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Abstract: This review deals with the effects of kinins, a family of octa- to decapeptides structurally related to bradykinin (BK), in adaptive immune responses. Herein, we discuss the experimental evidence that kinins may exert influence on multiple players of the immune system (i.e. macrophages, dendritic cells, T and B lymphocytes), and modulate the activation, proliferation, migration and effector functions of these cells. We also give an overview of the possible impact of kinins in human autoimmune diseases and corresponding animal models, with special emphasis on autoimmune neuroinflammation and arthritis. These studies indicate a possible immunomodulatory capacity of kinins beyond our current knowledge of kinin actions regarding the vascular system, and thus the way towards future therapeutic approaches. [Copyright &y& Elsevier]

Clinical course, outcome, radiological features, severity, and histopathology are heterogenous in multiple sclerosis (MS). Since MS is considered to be a polygenic disease, the genetic background may at least partly be responsible for this variability. Some MS cases are histopathologically characterized by a dramatic oligodendrocyte loss that is in part caused by apoptosis. A dysregulated apoptotic elimination of self-reactive T cells may also contribute to disease susceptibility. To analyze genetic differences in the apoptosis regulating factors bcl-2, bax, bcl-x and p53 we investigated polymorphisms of these genes in 105 patients with a relapsing remitting disease course and 99 controls by PCR-SSCP and direct sequencing. We identified so far unpublished sequence alterations in the promotor region of the bxl-x gene, in exon 7 of the p53 gene, and in exon 1 of the bax gene. No differences were observed between MS patients and controls. Additional known polymorphisms were found in intron 3 of the bax gene and in exon 6 of the p53 gene. No significant differences in the frequency of gene sequence variations were found between MS patients and controls. The apoptosis genes studied here therefore appear less likely to be important effector genes in MS. [Copyright &y& Elsevier]