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- W1529773650 abstract "Studies of the mouse strain have identified the gene, or closely linked group of genes, responsible for the immune defect, and it has been named “xid.” This chapter summarizes the known functional immune defects associated with xid and discusses the cellular basis for these defects. The X-chromosomes of mice and men influence the immunological function of these species in a number of interesting ways. In studies of the influence of the murine X-chromosome on serum IgM levels, it was shown that the mean values of serum IgM were higher in female mice than in males of two different mouse strains. However, in contrast to humans with Turner's syndrome (XO), who had lower mean serum IgM values than did normal XX females, the mean serum concentrations of IgM in XO mice were similar to that found in normal female mice. An X-linked form of severe combined immunodeficiency disease is described in the chapter. Children with this disease have variable degrees of lymphopenia, with small foci of lymphocytes in their lymph nodes and spleens. It is unclear if these patients have a primary B- or T-lymphocyte or stem cell defect. Spleens from either CBA/N or defective F1 male mice are considerably smaller than those of normal mice and the number of nucleated cells/spleen reflects this difference. The absence of thymus-independent type 2 (TI-2) responses in immune-defective mice and the apparent B-cell abnormality in this strain is related to an isolated dysfunction in otherwise normal B cells of these mice. It has been detected in studies that the xid defect could impair thymic-dependent (TD) responses by the induction of hapten-specific suppression without altering the development of memory B cells." @default.
- W1529773650 created "2016-06-24" @default.
- W1529773650 creator A5013496335 @default.
- W1529773650 date "1982-01-01" @default.
- W1529773650 modified "2023-10-03" @default.
- W1529773650 title "The CBA/N Mouse Strain: An Experimental Model Illustration the Influence of the X-Chromosome on Immunity" @default.
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