Independent roles for complement C3a and C5a receptors and the membrane attack complex in the pathogenesis of collagen antibody-induced arthritis in mice: Potential therapeutic implications

Banda, Nirmal K.; Hyatt, Stephanie; Glogowska, Magdalena J.; Takahashi, Kazue; Merkel, Tod J.; Stahl, Gregory L.; Liu, Bao; Gérard, Craig; Wetsel, Rick A.; Arend, William P.; Holers, V. Michael

doi:10.1016/j.molimm.2011.06.234

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“…It appears that this pathway may be less significant relatively to the alternative pathway in mice as compared to man. Mice lacking the C5aR or C3aR also have milder disease in arthritis models showing that at least a part of the pathology is related to anaphylatoxin production and the interaction between anaphylatoxins and their cellular receptors (Banda et al, 2011). Furthermore, deletion of complement receptor 2 (CR2) results in a diminished arthritis severity in the CIA model with lower antibody production towards collagen II and citrullinated peptides, showing the importance of complement mediated adaptive immune responses (Kuhn et al, 2008).…”

Section: Complement Activation In Arthritismentioning

confidence: 99%

Interactions of the complement system with molecules of extracellular matrix: Relevance for joint diseases

et al. 2012

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Rheumatoid arthritis (RA) is a highly disabling disease affecting all structures of the joint. Understanding the pathology behind the development of RA is essential for developing targeted therapeutic strategies as well as for developing novel markers to predict disease onset. Several molecules normally hidden within the cartilage tissue are exposed to complement components in the synovial fluid upon cartilage breakdown. Some of these have been shown to activate complement and toll-like receptors, which may enhance an already existing inflammatory response, thereby worsening the course of disease. Other cartilage-resident molecules have in contrast shown to possess complement-inhibitory properties. Knowledge about mechanisms behind pathological complement activation in the joints will hopefully lead to methods which allow us to distinguish patients with pathological complement activation from those where other inflammatory pathways are predominant. This will help to elucidate which patients will benefit from complement inhibitory therapies, which are thought to aid a specific subset of patients or patients at a certain stage of disease. Future challenges are to target the complement inhibition specifically to the joints to minimize systemic complement blockade.

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Section: Complement Activation In Arthritismentioning

confidence: 99%