The putative prophylactic and therapeutic effect of interferon-β€ (IFN-β€) on autoimmune inflammation of the peripheral nervous system was evaluated in experimental autoimmune neuritis (EAN), a well-known animal model of the human Guillain-Barre Β΄syndrome (GBS). We report that treatment of rats with 3
Depletion of CD8+ T cells suppresses the development of experimental autoimmune myasthenia gravis in Lewis rats
β Scribed by Guang-Xian Zhang; Cun-Gen Ma; Bao-Guo Xiao; Moiz Bakhiet; Hans Link; Tomas Olsson
- Publisher
- John Wiley and Sons
- Year
- 1995
- Tongue
- English
- Weight
- 921 KB
- Volume
- 25
- Category
- Article
- ISSN
- 0014-2980
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β¦ Synopsis
Depletion of CD8+ Tcells suppresses the development of experimental autoimmune myasthenia gravis in Lewis rats
To understand the role of CD8+ T cells in experimental autoimmune myasthenia gravis (EAMG), CD8+ Tcells were depleted by injecting a monoclonal anti-rat CD8 antibody (0x8) into Lewis rats immunized with Torpedo acetylcholine receptor (AChR) in complete Freund's adjuvant (CFA). CD8-depleted EAMG rats showed strikingly less muscle weakness and lower anti-AChR IgG antibody levels compared to Hy2-15-injected control EAMG rats. Moreover, the numbers of AChR-specific IgG antibody-secreting cells, AChR-reactive interferony-secreting T helper type 1-like cells and lymphocyte proliferation to AChR were lower in the CD8-depleted group than in control EAMG rats. These differences were significant among mononuclear cells from inguinal and popliteal lymph nodes, mesenteric lymph nodes and spleen, but not from thymus when examined 3,5 and 7 weeks post-immunization.We suggest that CD8+ T cells are involved in the induction and persistance of EAMG by directly or indirectly affecting AChR-reactive T cells and anti-AChR IgG antibody-secreting cells.
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## Abstract Natural killer (NK) cells are implicated in T cellβmediated autoimmune diseases. Experimental autoimmune neuritis (EAN) is a CD4+ T cellβmediated animal model of the GuillainβBarrΓ© syndrome in human. The role of NK cells in the initiation and development of EAN remains unclear. In the p