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1. Chemical composition and in-vitro antioxidant and antimicrobial activity of the essential oil of Citrus aurantifolia L. leaves grown in Eastern Oman

Author

Maha S. Al-Aamri, B. Pharm, Nour M. Al-Abousi, B. Pharm, Sausan S. Al-Jabri, B. Pharm, Tanveer Alam, Ph.D, and Shah A. Khan, Ph.D

Subjects
Medicine (General), R5-920
Abstract

الملخص: اهداف البحث: يدرس هذه البحث مضادات الأكسدة، ونشاط مضادات الميكروبات والتركيب الكيميائي للزيت الأساسي الذي تم عزله من الأجزاء الهوائية لحمض أورانتيفوليا. طرق البحث: تم جمع الأوراق الطازجة لحمض أورانتيفوليا من مزارع محلية في مدينة صور (المنطقة الشرقية) لسلطنة عمان خلال الفترة من يونيو- يوليو، ٢٠١٥. استخدمت طريقة التقطير المائي لعزل الزيت الأساسي. واستخدم الغاز اللوني- قياس الطيف الكتلي للتعرف ولتحديد كمية المكونات الكيمائية في الزيت. استخدمت طريقة الجرف الحرة للجذور في – المختبر لتحديد نشاط مضادات الأكسدة للزيت الذي تم عزله من أوراق الليمون، بينما تم تقييم النشاط المضاد للجراثيم ضد البكتيريا إيجابية الغرام والبكتيريا سلبية الغرام بطريقة انتشار القرص. النتائج: تم تحديد ما مجموعة ثلاثة وثلاثين مركبا كيميائيا وتم العثور على د- ليمونين (٦٣.٣٥٪) ليكون المكون الأساسي. تم تحديد مكونات رئيسة أخرى بنسب مختلفة. كما أظهر الزيت الأساسي لحمض أورانتيفوليا نشاطا ممتازا مضادا للجراثيم ضد المكورات العنقودية الذهبية ونشاط متوسطا ضد السلالات الإشريكية القولونية. وأظهر الزيت كذلك نشاطا واعدا لمضادات الأكسدة في المختبر ولكنه أظهر نشاطا مضادا للجراثيم متوسطا. الاستنتاجات: يتميز الزيت الأساسي لأوراق الليمون العماني بمحتوى عالي من د- ليمونين الذي يجعله مفيدا في الغذاء، والصناعات الدوائية والعطور. Abstract: Objectives: This study investigated the chemical composition and the antioxidant and antimicrobial activities of the essential oil isolated from the aerial parts of Citrus aurantifolia L. Methods: Fresh Citrus aurantifolia L. leaves were collected from farms in Sur city, located in the Al-Sharqia (Eastern) region of the Sultanate of Oman, during June–July of 2015. The essential oil was isolated using hydrodistillation. Gas chromatography–mass spectrometry (GC–MS) was used to identify and quantify the chemical constituents of the oil. An in-vitro 1,1-diphenyl-2-picrylhydrazyl (DPPH) free radical scavenging method was used to determine the antioxidant activity of the isolated oil from the lime leaves while a disc diffusion method was used to evaluate the antibacterial activity against Gram-negative and Gram-positive bacteria. Results: Thirty-three chemical compounds were identified, with d-limonene (63.35%) forming the major constituent. Other prominent constituents include 3,7-dimethyl-2,6-octadien-1-ol (7.07%), geraniol (6.23%), E-citral (4.35%), Z-citral (3.29%), and β-ocimene (2.25%). The essential oil of Citrus aurantifolia L. leaves showed excellent antibacterial activity against Staphylococcus aureus and moderate activity against pathogenic Escherichia coli strains. The oil exhibited promising in-vitro antioxidant activity (IC50 value = 21.57 μg/mL) but showed moderate antibacterial activities. Conclusions: The essential oil from Omani lime leaves is characterized by a high d-limonene content, making it useful for food, pharmaceutical, and perfumery industries. الكلمات المفتاحية: النشاط المضاد للجراثيم, حمض أورانتيفوليا, الزيت الأساسي, د- ليمونين, Keywords: Antibacterial activity, Citrus aurantifolia, d-limonene, Essential oil, GC–MS

Published
2018
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6. A multilayered immune system through the lens of unconventional T cells

Author

Mayassi, T, Barreiro, LB, Rossjohn, J, Jabri, B, Mayassi, T, Barreiro, LB, Rossjohn, J, and Jabri, B

Abstract

The unconventional T cell compartment encompasses a variety of cell subsets that straddle the line between innate and adaptive immunity, often reside at mucosal surfaces and can recognize a wide range of non-polymorphic ligands. Recent advances have highlighted the role of unconventional T cells in tissue homeostasis and disease. In this Review, we recast unconventional T cell subsets according to the class of ligand that they recognize; their expression of semi-invariant or diverse T cell receptors; the structural features that underlie ligand recognition; their acquisition of effector functions in the thymus or periphery; and their distinct functional properties. Unconventional T cells follow specific selection rules and are poised to recognize self or evolutionarily conserved microbial antigens. We discuss these features from an evolutionary perspective to provide insights into the development and function of unconventional T cells. Finally, we elaborate on the functional redundancy of unconventional T cells and their relationship to subsets of innate and adaptive lymphoid cells, and propose that the unconventional T cell compartment has a critical role in our survival by expanding and complementing the role of the conventional T cell compartment in protective immunity, tissue healing and barrier function.

Published
2021

7. Co-adjuvant effects of retinoic acid and IL-15 induce inflammatory immunity to dietary antigens

Author

DePaolo, R.W., Abadie, V., Tang, F., Fehlner-Peach, H., Hall, J.A., Wang, W., Marietta, E.V., Kasarda, D.D., Waldmann, T.A., Murray, J.A., Semrad, C., Kupfer, S.S., Belkaid, Y., Guandalini, S., and Jabri, B.

Subjects
Tretinoin -- Health aspects -- Physiological aspects, Immune response -- Research, Antigens -- Health aspects -- Physiological aspects, Environmental issues, Science and technology, Zoology and wildlife conservation
Abstract

Under physiological conditions the gut-associated lymphoid tissues not only prevent the induction of a local inflammatory immune response, but also induce systemic tolerance to fed antigens (1,2). A notable exception is coeliac disease, where genetically susceptible individuals expressing human leukocyte antigen (HLA) HLA-DQ2 or HLA-DQ8 molecules develop inflammatory T-cell and antibody responses against dietary gluten, a protein present in wheat (3). The mechanisms underlying this dysregulated mucosal immune response to a soluble antigen have not been identified. Retinoic acid, a metabolite of vitamin A, has been shown to have a critical role in the induction of intestinal regulatory responses (4-6). Here we find in mice that in conjunction with IL-15, a cytokine greatly upregulated in the gut of coeliac disease patients (3,7), retinoic acid rapidly activates dendritic cells to induce JNK (also known as MAPK8) phosphorylation and release the proinflammatory cytokines IL-12p70 and IL-23. As a result, in a stressed intestinal environment, retinoic acid acted as an adjuvant that promoted rather than prevented inflammatory cellular and humoral responses to fed antigen. Altogether, these findings reveal an unexpected role for retinoic acid and IL-15 in the abrogation of tolerance to dietary antigens., Induction of regulatory intestinal responses to oral antigens prevents the subsequent development of systemic T-helper type-1 ([T.sub.H]1) responses to those antigens, a phenomenon referred to as oral tolerance (2). An [...]

Published
2011
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9. Chronic Inflammation Permanently Reshapes Tissue-Resident Immunity in Celiac Disease

Author

Mayassi, T., Ladell, K., Gudjonson, H., McLaren, J.E., Shaw, D.G., Tran, M.T., Rokicka, J.J., Lawrence, I., Grenier, J.C., Unen, V. van, Ciszewski, C., Dimaano, M., Sayegh, H.E., Kumar, V., Wijmenga, C., Green, P.H., Gokhale, R., Jericho, H., Semrad, C.E., Guandalini, S., Dinner, A.R., Kupfer, S.S., Reid, H.H., Barreiro, L.B., Rossjohn, J., Price, D.A., Jabri, B., Mayassi, T., Ladell, K., Gudjonson, H., McLaren, J.E., Shaw, D.G., Tran, M.T., Rokicka, J.J., Lawrence, I., Grenier, J.C., Unen, V. van, Ciszewski, C., Dimaano, M., Sayegh, H.E., Kumar, V., Wijmenga, C., Green, P.H., Gokhale, R., Jericho, H., Semrad, C.E., Guandalini, S., Dinner, A.R., Kupfer, S.S., Reid, H.H., Barreiro, L.B., Rossjohn, J., Price, D.A., and Jabri, B.

Abstract

Contains fulltext : 215586.pdf (publisher's version ) (Open Access), Tissue-resident lymphocytes play a key role in immune surveillance, but it remains unclear how these inherently stable cell populations respond to chronic inflammation. In the setting of celiac disease (CeD), where exposure to dietary antigen can be controlled, gluten-induced inflammation triggered a profound depletion of naturally occurring Vgamma4(+)/Vdelta1(+) intraepithelial lymphocytes (IELs) with innate cytolytic properties and specificity for the butyrophilin-like (BTNL) molecules BTNL3/BTNL8. Creation of a new niche with reduced expression of BTNL8 and loss of Vgamma4(+)/Vdelta1(+) IELs was accompanied by the expansion of gluten-sensitive, interferon-gamma-producing Vdelta1(+) IELs bearing T cell receptors (TCRs) with a shared non-germline-encoded motif that failed to recognize BTNL3/BTNL8. Exclusion of dietary gluten restored BTNL8 expression but was insufficient to reconstitute the physiological Vgamma4(+)/Vdelta1(+) subset among TCRgammadelta(+) IELs. Collectively, these data show that chronic inflammation permanently reconfigures the tissue-resident TCRgammadelta(+) IEL compartment in CeD. VIDEO ABSTRACT.

Published
2019

10. Cytokine release and gastrointestinal symptoms after gluten challenge in celiac disease

Author

Goel, G, Tye-Din, JA, Qiao, S-W, Russell, AK, Mayassi, T, Ciszewski, C, Sarna, VK, Wang, S, Goldstein, KE, Dzuris, JL, Williams, LJ, Xavier, RJ, Lundin, KEA, Jabri, B, Sollid, LM, Anderson, RP, Goel, G, Tye-Din, JA, Qiao, S-W, Russell, AK, Mayassi, T, Ciszewski, C, Sarna, VK, Wang, S, Goldstein, KE, Dzuris, JL, Williams, LJ, Xavier, RJ, Lundin, KEA, Jabri, B, Sollid, LM, and Anderson, RP

Abstract

Celiac disease (CeD), caused by immune reactions to cereal gluten, is treated with gluten -elimination diets. Within hours of gluten exposure, either perorally or extraorally by intradermal injection, treated patients experience gastrointestinal symptoms. To test whether gluten exposure leads to systemic cytokine production time -related to symptoms, series of multiplex cytokine measurements were obtained in CeD patients after gluten challenge. Peptide injection elevated at least 15 plasma cytokines, with IL-2, IL-8, and IL-10 being most prominent (fold-change increase at 4 hours of 272, 11, and 1.2, respectively). IL-2 and IL-8 were the only cytokines elevated at 2 hours, preceding onset of symptoms. After gluten ingestion, IL-2 was the earliest and most prominent cytokine (15-fold change at 4 hours). Supported by studies of patient-derived gluten-specific T cell clones and primary lymphocytes, our observations indicate that gluten-specific CD4+ T cells are rapidly reactivated by antigen -exposure likely causing CeD-associated gastrointestinal symptoms.

Published
2019

12. A locus at 7p14.3 predisposes to refractory celiac disease progression from celiac disease

Author

Hrdlickova, B., Mulder, C.J., Malamut, G., Meresse, B., Platteel, M., Kamatani, Y., Ricano-Ponce, I., Wanrooij, R.L.J. van, Zorro, M.M., Bonder, M. Jan, Gutierrez-Achury, J., Cellier, C., Zhernakova, A., Nijeboer, P., Galan, P., Withoff, S., Lathrop, M., Bouma, G., Xavier, R.J., Jabri, B., Bensussan, N.C., Wijmenga, C., Kumar, V., Hrdlickova, B., Mulder, C.J., Malamut, G., Meresse, B., Platteel, M., Kamatani, Y., Ricano-Ponce, I., Wanrooij, R.L.J. van, Zorro, M.M., Bonder, M. Jan, Gutierrez-Achury, J., Cellier, C., Zhernakova, A., Nijeboer, P., Galan, P., Withoff, S., Lathrop, M., Bouma, G., Xavier, R.J., Jabri, B., Bensussan, N.C., Wijmenga, C., and Kumar, V.

Abstract

Item does not contain fulltext, BACKGROUND: Approximately 5% of patients with celiac disease (CeD) do not respond to a gluten-free diet and progress to refractory celiac disease (RCD), a severe progression that is characterized by infiltration of intraepithelial T lymphocytes. Patients with RCD type II (RCDII) show clonal expansions of intraepithelial T lymphocytes that result in a poor prognosis and a high mortality rate through development of aggressive enteropathy-associated T-cell lymphoma. It is not known whether genetic variations play a role in severe progression of CeD to RCDII. PATIENTS AND METHODS: We performed the first genome-wide association study to identify the causal genes for RCDII and the molecular pathways perturbed in RCDII. The genome-wide association study was performed in 38 Dutch patients with RCDII, and the 15 independent top-associated single nucleotide polymorphism (SNP) variants (P<5x10) were replicated in 56 independent French and Dutch patients with RCDII. RESULTS: After replication, SNP rs2041570 on chromosome 7 was significantly associated with progression to RCDII (P=2.37x10, odds ratio=2.36) but not with CeD susceptibility. SNP rs2041570 risk allele A was associated with lower levels of FAM188B expression in blood and small intestinal biopsies. Stratification of RCDII biopsies based on rs2041570 genotype showed differential expression of innate immune and antibacterial genes that are expressed in Paneth cells. CONCLUSION: We have identified a novel SNP associated with the severe progression of CeD to RCDII. Our data suggest that genetic susceptibility to CeD might be distinct from the progression to RCDII and suggest a role for Paneth cells in RCDII progression.

Published
2018

14. Reovirus infection triggers inflammatory responses to dietary antigens and development of celiac disease

Author

Bouziat, R. (Romain), Hinterleitner, R. (Reinhard), Brown, J.J. (Judy J.), Stencel-Baerenwald, J.E. (Jennifer E.), Ikizler, M. (Mine), Mayassi, T. (Toufic), Meisel, M. (Marlies), Kim, S.M. (Sangman M.), Discepolo, V. (Valentina), Pruijssers, A.J. (Andrea J.), Ernest, J.D. (Jordan D.), Iskarpatyoti, J.A. (Jason A.), Costes, L.M.M. (Léa), Lawrence, I. (Ian), Palanski, B.A. (Brad A.), Varma, M. (Mukund), Zurenski, M.A. (Matthew A.), Khomandiak, S. (Solomiia), McAllister, N. (Nicole), Aravamudhan, P. (Pavithra), Boehme, K.W. (Karl W.), Hu, F. (Fengling), Samsom, J.N. (Janneke), Reinecker, H.-C. (Hans-Christian), Kupfer, S.S. (Sonia S.), Guandalini, S. (Stefano), Semrad, C.E. (Carol E.), Abadie, V. (Valérie), Khosla, C. (Chaitan), Barreiro, L.B. (Luis B.), Xavier, R.J. (Ramnik J.), Ng, A. (Aylwin), Dermody, T.S. (Terence S.), Jabri, B. (Bana), Bouziat, R. (Romain), Hinterleitner, R. (Reinhard), Brown, J.J. (Judy J.), Stencel-Baerenwald, J.E. (Jennifer E.), Ikizler, M. (Mine), Mayassi, T. (Toufic), Meisel, M. (Marlies), Kim, S.M. (Sangman M.), Discepolo, V. (Valentina), Pruijssers, A.J. (Andrea J.), Ernest, J.D. (Jordan D.), Iskarpatyoti, J.A. (Jason A.), Costes, L.M.M. (Léa), Lawrence, I. (Ian), Palanski, B.A. (Brad A.), Varma, M. (Mukund), Zurenski, M.A. (Matthew A.), Khomandiak, S. (Solomiia), McAllister, N. (Nicole), Aravamudhan, P. (Pavithra), Boehme, K.W. (Karl W.), Hu, F. (Fengling), Samsom, J.N. (Janneke), Reinecker, H.-C. (Hans-Christian), Kupfer, S.S. (Sonia S.), Guandalini, S. (Stefano), Semrad, C.E. (Carol E.), Abadie, V. (Valérie), Khosla, C. (Chaitan), Barreiro, L.B. (Luis B.), Xavier, R.J. (Ramnik J.), Ng, A. (Aylwin), Dermody, T.S. (Terence S.), and Jabri, B. (Bana)

Abstract

Viral infections have been proposed to elicit pathological processes leading to the initiation of T helper 1 (TH1) immunity against dietary gluten and celiac disease (CeD). To test this hypothesis and gain insights into mechanisms underlying virus-induced loss of tolerance to dietary antigens, we developed a viral infection model that makes use of two reovirus strains that infect the intestine but differ in their immunopathological outcomes. Reovirus is an avirulent pathogen that elicits protective immunity, but we discovered that it can nonetheless disrupt intestinal immune homeostasis at inductive and effector sites of oral tolerance by suppressing peripheral regulatory T cell (pTreg) conversion and promoting TH1 immunity to dietary antigen. Initiation of TH1 immunity to dietary antigen was dependent on interferon regulatory factor 1 and dissociated from suppression of pTreg conversion, which was mediated by type-1 interferon. Last, our study in humans supports a role for infection with reovirus, a seemingly innocuous virus, in triggering the development of CeD.

Published
2017
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15. A.07 Genomics of atypical dyskinetic cerebral palsy – opportunities for improved diagnosis and management

Author

Goez, H, primary, Matthews, A, additional, Al Jabri, B, additional, Blydt-Hansen, I, additional, Andersen, J, additional, Tarailo-Graovac, M, additional, Drogemoller, B, additional, Shyr, C, additional, Lee, J, additional, Ghani, A, additional, Sinclair, G, additional, Ross, C, additional, Wasserman, W, additional, McKinnon, M, additional, Horvath, G, additional, and Van Karnebeek, C, additional

Published
2017
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16. Genomics of atypical dyskinetic cerebral palsy – opportunities for improved diagnosis and management

Author

Goez, H., primary, Matthews, A., additional, Al-Jabri, B., additional, Blydt-Hansen, I., additional, Andersen, J., additional, Tarailo-Graovac, M., additional, Drogemoller, B.I., additional, Shyr, C., additional, Lee, J., additional, Ghani, A., additional, Sinclair, G., additional, Ross, C.J., additional, Wassereman, W.W., additional, McKinnon, M., additional, Horvath, G., additional, and Van-Karnebeek, C., additional

Published
2017
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24. Interplay between type-1 interferon and IL15 in celiac disease

Author

Discepolo, V., primary, Bouziat, R., additional, Durling, B., additional, Lania, G., additional, Auricchio, R., additional, Cuomo, M., additional, Sarno, M., additional, Auricchio, S., additional, Troncone, R., additional, Barone, M.V., additional, Guandalini, S., additional, Barreiro, L.B., additional, and Jabri, B., additional

Published
2013
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25. CO33 BOTH GLIADIN PEPTIDE P31–43 AND TOLL-LIKE RECEPTOR 7 LIGAND, LOXORIBINE, ARE ABLE TO INDUCE IFN-ALPHA PATHWAY, INCREASING MXA EXPRESSION

Author

Sarno, M., primary, Nanayakkara, M., additional, Lania, G., additional, Maglio, M., additional, Gaito, A., additional, Ferrara, K., additional, Cuomo, M., additional, Ponticelli, D., additional, Aitoro, R., additional, Discepolo, V., additional, Jabri, B., additional, Troncone, R., additional, Auricchio, S., additional, and Barone, M.V., additional

Published
2012
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28. Distinction between coeliac disease and refractory sprue: a simple immunohistochemical method

Author

Patey‐Mariaud de Serre, N, primary, Cellier, C, additional, Jabri, B, additional, Delabesse, E, additional, Verkarre, V, additional, Roche, B, additional, Lavergne, A, additional, Brière, J, additional, Mauvieux, L, additional, Leborgne, M, additional, Barbier, J P, additional, Modigliani, R, additional, Matuchansky, C, additional, Macintyre, E, additional, Cerf‐Bensussan, N, additional, and Brousse, N, additional

Published
2000
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29. Refractory sprue maybe the missing link between celiac disease and enteropathy associated T-cell lymphoma. Clinical, pathological, phenotypic and molecular evidence in a national cooperative study

Author

Cellier, C., primary, Helmer, C., additional, Patey, N., additional, Delabesse, E., additional, Matuchansky, C., additional, Jabri, B., additional, Modigliani, R., additional, Lerebours, E., additional, Delchier, J-C, additional, Colombel, J-F, additional, Verkarre, V., additional, Barbier, J-P, additional, Caf-Bensussein, N., additional, and Brousse, N., additional

Published
2000
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30. Chronic Intestinal Pseudo-Obstruction Syndrome in Pediatric Patients

Author

Goulet, O., primary, Jobert-Giraud, A., additional, Michel, J., additional, Jaubert, F., additional, Lortat-Jacob, S., additional, Colomb, V., additional, Cuenod-Jabri, B., additional, Jan, D., additional, Brousse, N., additional, Gaillard, D., additional, Nihoul-Fékéte, C., additional, and Ricour, C., additional

Published
1999
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31. Small Bowel Transplantation Alone or With the Liver in Children: Changes by Using FK506

Author

Goulet, O., primary, Michel, J.L., additional, Jobert, A., additional, Damotte, D., additional, Colomb, V., additional, Cezard, J.P., additional, Lacaille, F., additional, Faure, C., additional, Jan, D., additional, Jabri, B., additional, Sarnacki, S., additional, Brousse, N., additional, Peuchmaur, M., additional, Aigrain, Y., additional, Ricour, C., additional, and Revillon, Y., additional

Published
1998
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32. Refractory spure: Histological and phenotypical features and outcome

Author

Cellier, C., primary, Helmer, C., additional, Patey, N., additional, Jabri, B., additional, Matuchansky, C., additional, Modigliani, R., additional, Lerebours, E., additional, Colombel, JF., additional, Delchier, JC., additional, Mauvieux, L., additional, Macintyre, E., additional, Cerf-Bensussan, N., additional, Brousse, N., additional, and Barbier, JP., additional

Published
1998
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34. Colites graves chez l'enfant de moins de 3 ans

Author

Cuénod-Jabri, B, primary, Patey, N, additional, Turck, D, additional, Canioni, D, additional, Besnard, M, additional, Mougenot, JF, additional, Martin de Lassalle, E, additional, Cézard, JP, additional, Fékété, N, additional, Lecomte, M, additional, Brousse, N, additional, Colomb, V, additional, Ricour, C, additional, and Goulet, O, additional

Published
1998
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38. SEVERE COLITIS IN CHILDREN BELOW 3 YEARS OF AGE.

Author

Cuenod-Jabri, B., primary, Patey, N., additional, Canioni, D., additional, Turck, D., additional, Martin-Delassale, M., additional, Besnard, M., additional, Mougenot, J-F., additional, Lecomte, E., additional, Fekete, C., additional, Cezard, J-P., additional, Brousse, N., additional, Colomb, V., additional, Ricour, C., additional, and Goulet, O., additional

Published
1997
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42. Relationship of HLA-DQ8 and severity of celiac disease: Comparison of New York and Parisian cohorts

Author

Johnson, T.C., Diamond, B., Memeo, L., Negulescu, H., Hovhanissyan, Z., Verkarre, V., Rotterdam, H., Fasano, A., Caillat-Zucman, S., Grosdidier, E., Winchester, R., Cellier, C., Jabri, B., and Green, P.H.R.

Abstract

Background & Aims: Celiac disease is a polygenic disorder associated with HLA-DQ2 or HLA-DQ8, which are present in greater than 90% of patients. The disease is considered milder in the United States compared with Europe. We assessed whether differences in the frequency of HLA type may account for differences in severity of the disease by using cohorts of patients from New York and Paris. Methods: HLA-DQ typing was performed on patients with celiac disease in New York and Paris. Clinical and pathologic data were compared between the New York and Parisian cohorts and also correlated with the different HLA types (HLA-DQ2, HLA-DQ2/-DQ8, HLA-DQ8). Results: Among these patients, the disease was milder in the New York cohort compared with the Parisian cohort. There were fewer patients with a classical presentation (45% and 89%, respectively; P < 0.001) and less severe pathology (total villous atrophy, 64% and 89%, respectively; P < 0.05), and less marked intraepithelial lymphocytosis (intraepithelial leukocytes [IELs]/100 enterocytes, 48.1 and 82.5, respectively; P < 0.0001). HLA-DQ2 homozygotes were less prevalent in the New York cohort compared with the Parisian cohort (59% and 79%, respectively; P = 0.08). HLA-DQ8 alleles were more prevalent in the New York cohort compared with the Parisian cohort (41% and 21%, respectively; P = 0.026). There was, however, no difference in the clinical or pathologic parameters of severity when we compared the groups based on HLA type. Conclusions: HLA-DQ8 alleles were increased in the New York cohort of patients with celiac disease; however, this did not account for less severe manifestations of the disease.

Published
2004
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43. Abnormal intestinal intraepithelial lymphocytes in refractory sprue

Author

Cellier, C., Patey, N., Mauvieux, L., Jabri, B., Delabesse, E., Cervoni, J., Burtin, M., Guy-Grand, D., Bouhnik, Y., Modigliani, R., Barbier, J., Macintyre, E., Brousse, N., and Cerf-Bensussan, N.

Abstract

Background & Aims: The etiology of refractory sprue is unclear. To gain insight into its pathogenesis, the phenotype and T-cell receptor (TCR) gene rearrangement status of intestinal lymphocytes were analyzed in a group of patients with clinical or biological features of celiac disease but either initially or subsequently refractory to a gluten-free diet. Methods: Intestinal biopsy specimens were obtained from 26 adults: 6 patients with refractory sprue, 7 patients with active celiac disease, and 13 normal controls. The phenotype of intestinal lymphocytes was studied by immunohistochemistry and, in 3 patients with refractory sprue, by cytometry of lymphocytes purified from intestinal biopsy specimens. TCR rearrangements were assessed by studying TCR@cV-J junctional regions from DNA extracted from intestinal biopsy specimens and purified intestinal lymphocytes. Results: In the 6 patients with refractory sprue, but not in normal controls or patients with active celiac disease, the intestinal epithelium was massively infiltrated by small lymphocytes that lacked CD8, CD4, and TCR, contained intracytoplasmic but not surface CD3@e chains, and exhibited restricted TCR@c gene rearrangements. Conclusions: Refractory sprue is associated with an abnormal subset of intraepithelial lymphocytes containing CD3@e and restricted rearrangements of the TCR@c chain but lacking surface expression of T-cell receptors. GASTROENTEROLOGY 1998;114:471-481

Published
1998
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44. Nexvax2 (R), a Peptide-Based Antigen-Specific Immunotherapy, Administered Intra-Dermally Three-Times Over 15-Days attenuates Responsiveness to Immuno-Dominant Gluten Peptides in HLA-DQ2.5+People With Celiac Disease (CeD)

Author

Goel, G., Andrews, J. M., Krause, R., Fogel, R., Barish, C. F., A James M Daveson, Epstein, R., King, T., Kinney, T., Krishnarajah, J., Miner, P. B., Tye-Din, J. A., Girardin, A., Taavela, J., Popp, A., Maki, M., Goldstein, K., Dzuris, J. L., Williams, L. J., Xavier, R., Sollid, L. M., Jabri, B., and Anderson, R. P.

45. A Single Intradermal (ID) Injection of Nexvax2 (R), a Peptide Composition With Dominant Epitopes for Gluten-Reactive CD4+T Cells, Activates T Cells and Triggers Acute Gastrointestinal Symptoms in HLA-DQ2.5+People With Celiac Disease (CeD)

Author

Goel, G., Mayassi, T., Qiao, S. W., Ciszewski, C., King, T., A James M Daveson, Andrews, J. M., Krishnarajah, J., Krause, R., Brown, G. J., Fogel, R., Barish, C. F., Epstein, R., Kinney, T., Miner, P. B., Tye-Din, J. A., Girardin, A., Goldstein, K., Dzuris, J. L., Williams, L. J., Xavier, R., Sollid, L. M., Jabri, B., and Anderson, R. P.

47. IL-15, gluten and HLA-DQ8 drive tissue destruction in coeliac disease

Author

Romain Bouziat, Cezary Ciszewski, Joseph A. Murray, Chaitan Khosla, Thomas Lejeune, Eric V. Marietta, Jean-Christophe Grenier, Olivier Tastet, Brad A. Palanski, Vania Yotova, Luis B. Barreiro, Irina E. Horwath, Matthew A. Zurenski, Bana Jabri, Ian Lawrence, Jordan D. Ernest, Jordan Voisine, Sangman M. Kim, Kaushik Panigrahi, Mohamed B.F. Hawash, Valérie Abadie, Valentina Discepolo, Anne Dumaine, Abadie, V., Kim, S. M., Lejeune, T., Palanski, B. A., Ernest, J. D., Tastet, O., Voisine, J., Discepolo, V., Marietta, E. V., Hawash, M. B. F., Ciszewski, C., Bouziat, R., Panigrahi, K., Horwath, I., Zurenski, M. A., Lawrence, I., Dumaine, A., Yotova, V., Grenier, J. -C., Murray, J. A., Khosla, C., Barreiro, L. B., and Jabri, B.

Subjects
CD4-Positive T-Lymphocytes, Male, Glutens, Tissue transglutaminase, Mice, Transgenic, Human leukocyte antigen, Biology, Coeliac disease, Article, Interferon-gamma, Mice, HLA-DQ Antigens, medicine, Cytotoxic T cell, Humans, Animals, Villous atrophy, Interleukin-15, Lamina propria, Multidisciplinary, Innate immune system, Animal, Microfilament Proteins, HLA-DQ Antigen, nutritional and metabolic diseases, medicine.disease, digestive system diseases, Celiac Disease, medicine.anatomical_structure, CD4-Positive T-Lymphocyte, Interleukin 15, Immunology, biology.protein, Female, Gluten, Human
Abstract

Coeliac disease is a complex, polygenic inflammatory enteropathy caused by exposure to dietary gluten that occurs in a subset of genetically susceptible individuals who express either the HLA-DQ8 or HLA-DQ2 haplotypes1,2. The need to develop non-dietary treatments is now widely recognized3, but no pathophysiologically relevant gluten- and HLA-dependent preclinical model exists. Furthermore, although studies in humans have led to major advances in our understanding of the pathogenesis of coeliac disease4, the respective roles of disease-predisposing HLA molecules, and of adaptive and innate immunity in the development of tissue damage, have not been directly demonstrated. Here we describe a mouse model that reproduces the overexpression of interleukin-15 (IL-15) in the gut epithelium and lamina propria that is characteristic of active coeliac disease, expresses the predisposing HLA-DQ8 molecule, and develops villous atrophy after ingestion of gluten. Overexpression of IL-15 in both the epithelium and the lamina propria is required for the development of villous atrophy, which demonstrates the location-dependent central role of IL-15 in the pathogenesis of coeliac disease. In addition, CD4+ T cells and HLA-DQ8 have a crucial role in the licensing of cytotoxic T cells to mediate intestinal epithelial cell lysis. We also demonstrate a role for the cytokine interferon-γ (IFNγ) and the enzyme transglutaminase 2 (TG2) in tissue destruction. By reflecting the complex interaction between gluten, genetics and IL-15-driven tissue inflammation, this mouse model provides the opportunity to both increase our understanding of coeliac disease, and develop new therapeutic strategies. An HLA- and gluten-dependent mouse model of coeliac disease with villous atrophy provides evidence for the cooperative role of IL-15 and gluten-specific CD4+ T cells in licensing the full activation of cytotoxic T cells that are necessary for inducing epithelial damage.

Published
2020

48. Tissue alarmins and adaptive cytokine induce dynamic and distinct transcriptional responses in tissue-resident intraepithelial cytotoxic T lymphocytes

Author

Rinse K. Weersma, Bana Jabri, Raul Aguirre-Gamboa, Sebo Withoff, Toufic Mayassi, Shixian Hu, Cezary Ciszewski, Yang Li, Maria M. Zorro, Iris Jonkers, Donatella Barisani, Cisca Wijmenga, Groningen Institute for Gastro Intestinal Genetics and Immunology (3GI), Molecular Neuroscience and Ageing Research (MOLAR), Department of Health and Life Sciences, Zorro, M, Aguirre-Gamboa, R, Mayassi, T, Ciszewski, C, Barisani, D, Hu, S, Weersma, R, Withoff, S, Li, Y, Wijmenga, C, Jabri, B, Jonkers, I, and CiiM, Zentrum für individualisierte Infektionsmedizin, Feodor-Lynen-Str.7, 30625 Hannover.

Subjects
0301 basic medicine, medicine.medical_treatment, Autoimmunity, Intraepithelial lymphocytes, DISEASE, Transcriptome, Tissue-resident lymphocytes, 0302 clinical medicine, Autoimmune disease, IL-21, Immunology and Allergy, Cytotoxic T cell, Alarmins, Intestinal Mucosa, Promoter Regions, Genetic, Interleukin-15, ARCHITECTURE, Interleukin, ASSOCIATION, 3. Good health, Cell biology, Cytokine, IL-15, Interleukin 15, Cytokines, EXPRESSION, SUSCEPTIBILITY LOCI, Immunology, EFFECTOR CTL, GENETIC RISK, IMMUNITY, Biology, IFN beta, Article, Tissue-resident lymphocyte, 03 medical and health sciences, medicine, Humans, Epigenetics, 030203 arthritis & rheumatology, Cytotoxic T lymphocyte, Intraepithelial lymphocyte, IDENTIFICATION, Gene Expression Profiling, medicine.disease, Inflammatory Bowel Diseases, Cytotoxic T lymphocytes, Celiac Disease, 030104 developmental biology, Gene Expression Regulation, CELLS, IFNβ, T-Lymphocytes, Cytotoxic
Abstract

The respective effects of tissue alarmins interleukin (IL)-15 and interferon beta (IFNβ), and IL-21 produced by T cells on the reprogramming of cytotoxic T lymphocytes (CTLs) that cause tissue destruction in celiac disease is poorly understood. Transcriptomic and epigenetic profiling of primary intestinal CTLs showed massive and distinct temporal transcriptional changes in response to tissue alarmins, while the impact of IL-21 was limited. Only anti-viral pathways were induced in response to all the three stimuli, albeit with differences in dynamics and strength. Moreover, changes in gene expression were primarily independent of changes in H3K27ac, suggesting that other regulatory mechanisms drive the robust transcriptional response. Finally, we found that IL-15/IFNβ/IL-21 transcriptional signatures could be linked to transcriptional alterations in risk loci for complex immune diseases. Together these results provide new insights into molecular mechanisms that fuel the activation of CTLs under conditions that emulate the inflammatory environment in patients with autoimmune diseases., Highlights • We report the epigenetic and transcriptomic response of IE-CTLs to tissue-derived alarmins and adaptive cytokine. • IL-15 and IFNβ induce massive and distinct transcriptional changes in IE-CTLs, while the impact of IL-21 was limited. • Genes associated with immune-mediated intestinal diseases are enriched in genes responding to IL-15, IFNβ and IL-21 in IE-CTLs.

Published
2019

49. Reovirus infection triggers inflammatory responses to dietary antigens and development of celiac disease

Author

Mine R. Ikizler, Fengling Hu, Matthew A. Zurenski, Bana Jabri, Karl W. Boehme, Hans Christian Reinecker, Chaitan Khosla, Brad A. Palanski, Sangman M. Kim, Romain Bouziat, Jason A. Iskarpatyoti, Valentina Discepolo, Ian Lawrence, Jordan D. Ernest, Léa M.M. Costes, Valérie Abadie, Mukund Varma, Janneke N. Samsom, Terence S. Dermody, Solomiia Khomandiak, Ramnik J. Xavier, Carol E. Semrad, Marlies Meisel, Andrea J. Pruijssers, Jennifer E. Stencel-Baerenwald, Nicole McAllister, Sonia S. Kupfer, Reinhard Hinterleitner, Toufic Mayassi, Pavithra Aravamudhan, Stefano Guandalini, Luis B. Barreiro, Judy J. Brown, Aylwin Ng, Bouziat, R., Hinterleitner, R., Brown, J. J., Stencel-Baerenwald, J. E., Ikizler, M., Mayassi, T., Meisel, M., Kim, S. M., Discepolo, V., Pruijssers, A. J., Ernest, J. D., Iskarpatyoti, J. A., Costes, L. M. M., Lawrence, I., Palanski, B. A., Varma, M., Zurenski, M. A., Khomandiak, S., Mcallister, N., Aravamudhan, P., Boehme, K. W., Hu, F., Samsom, J. N., Reinecker, H. -C., Kupfer, S. S., Guandalini, S., Semrad, C. E., Abadie, V., Khosla, C., Barreiro, L. B., Xavier, R. J., Ng, A., Dermody, T. S., Jabri, B., and Pediatrics

Subjects
0301 basic medicine, viruses, Autoimmunity, Receptor, Interferon alpha-beta, Disease, Mice, 0302 clinical medicine, Interferon, Reoviridae Infection, Pathogen, Multidisciplinary, Effector, Intestine, Intestines, medicine.anatomical_structure, Antigen, Interferon Type I, 030211 gastroenterology & hepatology, Genetic Engineering, Human, medicine.drug, Glutens, Regulatory T cell, Mice, Transgenic, Biology, Reoviridae, Article, Virus, 03 medical and health sciences, Immunity, Immune Tolerance, medicine, Animals, Humans, Antigens, Autoantibodies, Inflammation, Transglutaminases, Animal, Th1 Cells, biochemical phenomena, metabolism, and nutrition, Virology, Diet, Reoviridae Infections, Mice, Inbred C57BL, Celiac Disease, Disease Models, Animal, 030104 developmental biology, IRF1, Immunology, Gluten, Interferon Regulatory Factor-1
Abstract

Viral infections have been proposed to elicit pathological processes leading to the initiation of T helper 1 (TH1) immunity against dietary gluten and celiac disease (CeD). To test this hypothesis and gain insights into mechanisms underlying virus-induced loss of tolerance to dietary antigens, we developed a viral infection model that makes use of two reovirus strains that infect the intestine but differ in their immunopathological outcomes. Reovirus is an avirulent pathogen that elicits protective immunity, but we discovered that it can nonetheless disrupt intestinal immune homeostasis at inductive and effector sites of oral tolerance by suppressing peripheral regulatory T cell (pTreg) conversion and promoting TH1 immunity to dietary antigen. Initiation of TH1 immunity to dietary antigen was dependent on interferon regulatory factor 1 and dissociated from suppression of pTreg conversion, which was mediated by type-1 interferon. Last, our study in humans supports a role for infection with reovirus, a seemingly innocuous virus, in triggering the development of CeD.

Published
2017

50. Refractory sprue, coeliac disease, and enteropathy-associated T-cell lymphoma. French Coeliac Disease Study Group.

Author

Cellier, Christophe, Delabesse, Eric, Helmer, Christine, Patey, Natacha, Matuchansky, Claude, Jabri, Bana, Macintyre, Elizabeth, Cerf-Bensussan, Nadine, Brousse, Nicole, Cellier, C, Delabesse, E, Helmer, C, Patey, N, Matuchansky, C, Jabri, B, Macintyre, E, Cerf-Bensussan, N, and Brousse, N

Subjects
*SPRUE, *T cells, *CELIAC disease, *GENETIC mutation, *IMMUNOLOGY, *PHYSIOLOGY
Abstract

Background: Adult refractory sprue is a poorly defined disorder. We did a multicentre national study of patients with refractory sprue to characterise their clinical and pathological profile and outcome, and to assess the frequency and prognostic significance of phenotypic and molecular abnormalities in the intraepithelial T-cell population.Methods: Patients with severe symptomatic villous atrophy mimicking coeliac disease but refractory to a strict gluten-free diet, and with no initial evidence of overt lymphoma, were diagnosed at gastrointestinal referral centres between 1974 and 1998. Fixed and/or frozen duodenojejunal biopsy samples were reanalysed and immunostained with CD3 and CD8 monoclonal antibodies to find out the phenotype of intraepithelial lymphocytes (IEL). TCRgamma gene rearrangements were assessed on frozen biopsy samples by multiplex fluorescent PCR.Findings: There were 21 patients with refractory sprue and 20 controls with coeliacs disease. 16 (84%) of 19 assessed patients had an aberrant intraepithelial lymphoid intestinal population expressing intracytoplasmic CD3 but not surface CD8. Clonal intestinal TCRgamma gene rearrangements were found in 13 (76%) of 17 patients assessed; four (out of 12 assessed) had clonal dissemination to the blood. The 16 patients with an aberrant phenotype all had uncontrolled malabsorption; three subsequently developed overt T-cell lymphoma, and eight died. The three (16%) patients without aberrant clonal IEL made a complete clinical and histological recovery with steroid therapy plus a gluten-free diet.Interpretation: An immunophenotypically aberrant clonal intraepithelial T-cell population (similar to that of most cases of enteropathy-associated T-cell lymphoma) can be found in up to 75% of patients with refractory coeliac sprue; its identification by simple diagnostic techniques represents a marker of poor outcome (including occurrence of overt T-cell lymphoma). We suggest that refractory sprue associated with an aberrant clonal IEL may be the missing link between coeliac disease and T-cell lymphoma and may be classified as cryptic enteropathy-associated T-cell lymphoma. [ABSTRACT FROM AUTHOR]

Published
2000
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