scholarly journals Effects of Colonization of Gnotobiotic Swiss Webster Mice with Helicobacter bilis

2020 ◽  
Vol 70 (3) ◽  
pp. 216-232
Author(s):  
Mark T Whary ◽  
Chuanwu Wang ◽  
Catherine F Ruff ◽  
Mallory J DiVincenzo ◽  
Caralyn Labriola ◽  
...  
Keyword(s):  
T Cells ◽  
Mhc Class Ii ◽  
Lymphoid Tissue ◽  
Inbred Mice ◽  
Germinal Centers ◽  
Tertiary Lymphoid Tissue ◽  
Lower Bowel ◽  
Helicobacter Bilis ◽  
Class Ii Antigen ◽  
Mhc Class Ii Antigen

Helicobacter bilis (Hb) causes hepatitis in some strains of inbred mice. The current study confirmed that Hb directly causes portal hepatitis in outbred gnotobiotic Swiss Webster (SW) mice, as we previously reported for conventional SW mice. Hbmonoassociated SW mice also developed mild enterocolitis, expanded gut-associated lymphoid tissue (GALT), and tertiary lymphoid tissue in the lower bowel. At 1 and 10 mo after infection, Hb-induced GALT hyperplasia exhibited well-organized, ectopic germinal centers with increased mononuclear cell apoptosis, MHC class II antigen presentation, and pronounced endothelial venule formation, consistent with features of tertiary lymphoid tissue. In the lower bowel, Hb induced mainly B220+ cells as well as CD4+ IL17+, CD4+ IFNγ+, and CD4+ FoxP3+ regulatory T cells and significantly increased IL10 mRNA expression. This gnotobiotic model confirmed that Hb causes portal hepatitis in outbred SW mice but stimulated GALT with an antiinflammatory bias. Because Hb had both anti- and proinflammatory effects on GALT, it should be considered a 'pathosymbiont provocateur' and merits further evaluation in mouse models of human disease.

Clones of T Cells Discriminate between Native and Deglycosylated Forms of MHC Class II Antigen in Allostimulation

1993 ◽  
Vol 149 (2) ◽  
pp. 279-290
Author(s):  
Donald Culley ◽  
Deirdre Waldron-Edward ◽  
Puttaswamy Manjunath ◽  
Orval A. Mamer ◽  
Kushalappa Abikar ◽  
...  
Keyword(s):  
T Cells ◽  
Mhc Class Ii ◽  
Class Ii ◽  
Class Ii Antigen ◽  
Mhc Class Ii Antigen

scholarly journals Dendritic Cells Require TMEM176A/B Ion Channels for Optimal MHC Class II Antigen Presentation to Naive CD4+ T Cells

2021 ◽  
pp. ji2000498
Author(s):  
Melanie Lancien ◽  
Geraldine Bienvenu ◽  
Sonia Salle ◽  
Lucile Gueno ◽  
Magalie Feyeux ◽  
...  
Keyword(s):  
T Cells ◽  
Dendritic Cells ◽  
Ion Channels ◽  
Antigen Presentation ◽  
Mhc Class Ii ◽  
Cd4 T Cells ◽  
Class Ii ◽  
Class Ii Antigen ◽  
Mhc Class Ii Antigen

scholarly journals Activation of Dendritic Cells Alters the Mechanism of MHC Class II Antigen Presentation to CD4 T Cells

2020 ◽  
Vol 204 (6) ◽  
pp. 1621-1629 ◽  
Author(s):  
Kyung-Jin Cho ◽  
Satoshi Ishido ◽  
Laurence C. Eisenlohr ◽  
Paul A. Roche
Keyword(s):  
T Cells ◽  
Dendritic Cells ◽  
Antigen Presentation ◽  
Mhc Class Ii ◽  
Cd4 T Cells ◽  
Class Ii ◽  
Class Ii Antigen ◽  
Mhc Class Ii Antigen

scholarly journals Immunohistochemical Characterization of Inflammatory Cells in Brains of Dogs with Granulomatous Meningoencephalitis

1998 ◽  
Vol 35 (1) ◽  
pp. 43-52 ◽  
Author(s):  
A. Kipar ◽  
W. Baumgärtner ◽  
C. Vogl ◽  
K. Gaedke ◽  
M. Wellman
Keyword(s):  
T Cells ◽  
B Cells ◽  
Mhc Class Ii ◽  
Inflammatory Cells ◽  
Class Ii ◽  
Virus Antigen ◽  
Immunoglobulin M ◽  
Delayed Type Hypersensitivity ◽  
Class Ii Antigen ◽  
Mhc Class Ii Antigen

The inflammatory cells of eleven dogs with canine granulomatous meningoencephalitis were characterized immunohistochemically. Macrophages were identified by antibodies directed against lysozyme and the DH82 antigen (expressed by cells of a malignant histiocytosis). T cells were demonstrated by CD3, CD43, and CD45R antigen, and B cells by immunoglobulin G and immunoglobulin M expression. Furthermore, staining for the major histocompatibility complex (MHC) class II antigen was evaluated. Diseased animals ranged from 1 to 9 years of age. Small and medium-sized breeds were affected predominantly. Lesions were widespread and localized mainly in the brain stem, less frequently in the cerebrum or cerebellum. Alterations were represented by perivascular cuffs, parenchymal granulomas, and leptomeningeal infiltrates. Lymphocytes and macrophages comprised the dominant cell populations; their percentage varied substantially between different animals and between sections from the same individual. Immunohistochemically, the bulk of lymphocytes were CD3 antigen-positive T cells, while only a few cells were CD43 and CD45R antigen-positive or were classified as B cells. The majority of macrophages expressed both lysozyme and DH82 antigen; however, some were positive for only one antigen. MHC class II antigen-expression, observed only within and in close proximity to the lesions, was found on all inflammatory cells, pericytes/endothelial cells, and microglia. Results were negative for canine distemper virus antigen and nucleoprotein mRNA, rabies virus antigen, fungi, bacteria, and protozoal agents. This immunomorphologic study reveals that inflammatory lesions in canine granulomatous meningoencephalitis consist of a heterogeneous population of MHC class II antigen-positive macrophages and predominantly CD3 antigen-positive lymphocytes. The data suggest a T cell-mediated delayed-type hypersensitivity of an organ-specific autoimmune disease as a possible pathogenic mechanism for this unique canine brain lesion.

scholarly journals γδ+ T Cells Regulate Major Histocompatibility Complex Class II (IA and IE)-Dependent Susceptibility to Coxsackievirus B3-Induced Autoimmune Myocarditis

1999 ◽  
Vol 73 (7) ◽  
pp. 5630-5636 ◽  
Author(s):  
S. A. Huber ◽  
J. E. Stone ◽  
D. H. Wagner ◽  
J. Kupperman ◽  
L. Pfeiffer ◽  
...  
Keyword(s):  
T Cells ◽  
Major Histocompatibility Complex ◽  
Mhc Class Ii ◽  
Γδ T Cells ◽  
Class Ii ◽  
Histocompatibility Complex ◽  
Cvb3 Infection ◽  
Cardiac Lesions ◽  
Class Ii Antigen ◽  
Mhc Class Ii Antigen

ABSTRACT Coxsackievirus B3 (CVB3) infection induces myocardial inflammation and myocyte necrosis in some, but not all, strains of mice. C57BL/6 mice, which inherently lack major histocompatibility complex (MHC) class II IE antigen, develop minimal cardiac lesions despite high levels of virus in the heart. The present experiments evaluate the relative roles of class II IA and IE expression on myocarditis susceptibility in four transgenic C57BL/6 mouse strains differing in MHC class II antigen expression. Animals lacking MHC class II IE antigen (C57BL/6 [IA+ IE−] and ABo [IA− IE−]) developed minimal cardiac lesions subsequent to infection despite high concentrations of virus in the heart. In contrast, strains expressing IE (ABo Eα [IA− IE+] and Bl.Tg.Eα [IA+ IE+]) had substantial cardiac injury. Myocarditis susceptibility correlated to a Th1 (gamma interferon-positive) cell response in the spleen, while disease resistance correlated to a preferential Th2 (interleukin-4-positive) phenotype. Vγ/Vδ analysis indicates that distinct subpopulations of γδ+ T cells are activated after CVB3 infection of C57BL/6 and Bl.Tg.Eα mice. Depletion of γδ+ T cells abrogated myocarditis susceptibility in IE+ animals and resulted in a Th1→Th2 phenotype shift. These studies indicate that the MHC class II antigen haplotype controls myocarditis susceptibility, that this control is most likely mediated through the type of γδ T cells activated during CVB3 infection, and finally that different subpopulations of γδ+ T cells may either promote or inhibit Th1 cell responses.

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