C3a works with C5a to activate mast cells, recruit antibody, complement and phagocytic cells and increase fluid in the tissue, all of which contribute to the initiation of the adaptive immune response.

C3a has a regulatory process and a structure homologous to complement component C5a, with which it shares 36% of its sequence identity. [1] C3a induces an immunological response through a 482 residue G-protein-coupled receptor called C3a receptor (C3aR).

The anaphylatoxins (AT) C3a, C5a and C5a-desArg are generally considered pro-inflammatory polypeptides generated after proteolytic cleavage of C3 and C5 in response to complement activation. Their well appreciated effector functions include ...

C3a and C5a, the small (approximately 10KDa) cleavage fragments released by complement activation, are potent mediators of inflammation. They are anaphylatoxins and act as cell activators with nanomolar affinity, exerting their functions through binding to specific receptors (C3aR and C5aR or C5L2 r …

Oct 17, 2023 · A series of cryo-EM structures offer insights into how anaphylatoxins C3a and C5a engage complement receptors, illustrating agonist binding modes, pathways of receptor activation, and signaling bias that should facilitate the discovery of ligands and therapeutic candidates targeting these receptors.

May 11, 2023 · The complement receptors C3aR and C5aR1, whose signaling is selectively activated by anaphylatoxins C3a and C5a, are important regulators of both innate and adaptive immune responses.

This review provides a comprehensive overview of human C5a in the context of its structure and signaling under several pathophysiological conditions, including the current and future therapeutic applications targeting C5a.

Recent insights into the role of complement anaphylatoxins C3a and C5a in cancer provide new opportunities for the development of innovative biomarkers and therapeutic strategies. These two complement activation products can maintain chronic inflammation, promote an immunosuppressive microenvironmen …

Dec 1, 2015 · Serum C3a and C5a concentrations were assayed as markers of upper and terminal Complement activation. Upper Complement activation peaked as 39% of C3 molecules were converted to C3a. More than 31% upper Complement activation triggered significant activation of the terminal pathway.

Mar 14, 2008 · Here, we demonstrate that locally produced C5a and C3a anaphylatoxins interacting with their G protein-coupled receptors (GPCRs), C5aR and C3aR, on APCs and T cells both upstream and downstream of CD28 and CD40L signaling are integrally involved in T cell proliferation and differentiation.