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1. Therapeutic normal IgG intravenous immunoglobulin activates Wnt-β-catenin pathway in dendritic cells

Author

Sébastien Lacroix-Desmazes, Jagadeesh Bayry, Anupama Karnam, Melissa Bou-Jaoudeh, Srini V. Kaveri, Mrinmoy Das, Sandrine Delignat, Fabian Käsermann, Naresh Rambabu, Centre de Recherche des Cordeliers (CRC (UMR_S_1138 / U1138)), École pratique des hautes études (EPHE), Université Paris sciences et lettres (PSL)-Université Paris sciences et lettres (PSL)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Sorbonne Université (SU)-Université de Paris (UP), CLS Behring AG, Bern, Jagadeesh, Bayry, and Université Paris sciences et lettres (PSL)-Université Paris sciences et lettres (PSL)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Sorbonne Université (SU)-Université Paris Cité (UPCité)

Subjects
0301 basic medicine, Encephalomyelitis, Autoimmune, Experimental, [SDV.IMM] Life Sciences [q-bio]/Immunology, medicine.medical_treatment, Encephalomyelitis, Anti-Inflammatory Agents, Medicine (miscellaneous), Syk, Inflammation, Autoimmunity, T-Lymphocytes, Regulatory, General Biochemistry, Genetics and Molecular Biology, Article, 03 medical and health sciences, Mice, 0302 clinical medicine, hemic and lymphatic diseases, medicine, Animals, Humans, lcsh:QH301-705.5, Wnt Signaling Pathway, Cells, Cultured, beta Catenin, business.industry, Experimental autoimmune encephalomyelitis, Wnt signaling pathway, Immunoglobulins, Intravenous, LRP5, Immunotherapy, Dendritic Cells, medicine.disease, 3. Good health, Mice, Inbred C57BL, Gene regulation in immune cells, 030104 developmental biology, lcsh:Biology (General), Immunology, [SDV.IMM]Life Sciences [q-bio]/Immunology, Cytokines, Th17 Cells, Female, Signal transduction, medicine.symptom, General Agricultural and Biological Sciences, business, 030215 immunology
Abstract

Therapeutic normal IgG intravenous immunoglobulin (IVIG) is a well-established first-line immunotherapy for many autoimmune and inflammatory diseases. Though several mechanisms have been proposed for the anti-inflammatory actions of IVIG, associated signaling pathways are not well studied. As β-catenin, the central component of the canonical Wnt pathway, plays an important role in imparting tolerogenic properties to dendritic cells (DCs) and in reducing inflammation, we explored whether IVIG induces the β-catenin pathway to exert anti-inflammatory effects. We show that IVIG in an IgG-sialylation independent manner activates β-catenin in human DCs along with upregulation of Wnt5a secretion. Mechanistically, β-catenin activation by IVIG requires intact IgG and LRP5/6 co-receptors, but FcγRIIA and Syk are not implicated. Despite induction of β-catenin, this pathway is dispensable for anti-inflammatory actions of IVIG in vitro and for mediating the protection against experimental autoimmune encephalomyelitis in vivo in mice, and reciprocal regulation of effector Th17/Th1 and regulatory T cells., Karnam et al. show that the β-catenin pathway is dispensable for the anti-inflammatory actions of intravenous immunoglobulin (IVIG) in human dendritic cells and in protecting against experimental autoimmune encephalomyelitis. This study implicates an unknown signaling pathway as a mediator of the anti-inflammatory effects of therapeutic IVIG.

Published
2020
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2. Intravenous immunoglobulin protects from experimental allergic bronchopulmonary aspergillosis via a sialylation‐dependent mechanism

Author

Silvia Bozza, Luigina Romani, Fabian Käsermann, Jagadeesh Bayry, Srini V. Kaveri, Università degli Studi di Perugia (UNIPG), CLS Behring AG, Bern, Immunopathologie et immunointervention thérapeutique (CRC - Inserm U1138), Centre de Recherche des Cordeliers (CRC (UMR_S_1138 / U1138)), École pratique des hautes études (EPHE), Université Paris sciences et lettres (PSL)-Université Paris sciences et lettres (PSL)-Université Paris Diderot - Paris 7 (UPD7)-Université Paris Descartes - Paris 5 (UPD5)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Sorbonne Université (SU)-École pratique des hautes études (EPHE), Université Paris sciences et lettres (PSL)-Université Paris sciences et lettres (PSL)-Université Paris Diderot - Paris 7 (UPD7)-Université Paris Descartes - Paris 5 (UPD5)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Sorbonne Université (SU), Università degli Studi di Perugia = University of Perugia (UNIPG), and Bayry, Jagadeesh

Subjects
0301 basic medicine, Experimental allergic, Immunology, Tregs, Immunoglobulin E, [SDV.IMM.II]Life Sciences [q-bio]/Immunology/Innate immunity, T-Lymphocytes, Regulatory, Aspergillus fumigatus, Mice, 03 medical and health sciences, chemistry.chemical_compound, IL-17F, Th2 Cells, 0302 clinical medicine, Animals, Humans, Immunology and Allergy, [SDV.IMM.ALL]Life Sciences [q-bio]/Immunology/Allergology, [SDV.IMM.II] Life Sciences [q-bio]/Immunology/Innate immunity, Cells, Cultured, IVIG, biology, Mechanism (biology), Aspergillosis, Allergic Bronchopulmonary, Immunoglobulins, Intravenous, ABPA, biology.organism_classification, N-Acetylneuraminic Acid, Bronchopulmonary aspergillosis, Interleukin-10, 3. Good health, Eosinophils, Mice, Inbred C57BL, Interleukin 10, 030104 developmental biology, chemistry, biology.protein, Th17 Cells, Goblet Cells, Antibody, N-Acetylneuraminic acid, [SDV.IMM.ALL] Life Sciences [q-bio]/Immunology/Allergology, 030215 immunology
Abstract

International audience; Intravenous immunoglobuin (IVIG) exerts protective effects in experimental allergic bronchopulmonary aspergillosis (ABPA) via a sialylation-dependent mechanism. The protection was associated with reduced recruitment of eosinophils, diminished goblet cell hyperplasia, suppressed Th2 and Th17 responses and reciprocally enhanced regulatory T cells and IL-10, and decreased IgE levels in the circulation.

Published
2018
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3. Intravenous immunoglobulin mediates anti-inflammatory effects in peripheral blood mononuclear cells by inducing autophagy

Author

Olivier Benveniste, Varun K. Sharma, Maxime Lecerf, Anupama Karnam, Emmanuel Stephen-Victor, Bharat Bhatt, Fabian Käsermann, Veerupaxagouda Patil, Kithiganahalli Narayanaswamy Balaji, Jagadeesh Bayry, Naresh Rambabu, Srini V. Kaveri, Mrinmoy Das, Laurent Gilardin, Patrick Bruneval, Centre de Recherche des Cordeliers (CRC (UMR_S_1138 / U1138)), École pratique des hautes études (EPHE), Université Paris sciences et lettres (PSL)-Université Paris sciences et lettres (PSL)-Université Paris Diderot - Paris 7 (UPD7)-Université Paris Descartes - Paris 5 (UPD5)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Sorbonne Université (SU), CHU Pitié-Salpêtrière [AP-HP], Sorbonne Université-Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP), Department of Microbiology and Cell Biology [Bangalore, India], Université Paris Descartes - Paris 5 (UPD5), CSL Behring, Hôpital Européen Georges Pompidou [APHP] (HEGP), Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Hôpitaux Universitaires Paris Ouest - Hôpitaux Universitaires Île de France Ouest (HUPO), Centre de recherche en myologie, Association française contre les myopathies (AFM-Téléthon)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Sorbonne Université (SU)-Centre National de la Recherche Scientifique (CNRS), Hôpitaux Universitaires Paris Ouest - Hôpitaux Universitaires Île de France Ouest (HUPO)-Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP), Immuno-pathologie et immuno-intervention thérapeutique = Immunopathology and Therapeutic Immuno-intervention [CRC], Université Paris sciences et lettres (PSL)-Université Paris sciences et lettres (PSL)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Sorbonne Université (SU)-Université Paris Cité (UPCité)-École pratique des hautes études (EPHE), Université Paris sciences et lettres (PSL)-Université Paris sciences et lettres (PSL)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Sorbonne Université (SU)-Université Paris Cité (UPCité), Service de Département de médecine interne et immunologie clinique [CHU Pitié-Salpêtrière] (DMIIC), Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Sorbonne Université (SU)-Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Sorbonne Université (SU), Indian Institute of Science [Bangalore] (IISc Bangalore), Université Paris Cité - UFR Médecine [Santé] (UPCité UFR Médecine), Université Paris Cité (UPCité), CLS Behring AG, Bern, Service d'Anatomie et de Cytologie Pathologique (SACP), Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Hôpitaux Universitaires Paris Ouest - Hôpitaux Universitaires Île de France Ouest (HUPO)-Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Hôpitaux Universitaires Paris Ouest - Hôpitaux Universitaires Île de France Ouest (HUPO), Centre de recherche en Myologie – U974 SU-INSERM, Institut National de la Santé et de la Recherche Médicale (INSERM)-Sorbonne Université (SU), Jagadeesh, Bayry, Université Paris sciences et lettres (PSL)-Université Paris sciences et lettres (PSL)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Sorbonne Université (SU)-Université de Paris (UP)-École pratique des hautes études (EPHE), Université Paris sciences et lettres (PSL)-Université Paris sciences et lettres (PSL)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Sorbonne Université (SU)-Université de Paris (UP), Service de médecine interne et d'immunologie clinique [CHU Pitié-Salpêtrière], Sorbonne Université (SU)-Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Sorbonne Université (SU)-Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP), Université de Paris - UFR Médecine Paris Centre [Santé] (UP Médecine Paris Centre), Université de Paris (UP), Thérapie des maladies du muscle strié, and Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS)-Sorbonne Université (SU)

Subjects
Lipopolysaccharides, Cancer Research, medicine.medical_treatment, Anti-Inflammatory Agents, Autoimmunity, medicine.disease_cause, p38 Mitogen-Activated Protein Kinases, [SDV.IMM.II]Life Sciences [q-bio]/Immunology/Innate immunity, Monocytes, 0302 clinical medicine, hemic and lymphatic diseases, Phosphorylation, [SDV.IMM.ALL]Life Sciences [q-bio]/Immunology/Allergology, Microbiology & Cell Biology, 0303 health sciences, biology, lcsh:Cytology, TOR Serine-Threonine Kinases, Immunoglobulins, Intravenous, Endocytosis, Tissue Donors, 3. Good health, [SDV.IMM]Life Sciences [q-bio]/Immunology, Beclin-1, Immunotherapy, Antibody, [SDV.IMM] Life Sciences [q-bio]/Immunology, p38 mitogen-activated protein kinases, Immunology, [SDV.BC]Life Sciences [q-bio]/Cellular Biology, Article, Cell Line, Proinflammatory cytokine, Immunoglobulin Fab Fragments, 03 medical and health sciences, Cellular and Molecular Neuroscience, Immune system, Autophagy, medicine, Humans, lcsh:QH573-671, 030304 developmental biology, Organelles, Innate immune system, business.industry, Macrophages, Adenylate Kinase, Dendritic Cells, Cell Biology, [SDV.IMM.IMM]Life Sciences [q-bio]/Immunology/Immunotherapy, Translational research, Immunity, Innate, Leukocytes, Mononuclear, biology.protein, Phosphatidylinositol 3-Kinase, business, 030215 immunology
Abstract

Autophagy plays an important role in the regulation of autoimmune and autoinflammatory responses of the immune cells. Defective autophagy process is associated with various autoimmune and inflammatory diseases. Moreover, in many of these diseases, the therapeutic use of normal immunoglobulin G or intravenous immunoglobulin (IVIG), a pooled normal IgG preparation, is well documented. Therefore, we explored if IVIG immunotherapy exerts therapeutic benefits via induction of autophagy in the immune cells. Here we show that IVIG induces autophagy in peripheral blood mononuclear cells (PBMCs). Further dissection of this process revealed that IVIG-induced autophagy is restricted to inflammatory cells like monocytes, dendritic cells, and M1 macrophages but not in cells associated with Th2 immune response like M2 macrophages. IVIG induces autophagy by activating AMP-dependent protein kinase, beclin-1, class III phosphoinositide 3-kinase and p38 mitogen-activated protein kinase and by inhibiting mammalian target of rapamycin. Mechanistically, IVIG-induced autophagy is F(ab′)2-dependent but sialylation independent, and requires endocytosis of IgG by innate cells. Inhibition of autophagy compromised the ability of IVIG to suppress the inflammatory cytokines in innate immune cells. Moreover, IVIG therapy in inflammatory myopathies such as dermatomyositis, antisynthetase syndrome and immune-mediated necrotizing myopathy induced autophagy in PBMCs and reduced inflammatory cytokines in the circulation, thus validating the translational importance of these results. Our data provide insight on how circulating normal immunoglobulins maintain immune homeostasis and explain in part the mechanism by which IVIG therapy benefits patients with autoimmune and inflammatory diseases.

Published
2020
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4. Intravenous immunoglobulin induces IL-4 in human basophils by signaling through 1 surface-bound IgE

Author

Galeotti, Caroline, Stephen-Victor, Emmanuel, Karnam, Anupama, Das, Mrinmoy, Gilardin, Laurent, Maddur, Mohan, Wymann, Sandra, Vonarburg, Cédric, Chevailler, Alain, Dimitrov, Jordan, Benveniste, Olivier, Bruhns, Pierre, Kaveri, Srini, Bayry, Jagadeesh, Centre de Recherche des Cordeliers (CRC (UMR_S_1138 / U1138)), École pratique des hautes études (EPHE), Université Paris sciences et lettres (PSL)-Université Paris sciences et lettres (PSL)-Université Paris Diderot - Paris 7 (UPD7)-Université Paris Descartes - Paris 5 (UPD5)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Sorbonne Université (SU), Immunopathologie et immunointervention thérapeutique (CRC - Inserm U1138), Université Paris sciences et lettres (PSL)-Université Paris sciences et lettres (PSL)-Université Paris Diderot - Paris 7 (UPD7)-Université Paris Descartes - Paris 5 (UPD5)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Sorbonne Université (SU)-École pratique des hautes études (EPHE), AP-HP Hôpital Bicêtre (Le Kremlin-Bicêtre), Service de médecine interne et d'immunologie clinique [CHU Pitié-Salpêtrière], CHU Pitié-Salpêtrière [AP-HP], Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Sorbonne Université (SU)-Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Sorbonne Université (SU), Université Sorbonne Paris Cité (USPC), CLS Behring AG, Bern, Innate Immunity and Immunotherapy (CRCINA-ÉQUIPE 7), Centre de Recherche en Cancérologie et Immunologie Nantes-Angers (CRCINA), Institut National de la Santé et de la Recherche Médicale (INSERM)-Université de Nantes - UFR de Médecine et des Techniques Médicales (UFR MEDECINE), Université de Nantes (UN)-Université de Nantes (UN)-Centre hospitalier universitaire de Nantes (CHU Nantes)-Centre National de la Recherche Scientifique (CNRS)-Université d'Angers (UA)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Université de Nantes - UFR de Médecine et des Techniques Médicales (UFR MEDECINE), Université de Nantes (UN)-Université de Nantes (UN)-Centre hospitalier universitaire de Nantes (CHU Nantes)-Centre National de la Recherche Scientifique (CNRS)-Université d'Angers (UA), LabEX IGO Immunothérapie Grand Ouest, Centre Hospitalier Universitaire d'Angers (CHU Angers), PRES Université Nantes Angers Le Mans (UNAM), Centre de Recherche en Myologie, Institut National de la Santé et de la Recherche Médicale (INSERM)-Sorbonne Université (SU), Anticorps en thérapie et pathologie - Antibodies in Therapy and Pathology, Institut Pasteur [Paris]-Institut National de la Santé et de la Recherche Médicale (INSERM), Supported by Institut National de la Santé et de la Recherche Médicale (INSERM), Université Pierre et Marie Curie, Université Paris Descartes and CSL Behring, Switzerland. CG is a recipient of fellowship from La Fondation pour la Recherche Médicale (FDM20150633674), France, ESV and AK are recipient of fellowships from Indo-French Center for Promotion of Advanced Research (CEFIPRA)., École Pratique des Hautes Études (EPHE), Université Paris sciences et lettres (PSL)-Université Paris sciences et lettres (PSL)-Université Paris Diderot - Paris 7 (UPD7)-Université Paris Descartes - Paris 5 (UPD5)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Sorbonne Université (SU)-École Pratique des Hautes Études (EPHE), Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Sorbonne Université (SU), Université d'Angers (UA)-Université de Nantes (UN)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS)-Centre hospitalier universitaire de Nantes (CHU Nantes)-Université d'Angers (UA)-Université de Nantes (UN)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS)-Centre hospitalier universitaire de Nantes (CHU Nantes), Nantes Université (Nantes Univ), Centre de recherche en Myologie – U974 SU-INSERM, Institut Pasteur [Paris] (IP)-Institut National de la Santé et de la Recherche Médicale (INSERM), Service de Département de médecine interne et immunologie clinique [CHU Pitié-Salpêtrière] (DMIIC), Institut National de la Santé et de la Recherche Médicale (INSERM)-Institut Pasteur [Paris], and Gestionnaire, Hal Sorbonne Université

Subjects
FcγRIIB, DCIR, hemic and lymphatic diseases, FcεRI, Anti-IgE IgG, chemical and pharmacologic phenomena, hemic and immune systems, [SDV.IMM.IMM]Life Sciences [q-bio]/Immunology/Immunotherapy, [SDV.IMM.IMM] Life Sciences [q-bio]/Immunology/Immunotherapy, Antisynthetase syndrome, DC-SIGN, Dermatomyositis, Polymyositis
Abstract

International audience; BACKGROUND: Therapeutic normal IgG or intravenous immunoglobulin (IVIG) exerts anti-inflammatory effects through several mutually nonexclusive mechanisms. Recent data in mouse models of autoimmune disease suggest that IVIG induces IL-4 in basophils by enhancing IL-33 in SIGN-related 1-positive innate cells. However, translational insight on these data is lacking.OBJECTIVE: We sought to investigate the effect of IVIG on human basophil functions.METHODS: Isolated circulating basophils from healthy donors were cultured in the presence of IL-3, IL-33, GM-CSF, thymic stromal lymphopoietin, or IL-25. The effect of IVIG and F(ab')2 and Fc IVIG fragments was examined based on expression of various surface molecules, phosphorylation of spleen tyrosine kinase, induction of cytokines, and histamine release. Basophil phenotypes were also analyzed from IVIG-treated patients with myopathy. Approaches, such as depletion of anti-IgE reactivity from IVIG, blocking antibodies, or inhibitors, were used to investigate the mechanisms.RESULTS: We report that IVIG directly induces activation of IL-3-primed human basophils, but IL-33 and other cytokines were dispensable for this effect. Activation of basophils by IVIG led to enhanced expression of CD69 and secretion of IL-4, IL-6, and IL-8. IVIG-treated patients with myopathy displayed enhanced expression of CD69 on basophils. The spleen tyrosine kinase pathway is implicated in these functions of IVIG and were mediated by F(ab')2 fragments. Mechanistically, IVIG induced IL-4 in human basophils by interacting with basophil surface-bound IgE but independent of FcγRII, type II Fc receptors, C-type lectin receptors, and sialic acid-binding immunoglobulin-like lectins.CONCLUSION: These results uncovered a pathway of promoting the TH2 response by IVIG through direct interaction of IgG with human basophils.

Published
2019
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5. Monomeric immunoglobulin a from Plasma inhibits human Th17 responses In Vitro independent of Fcαri and Dc-sign

Author

Sandra Wymann, Meenu Sharma, Veerupaxagouda Patil, Jagadeesh Bayry, Emmanuel Stephen-Victor, Monika Jordi, Srini V. Kaveri, Mrinmoy Das, Cédric Vonarburg, Chaitrali Saha, Institut National de la Santé et de la Recherche Médicale (INSERM), Centre de Recherche des Cordeliers (CRC), Université Pierre et Marie Curie - Paris 6 (UPMC)-École Pratique des Hautes Études (EPHE), Université Paris sciences et lettres (PSL)-Université Paris sciences et lettres (PSL)-Université Paris Diderot - Paris 7 (UPD7)-Université Paris Descartes - Paris 5 (UPD5)-Institut National de la Santé et de la Recherche Médicale (INSERM), CLS Behring AG, Bern, Université Paris Descartes - Paris 5 (UPD5), Université Pierre et Marie Curie - Paris 6 (UPMC)-École pratique des hautes études (EPHE), Institut National de la Santé et de la Recherche Médicale ( INSERM ), Centre de Recherche des Cordeliers ( CRC ), Université Paris Diderot - Paris 7 ( UPD7 ) -École pratique des hautes études ( EPHE ) -Université Pierre et Marie Curie - Paris 6 ( UPMC ) -Université Paris Descartes - Paris 5 ( UPD5 ) -Institut National de la Santé et de la Recherche Médicale ( INSERM ), Université Paris Descartes - Paris 5 ( UPD5 ), and HAL UPMC, Gestionnaire

Subjects
0301 basic medicine, Immunoglobulin A, il-17, Fcαri, [SDV.IMM] Life Sciences [q-bio]/Immunology, medicine.medical_treatment, Immunology, Biology, cD89, Immunoglobulin G, 03 medical and health sciences, Immune system, natural antibodies, medicine, [ SDV.IMM ] Life Sciences [q-bio]/Immunology, Immunology and Allergy, Dc-sign, 3. Good health, DC-SIGN, monomeric IgA, Treg, 030104 developmental biology, Cytokine, biology.protein, STAT protein, iVig, [SDV.IMM]Life Sciences [q-bio]/Immunology, Interleukin 17, Th17, Antibody
Abstract

International audience; Circulating immunoglobulins including immunoglobulin G (IgG) and IgM play a critical role in the immune homeostasis by modulating functions of immune cells. These functions are mediated in part by natural antibodies. However, despite being second most abundant antibody in the circulation, the immunoregulatory function of IgA is relatively unexplored. As Th17 cells are the key mediators of a variety of autoimmune, inflamma-tory, and allergic diseases, we investigated the ability of monomeric IgA (mIgA) isolated from pooled plasma of healthy donors to modulate human Th17 cells. We show that mIgA inhibits differentiation and amplification of human Th17 cells and the production of their effector cytokine IL-17A. mIgA also suppresses IFN-γ responses under these experimental conditions. Suppressive effect of mIgA on Th17 responses is associated with reciprocal expansion of FoxP3-positive regulatory T cells. The effect of mIgA on Th17 cells is dependent on F(ab′)2 fragments and independent of FcαRI (CD89) and DC-SIGN. Mechanistically, the modulatory effect of mIgA on Th17 cells implicates suppression of phosphorylation of signal transducer and activator of transcription 3. Furthermore, mIgA binds to CD4 + T cells and recognizes in a dose-dependent manner the receptors for cytokines (IL-6Rα and IL-1RI) that mediate Th17 responses. Our findings thus reveal novel anti-inflammatory functions of IgA and suggest potential therapeutic utility of mIgA in autoimmune and inflammatory diseases that implicate Th17 cells.

Published
2017
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