The CD19–CD21 Complex Regulates Signal Transduction Thresholds Governing Humoral Immunity and Autoimmunity
1997; Cell Press; Volume: 6; Issue: 2 Linguagem: Inglês
10.1016/s1074-7613(00)80418-5
ISSN1097-4180
AutoresThomas F. Tedder, Makoto Inaoki, Shinichi Sato,
Tópico(s)Pediatric health and respiratory diseases
ResumoB lymphocytes respond to numerous stimuli that regulate negative selection in the bone marrow, the generation of humoral immune responses in the periphery, and the establishment and maintenance of tolerance and memory. The outcome of these developmental responses is determined in part by signal transduction through the B cell antigen (Ag)–receptor complex (Goodnow 1996). These signals are further regulated or “fine-tuned” by an array of cytoplasmic signal transduction molecules that amplify or dampen Ag–receptor signals during B cell development and during responses to self or foreign Ags. These downstream “response regulators” may be kinases, phosphatases, or other molecular mediators that greatly influence the magnitude and outcome of transmembrane signaling events. Cell surface response regulators may also inform B cells of their extracellular microenvironment and thereby define signaling thresholds within the B cell. Once signaling thresholds are established, transmembrane signaling events are interpreted in a predetermined context and appropriate responses are initiated. For example, immature B cells undergo apoptosis or clonal tolerance following surface Ag–receptor cross-linking, while this stimulus leads to a proliferative response in mature B cells (Cooper et al. 1980). Divergent response regulators may influence these events by either positively or negatively biasing the context of Ag–receptor signals during distinct stages of development.
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