Mechanisms of Mycobacterium avium-induced resistance against insulin-dependent diabetes mellitus (IDDM) in non-obese diabetic (NOD) mice: role of Fas and Th1 cells.

Important note: Information in this article was accurate in 1999. The state of the art may have changed since the publication date.

Mechanisms of Mycobacterium avium-induced resistance against insulin-dependent diabetes mellitus (IDDM) in non-obese diabetic (NOD) mice: role of Fas and Th1 cells.

Clin Exp Immunol. 1999 Feb;115(2):248-54. Unique Identifier : AIDSLINE MED/99132254
Martins TC; Aguas AP; Institute for Molecular and Cell Biology, Department of Anatomy; of the Institute Abel Salazar for the Biomedical Sciences,; University of Porto, Portugal.

Abstract: NOD mice spontaneously develop autoimmune diabetes. One of the manipulations that prevent diabetes in NOD mice is infection with mycobacteria or immunization of mice with mycobacteria-containing adjuvant. Infection of NOD mice with Mycobacterium avium, done before the mice show overt diabetes, results in permanent protection of the animals from diabetes and this protective effect is associated with increased numbers of CD4+ T cells and B220+ B cells. Here, we investigate whether the M. avium-induced protection of NOD mice from diabetes was associated with changes in the expression of Fas (CD95) and FasL by immune cells, as well as alterations in cytotoxic activity, interferon-gamma (IFN-gamma) and IL-4 production and activation of T cells of infected animals. Our data indicate that protection of NOD mice from diabetes is a Th1-type response that is mediated by up-regulation of the Fas-FasL pathway and involves an increase in the cytotoxicity of T cells. These changes are consistent with induction by the infection of regulatory T cells with the ability of triggering deletion or anergy of peripheral self-reactive lymphocytes that cause the autoimmune disease of NOD mice.

Keywords: JOURNAL ARTICLE Animal Antigens, CD/BIOSYNTHESIS Antigens, CD95/*IMMUNOLOGY Antigens, Differentiation, T-Lymphocyte/BIOSYNTHESIS Clonal Anergy Clonal Deletion Cytotoxicity, Immunologic Diabetes Mellitus, Insulin-Dependent/IMMUNOLOGY/*PREVENTION & CONTROL Interferon Type II/BIOSYNTHESIS Interleukin-4/BIOSYNTHESIS Membrane Glycoproteins/*IMMUNOLOGY Mice Mice, Inbred NOD Models, Immunological Mycobacterium avium/*IMMUNOLOGY Support, Non-U.S. Gov't Th1 Cells/*IMMUNOLOGY Tuberculosis/*IMMUNOLOGY
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A9950895

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