| Background: Multiple sclerosis (MS) is a characterized demyelinating disease of the CNS and postulated to be a autoimmune disease. The pathogenesis of MS has not been well understood, and mainly involves the follow causes such as virus infection, the abnormalities of immunoregulation, genetic factor, and environmental agent, et al. Nowadays, it is presumed to be a multi-pathogeny disease. Some individuals with congenital genetic predisposition are susceptible to the abnormalities of immunoregiilation. If affected by the extrinsic factors of the postnatal environment such as estrogen, infection, pregnancy, operation, and so on, the autoantigen, for instance, the myelin basic protein (MBP) ,originally secluded from immune system, will exposure and can not induce the immunologic tolerance of itself, which will interact with immunologically competent cells and induce specific immune response, and in turn result in the onset of MS.The competent cells participated in immunological response mainly involving lymphocyte and macrophage, most of whose immune regulating function was achieved by secreting cytokine (CK). Some cytokines with common biologic competence can react in a "cascade pattern". The typical case is the hpopolysaccharide (LPS) of G" bacteria can stimulate the monocyte / macrophage to secrete IL-12 and TNF a ,and the IL-12 can also stimulate the secretion of TNF a and IFN Y ,the TNF a can then stimulate the secretion of IL-1, which will in turn stimulate the secretion of IL-6. the IFN Y can turn round to excite the monocyte / macrophage to augment the4synthesis of IL-12 and TNFa.So a positive feedback circle is formed, which cause a increasing enlargement of immunologic reaction in vivo and mediate the onset of disease. This is the major mechanism that the CK mediate the onset of MS.The IL-16 is known as a chemoattractant factor and produced by activated CD8+ T lymphocytes. But, now, B cell and mast cell can also produce it. In 1982, in Boston umiversity ,Cruikshank discover a lymphocyte chemo- attractant factor (LCF). In 1995, in German, Baier cloned LCF of African monkey and named it IL-16, so become a new member of interleukines. As former reported, its major biologic activities is as follows: 1. induce the migration of human CD4+T cells,monocytes and eosinophils; 2. to bind to T cells via CD4+receptors; 3. to induce HIV-DR and IL-2 receptor expression, et al. But its function in the mechanism of MS? Some investigation has been carried out overseas, but, so far, none has been reported at home.Objiect: To investigate the variance of MBP and IL-16 in CSF and serum during the onset of MS, and the correlation between them and between MBP and the expanded disability status scale (EDSS) of MS, which will help to investigate the produce of IL-16 within CNS and in turn induce MS attack.Method: Group MS: Slinpatients with CSF and 32 outpatients were included, all of which were diagnosed as MS acording to Poser, excluding severe body disease. Before hospitalization, they all intake little-dose corticoid unregularly. Group inflammatory demyelinating poly-neuropathies (IDP): 24 onpatients including 19 AIDP and 5 CIDP were included, before specimen collecting they all also intake little-dose corticoid unregularly. Group health controls (HC): include 28 serum that were collected from the healthy blood donor of nanjing blood bank; and 24 CSF including 20 specimen that were collected from the selecting operation patients with haemorrhoids or anal fistula admited in nanjing traditional5Chinese medicine hospital and 3 patients with vascular headache and 1withhypokaluria paralysis admited in nanjing brain hospital.Result:1. CSF and serum levels of MBP all increased significantly in MS patients compared with that in IDP and in HC (P < 0.01).2. CSF levels of IL-16 increased significantly in MS patients compared with that in HC (p < 0.01), but no difference were found in serum between MSandHC.3. The MBP and IL-16 were detected simultaneously in 28 patients with CSF and se... |