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C-reactive protein (CRP) is produced by the liver in response to inflammation. The stimulation of CRP synthesis mainly occurs in response to pro-inflammatory cytokines, most notably IL-6 and to a lesser degree IL-1 and tumour necrosis alpha (TNF-α).1 2 Therefore, CRP is used as an inflammation marker for clinical purposes. CRP is a dynamic protein, has several conformational statuses, native pentameric CRP forms (pCRP), pentameric symmetrical forms (pCRP*), monomeric CRP forms (mCRP).1 2 pCRP can undergo dissociation into mCRP through pCRP*. pCRP binds to the cell surface via interaction with phosphocholine. Cell-bound pCRP undergoes a conformational change that leads to its dissociation to mCRP. For clinical purposes, pCRP is typically quantified rather than mCRP.1 2 pCRP does not have inflammatory activity.3 On the other hand, mCRP has pro-inflammatory function through the activation of endothelial cells, leukocytes and platelets via NF-κβ-regulated translation of proteins (e.g. IL-6, IL-8, MCP1), in addition to the complement pathway.1 2 This difference in function can be explained by the two isoforms binding to differing types of Fcgamma (Fcγ)-receptor involved in the signalling process. The mCRP uses the low-affinity immune complex binding immunoglobulin G (IgG) receptor called FcγRIIIb (CD16b) on neutrophils and FcγRIIIa (CD16a) on monocytes, while pCRP binds to the low-affinity IgG receptor FcγRIIa (CD32) (3 Khreiss T). Therefore, mCRP is a potential therapeutic target for the treatment of inflammatory diseases. In our previous study, we generated the anti-mCRP mAb to develop an anti-mCRP therapy. Clone 3C specifically recognised mCRP but not pCRP.4 Anti-mCRP mAb 3C suppressed arthritis and lupus nephritis in mouse model.4 In this study, we evaluated whether anti-mCRP mAb 3C attenuates aortitis in a Lactobacillus casei cell wall extract (LCWE)-induced Kawasaki disease-like vasculitis mouse model, a well-established animal model for vasculitis.5–7 In the LCWE mouse model, a single intraperitoneal injection of LCWE is sufficient to induce aortic root inflammation and/or coronary arteritis.5–7