The role of alpha 4 integrin and intercellular adhesion molecule-1 (ICAM-1) in murine experimental autoimmune thyroiditis.

Important note: Information in this article was accurate in 1997. The state of the art may have changed since the publication date.

The role of alpha 4 integrin and intercellular adhesion molecule-1 (ICAM-1) in murine experimental autoimmune thyroiditis.

Autoimmunity. 1996;23(1):9-23. Unique Identifier : AIDSLINE MED/97025579
McMurray RW; Tang H; Braley-Mullen H; Department of Internal Medicine, University of Missouri, Columbia; 65212, USA.

Abstract: Mouse-thyroglobulin (MTg)-sensitized spleen cells activated in vitro with MTg induce a lymphocytic form of experimental autoimmune thyroiditis (EAT) whereas activation of the same cell population with MTg in the presence of anti-interleukin 2 receptor antibody (M7/20) induces a granulomatous form of EAT. The thyroid infiltrate in both lymphocytic and granulomatous EAT includes both CD4+ and CD8+ T cells and CD4+ T cells are the primary effector cells for both forms of EAT. This investigation was undertaken to begin to define the roles of alpha 4 integrin, and intercellular adhesion molecule-1 (ICAM-1) in the migration of CD4+ and CD8+ T cells to the thyroid in EAT. The studies presented here demonstrate the expression of alpha 4 integrin and ICAM-1 on CD4+ and CD8+ T cells infiltrating the thyroid and the expression of vascular cell adhesion molecule (VCAM) and ICAM-1 on thyroid cells of mice with EAT. The effects of anti-alpha 4 and anti-ICAM mAb administration on EAT severity in recipient mice was also determined. Anti-alpha 4 administration reduced or abolished lymphocyte infiltration in the thyroid resulting in reduced severity of both lymphocytic and granulomatous EAT. In contrast, anti-ICAM mAb had little effect on EAT severity. These results suggest that these two adhesion molecules exhibit differential functional roles in the modulation of EAT disease severity and that alpha 4-VCAM interactions may be of particular importance in trafficking of effector cells to the thyroid.

Keywords: Animal Antigens, CD/*PHYSIOLOGY Antigens, CD44/METABOLISM Cyclophosphamide/METABOLISM CD8-Positive T-Lymphocytes/IMMUNOLOGY Doxorubicin/METABOLISM Etoposide/METABOLISM Female Immunization, Passive Intercellular Adhesion Molecule-1/*PHYSIOLOGY Lymphocyte Subsets/IMMUNOLOGY Methotrexate/METABOLISM Mice Mice, Inbred CBA Spleen/CYTOLOGY Support, U.S. Gov't, P.H.S. Thyroglobulin/IMMUNOLOGY Thyroid Gland/METABOLISM Thyroiditis, Autoimmune/*IMMUNOLOGY JOURNAL ARTICLE
970330
M9731088

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