9 results on '"Jabri, B"'
Search Results
2. Cytokine release and gastrointestinal symptoms after gluten challenge in celiac disease.
- Author
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Goel G, Tye-Din JA, Qiao SW, 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
- Subjects
- Adult, Aged, CD4-Positive T-Lymphocytes classification, CD4-Positive T-Lymphocytes metabolism, Celiac Disease immunology, Celiac Disease metabolism, Double-Blind Method, Female, Genotype, Glutens adverse effects, HLA Antigens genetics, Humans, Interleukin-10 blood, Interleukin-2 blood, Interleukin-8 blood, Male, Middle Aged, Placebo Effect, Vomiting etiology, Young Adult, Celiac Disease pathology, Cytokines blood, Glutens administration & dosage
- 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
- Full Text
- View/download PDF
3. Mitochondria maintain controlled activation state of epithelial-resident T lymphocytes.
- Author
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Konjar Š, Frising UC, Ferreira C, Hinterleitner R, Mayassi T, Zhang Q, Blankenhaus B, Haberman N, Loo Y, Guedes J, Baptista M, Innocentin S, Stange J, Strathdee D, Jabri B, and Veldhoen M
- Subjects
- Animals, Cardiolipins metabolism, Cells, Cultured, Coccidiosis parasitology, Disease Models, Animal, Eimeria immunology, Female, Humans, Intestinal Mucosa immunology, Intraepithelial Lymphocytes cytology, Lymphocyte Activation, Male, Mice, Mice, Inbred C57BL, Mice, Transgenic, Microscopy, Electron, Transmission, Mitochondria immunology, Mitochondria ultrastructure, Mitochondrial Membranes immunology, Mitochondrial Membranes metabolism, Mitochondrial Membranes ultrastructure, Primary Cell Culture, T-Lymphocytes cytology, Coccidiosis immunology, Intestinal Mucosa cytology, Intraepithelial Lymphocytes immunology, Mitochondria metabolism, T-Lymphocytes immunology
- Abstract
Epithelial-resident T lymphocytes, such as intraepithelial lymphocytes (IELs) located at the intestinal barrier, can offer swift protection against invading pathogens. Lymphocyte activation is strictly regulated because of its potential harmful nature and metabolic cost, and most lymphocytes are maintained in a quiescent state. However, IELs are kept in a heightened state of activation resembling effector T cells but without cytokine production or clonal proliferation. We show that this controlled activation state correlates with alterations in the IEL mitochondrial membrane, especially the cardiolipin composition. Upon inflammation, the cardiolipin composition is altered to support IEL proliferation and effector function. Furthermore, we show that cardiolipin makeup can particularly restrict swift IEL proliferation and effector functions, reducing microbial containment capability. These findings uncover an alternative mechanism to control cellular activity, special to epithelial-resident T cells, and a novel role for mitochondria, maintaining cells in a metabolically poised state while enabling rapid progression to full functionality., (Copyright © 2018 The Authors, some rights reserved; exclusive licensee American Association for the Advancement of Science. No claim to original U.S. Government Works.)
- Published
- 2018
- Full Text
- View/download PDF
4. Natural polyreactive IgA antibodies coat the intestinal microbiota.
- Author
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Bunker JJ, Erickson SA, Flynn TM, Henry C, Koval JC, Meisel M, Jabri B, Antonopoulos DA, Wilson PC, and Bendelac A
- Subjects
- Animals, Antibodies, Monoclonal genetics, Antibodies, Monoclonal immunology, Antigens immunology, B-Lymphocytes immunology, Bacteria immunology, Germ-Free Life immunology, Immunoglobulin A genetics, Intestinal Mucosa immunology, Intestinal Mucosa microbiology, Mice, Mice, Inbred C57BL, Peyer's Patches immunology, Symbiosis, Gastrointestinal Microbiome immunology, Immunoglobulin A immunology, Plasma Cells immunology
- Abstract
Large quantities of immunoglobulin A (IgA) are constitutively secreted by intestinal plasma cells to coat and contain the commensal microbiota, yet the specificity of these antibodies remains elusive. Here we profiled the reactivities of single murine IgA plasma cells by cloning and characterizing large numbers of monoclonal antibodies. IgAs were not specific to individual bacterial taxa but rather polyreactive, with broad reactivity to a diverse, but defined, subset of microbiota. These antibodies arose at low frequencies among naïve B cells and were selected into the IgA repertoire upon recirculation in Peyer's patches. This selection process occurred independent of microbiota or dietary antigens. Furthermore, although some IgAs acquired somatic mutations, these did not substantially influence their reactivity. These findings reveal an endogenous mechanism driving homeostatic production of polyreactive IgAs with innate specificity to microbiota., (Copyright © 2017 The Authors, some rights reserved; exclusive licensee American Association for the Advancement of Science. No claim to original U.S. Government Works.)
- Published
- 2017
- Full Text
- View/download PDF
5. Reovirus infection triggers inflammatory responses to dietary antigens and development of celiac disease.
- Author
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Bouziat R, Hinterleitner R, Brown JJ, Stencel-Baerenwald JE, Ikizler M, Mayassi T, Meisel M, Kim SM, Discepolo V, Pruijssers AJ, Ernest JD, Iskarpatyoti JA, Costes LM, Lawrence I, Palanski BA, Varma M, Zurenski MA, Khomandiak S, McAllister N, Aravamudhan P, Boehme KW, Hu F, Samsom JN, Reinecker HC, Kupfer SS, Guandalini S, Semrad CE, Abadie V, Khosla C, Barreiro LB, Xavier RJ, Ng A, Dermody TS, and Jabri B
- Subjects
- Animals, Diet adverse effects, Disease Models, Animal, Genetic Engineering, Humans, Immune Tolerance, Inflammation immunology, Interferon Regulatory Factor-1 genetics, Interferon Regulatory Factor-1 immunology, Interferon Type I genetics, Interferon Type I immunology, Intestines immunology, Intestines pathology, Intestines virology, Mice, Mice, Inbred C57BL, Mice, Transgenic, Receptor, Interferon alpha-beta genetics, Reoviridae genetics, Antigens immunology, Celiac Disease immunology, Celiac Disease virology, Glutens immunology, Inflammation virology, Reoviridae Infections complications, Reoviridae Infections immunology, Th1 Cells immunology
- Abstract
Viral infections have been proposed to elicit pathological processes leading to the initiation of T helper 1 (T
H 1) 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 TH 1 immunity to dietary antigen. Initiation of TH 1 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., (Copyright © 2017, American Association for the Advancement of Science.)- Published
- 2017
- Full Text
- View/download PDF
6. Commensal Bifidobacterium promotes antitumor immunity and facilitates anti-PD-L1 efficacy.
- Author
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Sivan A, Corrales L, Hubert N, Williams JB, Aquino-Michaels K, Earley ZM, Benyamin FW, Lei YM, Jabri B, Alegre ML, Chang EB, and Gajewski TF
- Subjects
- Animals, Bifidobacterium genetics, CD8-Positive T-Lymphocytes immunology, Dendritic Cells immunology, Fecal Microbiota Transplantation, Gene Expression Regulation, Humans, Immunity genetics, Immunotherapy methods, Lymphocyte Activation, Mice, Mice, Inbred C57BL, RNA, Ribosomal, 16S genetics, Symbiosis, T-Lymphocytes immunology, Tumor Microenvironment immunology, Antibodies, Monoclonal therapeutic use, B7-H1 Antigen immunology, Bifidobacterium immunology, Gastrointestinal Microbiome immunology, Melanoma immunology, Melanoma therapy, Skin Neoplasms immunology, Skin Neoplasms therapy
- Abstract
T cell infiltration of solid tumors is associated with favorable patient outcomes, yet the mechanisms underlying variable immune responses between individuals are not well understood. One possible modulator could be the intestinal microbiota. We compared melanoma growth in mice harboring distinct commensal microbiota and observed differences in spontaneous antitumor immunity, which were eliminated upon cohousing or after fecal transfer. Sequencing of the 16S ribosomal RNA identified Bifidobacterium as associated with the antitumor effects. Oral administration of Bifidobacterium alone improved tumor control to the same degree as programmed cell death protein 1 ligand 1 (PD-L1)-specific antibody therapy (checkpoint blockade), and combination treatment nearly abolished tumor outgrowth. Augmented dendritic cell function leading to enhanced CD8(+) T cell priming and accumulation in the tumor microenvironment mediated the effect. Our data suggest that manipulating the microbiota may modulate cancer immunotherapy., (Copyright © 2015, American Association for the Advancement of Science.)
- Published
- 2015
- Full Text
- View/download PDF
7. IMMUNOLOGY. Breaching the gut-vascular barrier.
- Author
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Bouziat R and Jabri B
- Subjects
- Animals, Humans, Capillary Permeability immunology, Intestines immunology, Intestines microbiology, Microbiota immunology, Salmonella Infections immunology, Salmonella typhimurium immunology
- Published
- 2015
- Full Text
- View/download PDF
8. The Toll-like receptor 2 pathway establishes colonization by a commensal of the human microbiota.
- Author
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Round JL, Lee SM, Li J, Tran G, Jabri B, Chatila TA, and Mazmanian SK
- Subjects
- Animals, Colon immunology, Colon microbiology, Germ-Free Life, Homeostasis, Humans, Immunity, Mucosal, Interleukin-10 metabolism, Metagenome, Mice, Mice, Inbred C57BL, Models, Biological, Polysaccharides, Bacterial immunology, Signal Transduction, Specific Pathogen-Free Organisms, Symbiosis, T-Lymphocytes, Regulatory immunology, Th17 Cells immunology, Toll-Like Receptor 2 immunology, Bacteroides fragilis growth & development, Bacteroides fragilis immunology, Immune Tolerance, Intestinal Mucosa immunology, Intestinal Mucosa microbiology, Polysaccharides, Bacterial metabolism, Toll-Like Receptor 2 metabolism
- Abstract
Mucosal surfaces constantly encounter microbes. Toll-like receptors (TLRs) mediate recognition of microbial patterns to eliminate pathogens. By contrast, we demonstrate that the prominent gut commensal Bacteroides fragilis activates the TLR pathway to establish host-microbial symbiosis. TLR2 on CD4(+) T cells is required for B. fragilis colonization of a unique mucosal niche in mice during homeostasis. A symbiosis factor (PSA, polysaccharide A) of B. fragilis signals through TLR2 directly on Foxp3(+) regulatory T cells to promote immunologic tolerance. B. fragilis lacking PSA is unable to restrain T helper 17 cell responses and is defective in niche-specific mucosal colonization. Therefore, commensal bacteria exploit the TLR pathway to actively suppress immunity. We propose that the immune system can discriminate between pathogens and the microbiota through recognition of symbiotic bacterial molecules in a process that engenders commensal colonization.
- Published
- 2011
- Full Text
- View/download PDF
9. Plague bacteria target immune cells during infection.
- Author
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Marketon MM, DePaolo RW, DeBord KL, Jabri B, and Schneewind O
- Subjects
- Animals, B-Lymphocytes immunology, B-Lymphocytes metabolism, B-Lymphocytes microbiology, Bacterial Outer Membrane Proteins genetics, Dendritic Cells immunology, Dendritic Cells metabolism, Flow Cytometry, Fluorescence, HeLa Cells, Humans, Macrophages immunology, Macrophages metabolism, Macrophages, Peritoneal microbiology, Mice, Mice, Inbred BALB C, Mice, Inbred C57BL, Microscopy, Fluorescence, Neutrophils immunology, Neutrophils metabolism, Plague immunology, Recombinant Fusion Proteins metabolism, T-Lymphocytes immunology, T-Lymphocytes metabolism, T-Lymphocytes microbiology, Transformation, Bacterial, Yersinia pestis metabolism, Bacterial Outer Membrane Proteins metabolism, Dendritic Cells microbiology, Macrophages microbiology, Neutrophils microbiology, Plague microbiology, Yersinia pestis pathogenicity
- Abstract
The plague is caused by the bacterium Yersinia pestis. Plague bacteria are thought to inject effector Yop proteins into host cells via the type III pathway. The identity of the host cells targeted for injection during plague infection is unknown. We found, using Yop beta-lactamase hybrids and fluorescent staining of live cells from plague-infected animals, that Y. pestis selected immune cells for injection. In vivo, dendritic cells, macrophages, and neutrophils were injected most frequently, whereas B and T lymphocytes were rarely selected. Thus, it appears that Y. pestis disables these cell populations to annihilate host immune responses during plague.
- Published
- 2005
- Full Text
- View/download PDF
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