Sudden infant death syndrome and the genetics of inflammation.

摘要: Several studies report signs of slight infection prior to death in cases sudden infant syndrome (SIDS). Based on this, a hypothesis an altered immunological homeostasis has been postulated. The cytokines are important cellular mediators that crucial for health by regulating cell activity during the inflammatory process. pro-inflammatory favor inflammation; most these IL-1α, IL-1β, IL-6, IL-8, IL-12, IL-18, TNF-α, and IFN-γ. These controlled anti-inflammatory cytokines. This is accomplished reducing cytokine production, thus counteracts their biological effect. major interleukin-1 receptor antagonist (IL-1ra), IL-4, IL-10, IL-11, IL-13. last decade there focused genetic within genes immune system, SIDS with special interest encoding because considered be likely explain vulnerability infection, several have investigated attempt uncover associations between different variants. So far, IL-1, TNF-α research, indicate specific variants SIDS. Taken together, this may at least subset predisposing involved. However, system network complex, more needed order better understand interplay variations how contribute unfavorable response.