Humoral Immune Factors

In the last decades, postinfectious molecular mimicry has been postulated as the foremost putative mechanism underlying GBS. This implies that antigenic determinants are shared between an infectious agent and the peripheral nervous system. Thus the initial antigenic stimulation by the infectious agent results 

In any chronic autoimmune inflammatory condition, several antigens may be involved via epitope spreading (Lehmann et al., 1992), making it difficult to identify the culprit antigen in an individual patient. Moreover, antibodies display a variety of affinities and avidities and some may activate the complement cascade while others may not (Janeway et al., 

Therefore, it is not easy to define the pathogenic role of individual antigen binding specificities. Given the heterogeneity of GBS and CIDP, it is likely that different antibodies are sequentially or even collectively involved in the pathogenesis of this disease. 

Yan et al., 2001 stndied the sera of 21 CIDP patients for antimyehn activity nsing immunoflnorescence and for binding to myehn proteins nsing Western blot analysis. Results showed that the sera of six patients (29%) contained anti-P IgG antibodies, and four of these caused conduction block and demyelination when injected intraneurally into experimental animals. These results suggest that P is an autoantigen in 

Briefly summarize the different experimental neuritis models in relation to the human diseases. 

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Yamashita reported anti-inflammatory effect of astaxanthin when administered with aspirin. An oral preparation has been developed by Alejung and Wadstroem for the treatment of Helicobacter infections of the mammalian gastrointestinal tract. Strong evidence suggested that astaxanthin modulated the humoral and non-humoral immune systems. It enhanced the release of interleukin-1 and tumor necrosis factor-... 

IL-2 acts as a critical autocrine growth factor for T-cells, and the magnitude of the T-cell response is largely dependent upon the level of IL-2 produced. IL-2 also serves as a growth factor for activated B-lymphocytes. In addition to promoting proliferation of these cells, IL-2 (as well as some other interleukins) stimulates enhanced antibody production and secretion. In this way, it effectively potentates the humoral immune response. 

Beckmen, K.B. et al., Organochlorine contaminant exposure and associations with hematological and humoral immune functional assays with dam age as a factor in free-ranging northern fur seal pups (Callorhinus ursinus), Mar. Pollut. Bull., 46, 594, 2003. 

Dai Y, Schwarz EM, Gu D, Zhang WW, Sarvetnick N, Verma IM. Cellular and humoral immune responses to adenoviral vectors containing factor IX gene tolerization of factor IX and vector antigens allows for long-term expression. Proc Natl Acad Sci USA 1995 92 1401-1405. 

Corticosteroids suppress both humoral and cellular immunity. Single doses produce a redistribution of lymphocytes with a concentration dependent decrease of CD4 and CDS positive cells. This in vivo lymphopenic effect correlates with the in vitro inhibition of stimulated T-cell proliferation. Furthermore, corticosteroids are able to inhibit the expression of genes coding for IL-1, IL-2, IL-6, interferon a, and tumor necrosis factor, TNE-a. Chronic administration decreases the size and also the cellu-larity of lymphoid tissues like lymph nodes, spleen, and thymus. Corticosteroids have more effect on the primary immune response and are less effective against previously sensitized immune responses. Their suppressive effects are more pronounced for T-cell immune responses than for the humoral immune response. 

Mectianism of Action A cyclic polypeptide that inhibits both cellular and humoral immune responses by inhibiting interleukin-2, a proliferative factor needed for T-cell ac-tivityT herapeuticEffect Prevenfs organ rejecfion and relieves sympfoms of psoriasis and arfhrifis. 

The importance of the plasma membrane as the site of action of im-munologically mediated cytotoxicity reactions involving humoral or cellular factors has recently become evident. In this regard, several studies have shown that humoral immune killing reactions involve a complex series of biochemical interactions between the attacker moieties and the cell surface membrane.One approach in studying and elucidating such interactions could therefore focus on the effects of the immune attack processes on the synthesis and/or turnover of cell surface macromolecules known to be structural and functional components of the plasma membrane (e.g., proteins and lipids). 

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