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2. Identifying quantitative sncRNAs signature using global sequencing as a potential biomarker for tuberculosis diagnosis and their role in regulating host response

Author

Kaul, Sheetal, Nair, Vivek, Gcanga, Lorna, Lakshmanan, Vairavan, Kalamuddin, M., Anang, Vandana, Rathore, Sumit, Dhawan, Shikha, Alam, Tanvir, Khanna, Vishal, Lohiya, Sheelu, Ali, Shakir, Mannan, Shamim, Rade, Kirankumar, Parihar, Suraj P., Khanna, Ashwani, Malhotra, Pawan, Brombacher, Frank, Dasaradhi, Palakodeti VN, Guler, Reto, and Mohmmed, Asif

Published
2024
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6. The divergent outcome of IL-4Ra signalling on Foxp3 T regulatory cells in listeriosis and tuberculosis.

Author

Chia, Julius E., Rousseau, Robert P., Ozturk, Mumin, Poswayo, Sibongiseni K. L., Lucas, Rodney, Brombacher, Frank, and Parihar, Suraj P.

Subjects
REGULATORY T cells, TRANSCRIPTION factors, T cells, MYCOBACTERIUM tuberculosis, LISTERIOSIS
Abstract

Introduction: Forkhead box P3 (Foxp3) T regulatory cells are critical for maintaining self-tolerance, immune homeostasis, and regulating the immune system. Methods: We investigated interleukin-4 receptor alpha (IL-4Ra) signalling on T regulatory cells (Tregs) during Listeria monocytogenes (L. monocytogenes) infection using a mouse model on a BALB/c background, specifically with IL4Ra knockdown in Tregs (Foxp3creIL-4Ra−/lox). Results: We showed an impairment of Treg responses, along with a decreased bacterial burden and diminished tissue pathology in the liver and spleen, which translated into better survival. Mechanistically, we observed an enhancement of the Th1 signature, characterised by increased expression of the T-bet transcription factor and a greater number of effector T cells producing IFN-g, IL-2 following ex-vivo stimulation with heat-killed L. monocytogenes in Foxp3creIL-4Ra-/lox mice. Furthermore, CD8 T cells from Foxp3creIL-4Ra-/lox mice displayed increased cytotoxicity (Granzyme-B) with higher proliferation capacity (Ki-67), better survival (Bcl-2) with concomitant reduced apoptosis (activated caspase 3). In contrast to L. monocytogenes, Foxp3creIL-4Ra-/lox mice displayed similar bacterial burdens, lung pathology and survival during Mycobacterium tuberculosis (M. tuberculosis) infection, despite increased T cell numbers and IFN-g, TNF and IL-17 production. Conclusion: Our results demonstrated that the diminished IL-4Ra signalling on Foxp3+ T regulatory cells resulted in a loss of their functionality, leading to survival benefits in listeriosis but not in tuberculosis. [ABSTRACT FROM AUTHOR]

Published
2024
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7. Novel IL-4/HB-EGF-dependent crosstalk between eosinophils and macrophages controls liver regeneration after ischaemia and reperfusion injury.

Author

Yang Yang, Long Xu, Atkins, Constance, Kuhlman, Lily, Jie Zhao, Jong-Min Jeong, Yankai Wen, Moreno, Nicolas, Kang Ho Kim, Yu A. An, Fenfen Wang, Bynon, Steve, Villani, Vincenzo, Bin Gao, Brombacher, Frank, Harris, Raymond, Eltzschig, Holger K., Jacobsen, Elizabeth, and Ju, Cynthia

Subjects
PROLIFERATING cell nuclear antigen, EPIDERMAL growth factor receptors, KILLER cells, LIVER cells, CYTOTOXIC T cells, LIVER histology, LIVER surgery, LIPOXINS, HEPARIN
Published
2024
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9. Homeostatic IL-13 in healthy skin directs dendritic cell differentiation to promote TH2 and inhibit TH17 cell polarization

Author

Mayer, Johannes U., Hilligan, Kerry L., Chandler, Jodie S., Eccles, David A., Old, Samuel I., Domingues, Rita G., Yang, Jianping, Webb, Greta R., Munoz-Erazo, Luis, Hyde, Evelyn J., Wakelin, Kirsty A., Tang, Shiau-Choot, Chappell, Sally C., von Daake, Sventja, Brombacher, Frank, Mackay, Charles R., Sher, Alan, Tussiwand, Roxane, Connor, Lisa M., Gallego-Ortega, David, Jankovic, Dragana, Le Gros, Graham, Hepworth, Matthew R., Lamiable, Olivier, and Ronchese, Franca

Published
2021
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10. IgM and IgD B cell receptors differentially respond to endogenous antigens and control B cell fate.

Author

Noviski, Mark, Mueller, James L, Satterthwaite, Anne, Garrett-Sinha, Lee Ann, Brombacher, Frank, and Zikherman, Julie

Subjects
Germinal Center, B-Lymphocytes, Animals, Mice, Immunoglobulin D, Immunoglobulin M, Receptors, Antigen, B-Cell, Autoantibodies, Antigens, Signal Transduction, Immune Tolerance, Cell Lineage, B cell receptor, IgD, IgM, antibody responses, autoimmune response/disease, immunology, inflammation, mouse, signal transduction, Receptors, Antigen, B-Cell, Biochemistry and Cell Biology
Abstract

Naive B cells co-express two BCR isotypes, IgM and IgD, with identical antigen-binding domains but distinct constant regions. IgM but not IgD is downregulated on autoreactive B cells. Because these isotypes are presumed to be redundant, it is unknown how this could impose tolerance. We introduced the Nur77-eGFP reporter of BCR signaling into mice that express each BCR isotype alone. Despite signaling strongly in vitro, IgD is less sensitive than IgM to endogenous antigen in vivo and developmental fate decisions are skewed accordingly. IgD-only Lyn-/- B cells cannot generate autoantibodies and short-lived plasma cells (SLPCs) in vivo, a fate thought to be driven by intense BCR signaling induced by endogenous antigens. Similarly, IgD-only B cells generate normal germinal center, but impaired IgG1+ SLPC responses to T-dependent immunization. We propose a role for IgD in maintaining the quiescence of autoreactive B cells and restricting their differentiation into autoantibody secreting cells.

Published
2018

13. A Myeloid-Specific Lack of IL-4Rα Prevents the Development of Alternatively Activated Macrophages and Enhances Immunity to Experimental Cysticercosis

Author

Olguín, Jonadab E., primary, Corano-Arredondo, Edmundo, additional, Hernández-Gómez, Victoria, additional, Rivera-Montoya, Irma, additional, Rodríguez, Mario A., additional, Medina-Andrade, Itzel, additional, Arendse, Berenice, additional, Brombacher, Frank, additional, and Terrazas, Luis I., additional

Published
2024
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16. mTOR inhibition rescues osteopenia in mice with systemic sclerosis

Author

Chen, Chider, Akiyama, Kentaro, Wang, Dandan, Xu, Xingtian, Li, Bei, Moshaverinia, Alireza, Brombacher, Frank, Sun, Lingyun, and Shi, Songtao

Subjects
Stem Cell Research, Rare Diseases, Genetics, Osteoporosis, Underpinning research, 1.1 Normal biological development and functioning, Adipogenesis, Animals, Bone Diseases, Metabolic, Cell Differentiation, Cells, Cultured, Female, Fibrillin-1, Fibrillins, Flow Cytometry, Immunoblotting, Immunosuppressive Agents, Male, Mesenchymal Stem Cells, Mice, 129 Strain, Mice, Inbred C57BL, Mice, Knockout, Mice, Transgenic, Microfilament Proteins, Microscopy, Fluorescence, Osteogenesis, RNA Interference, Receptors, Cell Surface, Scleroderma, Systemic, Signal Transduction, Sirolimus, TOR Serine-Threonine Kinases, Transforming Growth Factor beta, Medical and Health Sciences, Immunology
Abstract

Fibrillin-1 (FBN1) deficiency-induced systemic sclerosis is attributed to elevation of interleukin-4 (IL4) and TGF-β, but the mechanism underlying FBN1 deficiency-associated osteopenia is not fully understood. We show that bone marrow mesenchymal stem cells (BMMSCs) from FBN1-deficient (Fbn1(+/-)) mice exhibit decreased osteogenic differentiation and increased adipogenic differentiation. Mechanistically, this lineage alteration is regulated by IL4/IL4Rα-mediated activation of mTOR signaling to down-regulate RUNX2 and up-regulate PPARγ2, respectively, via P70 ribosomal S6 protein kinase (P70S6K). Additionally, we reveal that activation of TGF-β/SMAD3/SP1 signaling results in enhancement of SP1 binding to the IL4Rα promoter to synergistically activate mTOR pathway in Fbn1(+/-) BMMSCs. Blockage of mTOR signaling by osteoblastic-specific knockout or rapamycin treatment rescues osteopenia phenotype in Fbn1(+/-) mice by improving osteogenic differentiation of BMMSCs. Collectively, this study identifies a previously unrecognized role of the FBN1/TGF-β/IL4Rα/mTOR cascade in BMMSC lineage selection and provides experimental evidence that rapamycin treatment may provide an anabolic therapy for osteopenia in Fbn1(+/-) mice.

Published
2015

17. Author Correction: Homeostatic IL-13 in healthy skin directs dendritic cell differentiation to promote TH2 and inhibit TH17 cell polarization

Author

Mayer, Johannes U., Hilligan, Kerry L., Chandler, Jodie S., Eccles, David A., Old, Samuel I., Domingues, Rita G., Yang, Jianping, Webb, Greta R., Munoz-Erazo, Luis, Hyde, Evelyn J., Wakelin, Kirsty A., Tang, Shiau-Choot, Chappell, Sally C., von Daake, Sventja, Brombacher, Frank, Mackay, Charles R., Sher, Alan, Tussiwand, Roxane, Connor, Lisa M., Gallego-Ortega, David, Jankovic, Dragana, Le Gros, Graham, Hepworth, Matthew R., Lamiable, Olivier, and Ronchese, Franca

Published
2022
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18. Immunoglobulin M regulates airway hyperresponsiveness independent of T helper 2 allergic inflammation

Author

Hadebe, Sabelo, primary, Savulescu, Anca Flavia, additional, Khumalo, Jermaine, additional, Jones, Katelyn, additional, Mangali, Sandisiwe, additional, Mthembu, Nontobeko, additional, Musaigwa, Fungai, additional, Maepa, Welcome, additional, Ndlovu, Hlumani, additional, Ngomti, Amkele, additional, Scibiorek, Martyna, additional, Okendo, Javan, additional, and Brombacher, Frank, additional

Published
2023
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23. Intestinal epithelial cell secretion of RELM-β protects against gastrointestinal worm infection

Author

Herbert, De'Broski R, Yang, Jun-Qi, Hogan, Simon P, Groschwitz, Kathryn, Khodoun, Marat, Munitz, Ariel, Orekov, Tatyana, Perkins, Charles, Wang, Quan, Brombacher, Frank, Urban, Joseph F, Rothenberg, Marc E, and Finkelman, Fred D

Subjects
Vaccine Related, Digestive Diseases, Autoimmune Disease, Infectious Diseases, Aetiology, 2.1 Biological and endogenous factors, Infection, Animals, Gastrointestinal Tract, Hormones, Ectopic, Intercellular Signaling Peptides and Proteins, Interleukin-13, Interleukin-4, Intestinal Mucosa, Mice, Mice, Inbred BALB C, Mice, Inbred C57BL, Nematospiroides dubius, Nippostrongylus, Medical and Health Sciences, Immunology
Abstract

Th2 cells drive protective immunity against most parasitic helminths, but few mechanisms have been demonstrated that facilitate pathogen clearance. We show that IL-4 and IL-13 protect against intestinal lumen-dwelling worms primarily by inducing intestinal epithelial cells (IECs) to differentiate into goblet cells that secrete resistin-like molecule (RELM) beta. RELM-beta is essential for normal spontaneous expulsion and IL-4-induced expulsion of Nippostrongylus brasiliensis and Heligmosomoides polygyrus, which both live in the intestinal lumen, but it does not contribute to immunity against Trichinella spiralis, which lives within IEC. RELM-beta is nontoxic for H. polygyrus in vitro but directly inhibits the ability of worms to feed on host tissues during infection. This decreases H. polygyrus adenosine triphosphate content and fecundity. Importantly, RELM-beta-driven immunity does not require T or B cells, alternative macrophage activation, or increased gut permeability. Thus, we demonstrate a novel mechanism for host protection at the mucosal interface that explains how stimulation of epithelial cells by IL-4 and IL-13 contributes to protection against parasitic helminthes that dwell in the intestinal lumen.

Published
2009

24. Intestinal epithelial cell secretion of RELM-beta protects against gastrointestinal worm infection.

Author

Herbert, De'Broski R, Yang, Jun-Qi, Hogan, Simon P, Groschwitz, Kathryn, Khodoun, Marat, Munitz, Ariel, Orekov, Tatyana, Perkins, Charles, Wang, Quan, Brombacher, Frank, Urban, Joseph F, Rothenberg, Marc E, and Finkelman, Fred D

Subjects
Gastrointestinal Tract, Intestinal Mucosa, Animals, Mice, Inbred BALB C, Mice, Inbred C57BL, Mice, Nematospiroides dubius, Nippostrongylus, Hormones, Ectopic, Interleukin-4, Interleukin-13, Hormones, Ectopic, Inbred BALB C, Inbred C57BL, Medical and Health Sciences, Immunology
Abstract

Th2 cells drive protective immunity against most parasitic helminths, but few mechanisms have been demonstrated that facilitate pathogen clearance. We show that IL-4 and IL-13 protect against intestinal lumen-dwelling worms primarily by inducing intestinal epithelial cells (IECs) to differentiate into goblet cells that secrete resistin-like molecule (RELM) beta. RELM-beta is essential for normal spontaneous expulsion and IL-4-induced expulsion of Nippostrongylus brasiliensis and Heligmosomoides polygyrus, which both live in the intestinal lumen, but it does not contribute to immunity against Trichinella spiralis, which lives within IEC. RELM-beta is nontoxic for H. polygyrus in vitro but directly inhibits the ability of worms to feed on host tissues during infection. This decreases H. polygyrus adenosine triphosphate content and fecundity. Importantly, RELM-beta-driven immunity does not require T or B cells, alternative macrophage activation, or increased gut permeability. Thus, we demonstrate a novel mechanism for host protection at the mucosal interface that explains how stimulation of epithelial cells by IL-4 and IL-13 contributes to protection against parasitic helminthes that dwell in the intestinal lumen.

Published
2009

26. Autoimmune Valvular Carditis Requires Endothelial Cell TNFR1 Expression

Author

Faragher, Jessica L., primary, Auger, Jennifer L., additional, Osinski, Victoria, additional, Meier, Lee A., additional, Engelson, Brianna J., additional, Firulyova, Maria M., additional, Gonzalez-Torres, Mayra I., additional, Brombacher, Frank, additional, Zaitsev, Konstantin, additional, Marath, Aubyn, additional, and Binstadt, Bryce A., additional

Published
2023
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31. Delayed Goblet Cell Hyperplasia, Acetylcholine Receptor Expression, and Worm Expulsion in SMC-Specific IL-4Rα–Deficient Mice

Author

Horsnell, William GC, Cutler, Antony J, Hoving, Claire J, Mearns, Helen, Myburgh, Elmarie, Arendse, Berenice, Finkelman, Fred D, Owens, Gary K, Erle, Dave, and Brombacher, Frank

Subjects
Biomedical and Clinical Sciences, Immunology, Digestive Diseases, Infectious Diseases, 2.1 Biological and endogenous factors, Aetiology, Inflammatory and immune system, Animals, Gene Expression, Goblet Cells, Hyperplasia, Interleukin-4 Receptor alpha Subunit, Mice, Muscle, Smooth, Nematode Infections, Receptors, Cholinergic, Microbiology, Medical Microbiology, Virology, Medical microbiology
Abstract

Interleukin 4 receptor alpha (IL-4Ralpha) is essential for effective clearance of gastrointestinal nematode infections. Smooth muscle cells are considered to play a role in the type 2 immune response-driven expulsion of gastrointestinal nematodes. Previous studies have shown in vitro that signal transducer and activator of transcription 6 signaling in response to parasitic nematode infection significantly increases smooth muscle cell contractility. Inhibition of the IL-4Ralpha pathway inhibits this response. How this response manifests itself in vivo is unknown. In this study, smooth muscle cell IL-4Ralpha-deficient mice (SM-MHC(Cre)IL-4Ralpha(-/lox)) were generated and characterized to uncover any role for IL-4/IL-13 in this non-immune cell type in response to Nippostrongylus brasiliensis infection. IL-4Ralpha was absent from alpha-actin-positive smooth muscle cells, while other cell types showed normal IL-4Ralpha expression, thus demonstrating efficient cell-type-specific deletion of the IL-4Ralpha gene. N. brasiliensis-infected SM-MHC(Cre)IL-4Ralpha(-/lox) mice showed delayed ability to resolve infection with significantly prolonged fecal egg recovery and delayed worm expulsion. The delayed expulsion was related to a delayed intestinal goblet cell hyperplasia, reduced T helper 2 cytokine production in the mesenteric lymph node, and reduced M3 muscarinic receptor expression during infection. Together, these results demonstrate that in vivo IL-4Ralpha-responsive smooth muscle cells are beneficial for N. brasiliensis expulsion by coordinating T helper 2 cytokine responses, goblet hyperplasia, and acetylcholine responsiveness, which drive smooth muscle cell contractions.

Published
2007

37. ajpheart.2020.pdf

Author

Song, Jianrui, Frieler, Ryan, E. Whitesall, Steven, Chung, Yutein, Vigil, Thomas, Muir, Lindsey A., Ma, Jun, Brombacher, Frank, N. Goonewardena, Sascha, Lumeng, Carey N., Goldstein, Daniel, and Mortensen, Richard M.

Subjects
Cardiology (incl. cardiovascular diseases)
Abstract

Interleukin-4 receptor a (IL4Ra) signaling plays an important role in cardiac remodeling during myocardial infarction (MI). However, the target cell type(s) of IL4Ra signaling during this remodeling remains unclear. Here, we investigated the contribution of endogenous myeloid-specific IL4Ra signaling in cardiac remodeling post-MI. We established a murine myeloid-specific IL4Ra knockout (MyIL4RaKO) model with LysM promoter-driven Cre recombination. Macrophages from MyIL4RaKO mice showed significant downregulation of alternatively activated macrophage markers but an upregulation of classical activated macrophage markers both in vitro and in vivo, indicating the successful inactivation of IL4Ra signaling in macrophages. To examine the role of myeloid IL4Ra during MI, we subjected MyIL4RaKO and littermate floxed control (FC) mice to MI. We found that cardiac function was significantly impaired as a result of myeloid-specific IL4Ra deficiency. This deficiency resulted in a dysregulated inflammatory response consisting of decreased production of anti-inflammatory cytokines. Myeloid IL4Ra deficiency also led to reduced collagen 1 deposition and an imbalance of matrix metalloproteinases (MMPs)/tissue inhibitors of metalloproteinases (TIMPs), with upregulated MMPs and downregulated TIMPs, which resulted in insufficient fibrotic remodeling. In conclusion, this study identifies that myeloid-specific IL4Ra signaling regulates inflammation and fibrotic remodeling during MI. Therefore, myeloid- specific activation of IL4Ra signaling could offer protective benefits after MI

Published
2023
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38. JAHA.2021.pdf

Author

Song, Jianrui, Frieler, Ryan, Vigil, Thomas, Ma, Jun, Brombacher, Frank, N. Goonewardena, Sascha, Goldstein, Daniel, and Mortensen, Richard M.

Subjects
Cardiology (incl. cardiovascular diseases)
Abstract

BACKGROUND: Hypertension-induced cardiovascular remodeling is characterized by chronic low-grade inflammation. Interleukin-4 receptor α (IL-4Rα) signaling is importantly involved in cardiovascular remodeling, however, the target cell type(s) is unclear. Here, we investigated the role of myeloid-specific IL-4Rα signaling in cardiovascular remodeling induced by angiotensin II and high salt. METHODS AND RESULTS: Myeloid IL-4Rα deficiency suppressed both the in vitro and in vivo expression of alternatively activated macrophage markers including Arg1 (arginase 1), Ym1 (chitinase 3-like 3), and Relmα/Fizz1 (resistin-like molecule α). After angiotensin II and high salt treatment, myeloid-specific IL-4Rα deficiency did not change hypertrophic remodeling within the heart and aorta. However, myeloid IL-4Rα deficiency resulted in a substantial reduction in fibrosis through the suppression of profibrotic pathways and the enhancement of antifibrotic signaling. Decreased fibrosis was associated with significant preservation of myocardial function in MyIL4RαKO mice and was mediated by attenuated alternative macrophage activation. CONCLUSIONS: Myeloid IL-4Rα signaling is substantially involved in fibrotic cardiovascular remodeling by controlling alternative macrophage activation and regulating fibrosis-related signaling. Inhibiting myeloid IL-4Rα signaling may be a potential strategy to prevent hypertensive cardiovascular diseases.

Published
2023
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39. Transcribed enhancers lead waves of coordinated transcription in transitioning mammalian cells

Author

FANTOM Consortium, Arner, Erik, Daub, Carsten O., Vitting-Seerup, Kristoffer, Andersson, Robin, Lilje, Berit, Drabløs, Finn, Lennartsson, Andreas, Rönnerblad, Michelle, Hrydziuszko, Olga, Vitezic, Morana, Freeman, Tom C., Alhendi, Ahmad M. N., Arner, Peter, Axton, Richard, Baillie, J. Kenneth, Beckhouse, Anthony, Bodega, Beatrice, Briggs, James, Brombacher, Frank, Davis, Margaret, Detmar, Michael, Ehrlund, Anna, Endoh, Mitsuhiro, Eslami, Afsaneh, Fagiolini, Michela, Fairbairn, Lynsey, Faulkner, Geoffrey J., Ferrai, Carmelo, Fisher, Malcolm E., Forrester, Lesley, Goldowitz, Daniel, Guler, Reto, Ha, Thomas, Hara, Mitsuko, Herlyn, Meenhard, Ikawa, Tomokatsu, Kai, Chieko, Kawamoto, Hiroshi, Khachigian, Levon M., Klinken, S. Peter, Kojima, Soichi, Koseki, Haruhiko, Klein, Sarah, Mejhert, Niklas, Miyaguchi, Ken, Mizuno, Yosuke, Morimoto, Mitsuru, Morris, Kelly J., Mummery, Christine, Nakachi, Yutaka, Ogishima, Soichi, Okada-Hatakeyama, Mariko, Okazaki, Yasushi, Orlando, Valerio, Ovchinnikov, Dmitry, Passier, Robert, Patrikakis, Margaret, Pombo, Ana, Qin, Xian-Yang, Roy, Sugata, Sato, Hiroki, Savvi, Suzana, Saxena, Alka, Schwegmann, Anita, Sugiyama, Daisuke, Swoboda, Rolf, Tanaka, Hiroshi, Tomoiu, Andru, Winteringham, Louise N., Wolvetang, Ernst, Yanagi-Mizuochi, Chiyo, Yoneda, Misako, Zabierowski, Susan, Zhang, Peter, Abugessaisa, Imad, Bertin, Nicolas, Diehl, Alexander D., Fukuda, Shiro, Furuno, Masaaki, Harshbarger, Jayson, Hasegawa, Akira, Hori, Fumi, Ishikawa-Kato, Sachi, Ishizu, Yuri, Itoh, Masayoshi, Kawashima, Tsugumi, Kojima, Miki, Kondo, Naoto, Lizio, Marina, Meehan, Terrence F., Mungall, Christopher J., Murata, Mitsuyoshi, Nishiyori-Sueki, Hiromi, Sahin, Serkan, Nagao-Sato, Sayaka, Severin, Jessica, de Hoon, Michiel J. L., Kawai, Jun, Kasukawa, Takeya, Lassmann, Timo, Suzuki, Harukazu, Kawaji, Hideya, Summers, Kim M., Wells, Christine, Hume, David A., Forrest, Alistair R. R., Sandelin, Albin, Carninci, Piero, and Hayashizaki, Yoshihide

Published
2015

40. Arteannuin-B and (3-Chlorophenyl)-2-Spiroisoxazoline Derivative Exhibit Anti-Inflammatory Effects in LPS-Activated RAW 264.7 Macrophages and BALB/c Mice-Induced Proinflammatory Responses via Downregulation of NF-κB/P38 MAPK Signaling

Author

Sawhney, Gifty, primary, Rasool, Javeed Ur, additional, Saroch, Diksha, additional, Ozturk, Mumin, additional, Brombacher, Frank, additional, Ahmad, Bilal, additional, Bhagat, Asha, additional, Ali, Asif, additional, Parihar, Suraj P., additional, and Ahmed, Zabeer, additional

Published
2022
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41. Host-Directed Targeting of LincRNA-MIR99AHG Suppresses Intracellular Growth of Mycobacterium tuberculosis

Author

Gcanga, Lorna, primary, Tamgue, Ousman, additional, Ozturk, Mumin, additional, Pillay, Shandre, additional, Jacobs, Raygaana, additional, Chia, Julius Ebua, additional, Mbandi, Stanley Kimbung, additional, Davids, Malika, additional, Dheda, Keertan, additional, Schmeier, Sebastian, additional, Alam, Tanvir, additional, Roy, Sugata, additional, Suzuki, Harukazu, additional, Brombacher, Frank, additional, and Guler, Reto, additional

Published
2022
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43. Interleukin‐4 receptor alpha signaling regulates monocyte homeostasis

Author

Haider, Patrick, primary, Kral‐Pointner, Julia B., additional, Salzmann, Manuel, additional, Moik, Florian, additional, Bleichert, Sonja, additional, Schrottmaier, Waltraud C., additional, Kaun, Christoph, additional, Brekalo, Mira, additional, Fischer, Michael B., additional, Speidl, Walter S., additional, Hengstenberg, Christian, additional, Podesser, Bruno K., additional, Huber, Kurt, additional, Pabinger, Ingrid, additional, Knapp, Sylvia, additional, Brombacher, Frank, additional, Brostjan, Christine, additional, Ay, Cihan, additional, Wojta, Johann, additional, and Hohensinner, Philipp J., additional

Published
2022
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44. Lyl1-deficiency promotes inflammatory responses and increases mycobacterial burden in response to Mycobacterium tuberculosis infection in mice

Author

Jones, Shelby-Sara, primary, Ozturk, Mumin, additional, Kieswetter, Nathan Scott, additional, Poswayo, Sibongiseni K. L., additional, Hazra, Rudranil, additional, Tamgue, Ousman, additional, Parihar, Suraj P., additional, Suzuki, Harukazu, additional, Brombacher, Frank, additional, and Guler, Reto, additional

Published
2022
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48. Arteannuin-B and its Spiro-isoxazoline Derivative Inhibits LPS Induced Pro-Inflammatory Responses in RAW 264.7 Macrophages and BALB/c Mice via down-regulation of NF-κβ/P38 MAPK Mediated Stress Signalling

Author

Sawhney, Gifty, primary, Rasool, Javeed Ur, additional, Saroch, Diksha, additional, Ozturk, Mumin, additional, Parihar, Suraj, additional, Brombacher, Frank, additional, Ahmad, Bilal, additional, Bhagat, Asha, additional, Ali, Asif, additional, and Ahmed, Zabeer, additional

Published
2022
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