Response To Immunosuppressive Therapies Suggests An Autoimmune Etiology

Immunomodulating and immunosuppressive therapies constitute the cornerstones of therapy for MS and will be discussed in detail in later chapters of this book. These agents include glucocorticoids, immunosuppressive agents such as mitoxantrone, immunomodulators such as interferon-p, and glatiramer acetate. All of these agents are partially effective and are thought to act by modulating the immune response. Glucocorticoids are useful for hastening recovery of acute relapses.

Glucocorticoids have a multitude of inhibitory effects on the immune system. They decrease expression of pro-inflammatory cytokines such as TNFa, IL-2, and IFN-y (117,118). In most studies, they have been shown to increase expression of anti-inflammatory cytokines such as IL-10 and TGFp-1 (119,120). Glucocorticoids also decrease MHC I and MHC II expression (121), induce T-cell apoptosis (122), inhibit nitric oxide synthesis (123), decrease expression of the adhesion molecules E selectin and ICAM-1 (124), decrease CSF matrix metalloproteinase 9 levels (125), decrease CSF IgG (126), and inhibit macrophage phagocytosis (127). Likewise, IFN-p induces a shift toward Th2 T-cell responses (128), inhibits T-cell activation (129), inhibits metalloproteinase-9 production (130), decreases Thl cytokine levels (131), modulates adhesion molecule activity (130,132), and has other anti-inflammatory effects that are still being elucidated (133). Glatiramer acetate alters the Th1 :Th2 balance toward Th2 cytokine production (134). Mitoxantrone, FDA-approved for relapsing-remitting and secondary progressive MS, is an immu-nosuppressive agent that decreases the number and activity of T- and B-lymphocytes and suppresses humoral immunity (135). The beneficial effects of these medications, which all inhibit or modulate the immune system, support the notion that MS is an immune-mediated disorder, perhaps initiated and sustained by autoimmunity.

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