Abstract:
:The complement system is known to be involved in autoimmunity at several levels. Activated complement contributes to the inflammatory tissue injury characteristic of many autoimmune disease settings. On the other hand, early components of the classical pathway, including C1q, C4 and C2, are thought to be important for disposing apoptotic cellular autoantigens and/or the induction of B cell tolerance in the bone marrow, and their deficiency is a strong risk factor for systemic autoimmunity. Recent studies using transgenic mice have revealed membrane complement regulatory proteins as important modulators in the pathogenesis and manifestation of autoimmune injury. Available evidence suggests that these regulatory proteins may act to suppress autoimmunity via both complement-dependent and -independent mechanisms.
journal_name
Autoimmunityjournal_title
Autoimmunityauthors
Song WCdoi
10.1080/08916930600739647subject
Has Abstractpub_date
2006-08-01 00:00:00pages
403-10issue
5eissn
0891-6934issn
1607-842Xpii
P51130881J044233journal_volume
39pub_type
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