Massive system shock 5e1/30/2024 ![]() ![]() Because the clinical, epidemiological, immunological, and pathological findings in PP-MS are notably different from those described for other forms of MS, 3,4 the question arises whether PP-MS and RR-MS are two distinct disease entities. RR disease is often followed by progression (SP-MS). In contrast, PP-MS continuously progresses from the onset. ![]() ![]() 2 RR-MS is defined by relapses with full recovery or with sequelae. Based on either the presence or absence of relapses and remissions or progression of neurological deficits, the clinical course of MS can be categorized into four forms: relapsing-remitting (RR), primary progressive (PP), secondary progressive (SP), and progressive relapsing (PR). 1 The spectrum of clinical disease for MS is diverse. Multiple sclerosis (MS) is an inflammatory demyelinating disease of the central nervous system (CNS). We suggest that induction of lymphoid apoptosis alters the balance of Th1 versus Th2 immune responses and increases MOG antibody production, leading to exacerbation of demyelination and subsequent disease progression. Spleen cells from mice with progressive EAE produced less interferon-γ than those from RR-EAE when stimulated with mitogen. SJL/J mice with SP-EAE had large areas of demyelination, high MOG antibody titers and atrophic lymphoid organs. Injection of apoptotic cells resulted in greater than 20% of mice developing SP-EAE with ataxia. To test whether lymphoid apoptosis itself contributes to disease progression, we injected SJL/J mice with apoptotic thymocytes. In A.SW progressive EAE, we found atrophy of the thymus, spleen, and lymph nodes with depletion of T and B cells and massive apoptosis, as demonstrated by immunohistochemistry, terminal dUTP nick-end labeling, and DNA agarose gel electrophoresis. A.SW mice develop PP or SP-experimental allergic encephalomyelitis (EAE) with large areas of demyelination and high titers of MOG antibody whereas SJL/J mice develop RR-EAE with perivascular T cells and mild demyelination. Using myelin oligodendrocyte glycoprotein (MOG) 92-106, we have established animal models that mimic the different types of multiple sclerosis. The mechanism(s) responsible for generating the different forms of multiple sclerosis, primary progressive (PP) and secondary progressive (SP) versus relapsing-remitting (RR), is not well understood. ![]()
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