By Louis B. Justement (auth.), Louis B. Justement Ph.D., Professor Katherine A. Siminovitch M.D. (eds.)
Proper improvement and differentiation of B lymphocytes is es sential to make sure that an organism has the power to mount a good humoral immune reaction opposed to international antigens. The immune approach needs to hold a stability among the deletion of destructive self-reactive B cells and the new release of a various rep ertoire of B cells that has the power to acknowledge a virtually un constrained array of overseas antigens. the necessity to delete self-reactive cells is tempered via the necessity to stay away from the new release of enormous practical holes within the repertoire of international antigen-specific B cells that patrol the outer edge. to complete this, the immune procedure needs to succeed in a compromise by means of removing basically the main harmful autoreactive clones, whereas permitting much less destructive au toreactive B cells to exist within the outer edge the place they could com plement the organism's skill to mount a fast reaction opposed to invading micro-organisms. these autoreactive cells that do input the peripheral pool are topic to a couple of conditional re straints that successfully attenuate their skill to reply to self antigens. Deleterious changes within the homeostasis among tolerance induction and recruitment of B cells into the practical repertoire could lead to elevated susceptibility to autoimmune illness or an infection, respectively. accordingly, delineation of the molecular approaches that continue immunological homeostasis within the B telephone compartment is critical.
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Additional info for Signal Transduction and the Coordination of B Lymphocyte Development and Function I: Transduction of BCR Signals from the Cell Membrane to the Nucleus
As previously discussed, the Src family PTKs as a group are involved in regulating the activation of both Syk and Btk (KUROSAKI et al. 1994; RAWLINGS et al. 1996). Therefore, elimination or alteration of Src family PTK function could exert either a direct or indirect effect, or both, on the phosphorylation of downstream effector proteins. Clearly, changes in the phosphorylation of effector proteins that are direct substrates for Src kinases would be expected. Alternatively, changes in substrate phosphorylation could also result from an indirect process in which downstream PTKs such as Syk or Btk are dysregulated.
1993; TSUI and TsUI 1994; CYSTER and GOODNOW 1995; PANI et al. 1995). Both strains of mice exhibit severe defects in the B-cell compartment resulting in B-cell immune deficiency and the breakdown of self-tolerance, leading to the production of autoantibodies. B. Justement conventional B cells and, therefore, mount a weak humoral response when challenged with antigens. Nevertheless, these mice also develop autoantibodies by 4 weeks of age. Presumably, the increased prevalence of autoantibodies is due to the abnormal peripheral expansion of CD5+ B cells, which constitute a putative autoreactive B-cell subpopulation that is normally localized in the peritoneal and pleural cavities (KOZLOWSKI et al.
DAG and IP3) that regulate PKC activity and Ca2+ mobilization, leading to nuclear translocation of the transcription factor NF-AT (RAO et al. 1997). The She-dependent pathway mediates recruitment of the Grb2/Sos complex to the membrane where Sos acts as a guanine nucleotide exchange factor (GEF) that promotes activation of the Ras/Raf pathway leading to activation of ERKI/2 MAPKs (GOLD et al. 1992; HARWOOD and CAMBIER 1993; LAZARUS et al. 1993; SUTHERLAND et al. 1996). These MAPKs are involved in regulating the function of the transcription factors Elkl and Sap-la (Su and KARIN 1996; JANKNECHT and HUNTER 1997).