High impact information on C4a

• In addition to C3a, C3a-desArg and C4a but not C5a, are potent enhancers of CXCL12-induced chemotaxis of human and murine bone marrow (BM) stem/progenitor cells and B lineage cells [1].
• The active site of the anaphylatoxin C4a matches to a splice junction [2].
• Activation of C4 releases into the fluid phase a fragment of the alpha chain, C4a [3].
• Unlike the analogous fragments of C3 and C2, there is no evidence for an anaphylatoxic effect of C4a [3].
• Subsequently, an alternative C4a isolation scheme was utilized, via cleavage in vitro of purified C4 [4].

Biological context of C4a

• The role of complement activation by 4-day T cells is pivotal as complement depletion of recipient mice by cobra venom factor (CVF) inhibits the immunizing capacity of untreated 4-day T cells, while 4-day T cells treated with complement in vitro and injected together with C4a anaphylatoxin are able to immunize recipient mice [5].

Anatomical context of C4a

• Concentrations of this latter C4a preparation, of up to 3.3 microM, had no effect on calcium mobilization in human neutrophils or in cells stably expressing the cloned C3a receptors, an indication that C4a does not interact with the C3a receptor [4].

Analytical, diagnostic and therapeutic context of C4a

• Radioimmunoassays for C3a and C4a have been used to measure the activation of complement during the formation of immune complexes in human serum by the interaction of DNP-BSA and each of 11 mouse anti-DNP monoclonal antibodies of varied isotype and affinity [6].

References