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IMMUNOREGULATION OF EXPERIMENTAL MYASTHENIA GRAVIS
Author(s) -
Sheng JianRong,
Prabhakar Bellur S,
Meriggioli Matthew N
Publication year - 2008
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.22.1_supplement.1065.1
Subject(s) - myasthenia gravis , immunology , granulocyte macrophage colony stimulating factor , autoimmune disease , il 2 receptor , antibody , medicine , cytokine , dendritic cell , t cell , antigen , immune system
Recently, dendritic cells (DCs) and regulatory T‐cells (Tregs) have been shown to possess potent capabilities to tolerize T‐cells in an antigen‐specific manner. Strategies mobilizing specific subsets of DCs and Tregs have shown promise in experimental models of T‐cell mediated autoimmune disease. We have observed that the selective activation of particular subsets of DCs utilizing granulocyte‐macrophage colony‐stimulating factor (GM‐CSF) had profound effects on the induction of the antibody mediated autoimmune disease, experimental autoimmune myasthenia gravis (EAMG). We now show that treatment with GM‐CSF significantly ameliorates well‐established, chronic EAMG and effectively down‐modulates anti‐AChR T cell and pathogenic antibody responses. Furthermore, we show that GM‐CSF treatment shifts the cytokine response to a Th2 pattern and that CD4+CD25+ cells are critically involved in the disease suppressive effect.