Inhibition of Experimental Autoimmune Encephalomyelitis in Human C-Reactive Protein Transgenic Mice Is FcγRIIB Dependent. (27th September 2010)

• Record Type: Journal Article
• Authors: Hu, Xian-Zhen; Wright, Tyler T.; Jones, Nicholas R.; Ramos, Theresa N.; Skibinski, Gregory A.; McCrory, Mark A.; Barnum, Scott R.; Szalai, Alexander J.
• Other Names: Isobe Noriko Academic Editor.
• Is Part Of: Autoimmune diseases. Volume 2011(2011)
• Publication Date: 2010-09-27
• Subjects: Autoimmune diseases -- Periodicals; 571.97305
• DOI: 10.4061/2011/484936
• Languages: English
• ISSNs: 2090-0422

Abstract

Abstract : We showed earlier that experimental autoimmune encephalomyelitis (EAE) in human C-reactive protein (CRP) transgenic mice (CRPtg) has delayed onset and reduced severity compared to wild-type mice. Since human CRP is known to engage Fc receptors and Fc receptors are known to play a role in EAE in the mouse, we sought to determine if Fcγ RI, Fcγ RIIb, or Fcγ RIII was needed to manifest human CRP-mediated protection of CRPtg. We report here that in CRPtg lacking either of the two activating receptors, Fcγ RI and Fcγ RIII, the beneficial effects of human CRP are still observed. In contrast, if CRPtg lack expression of the inhibitory receptor Fcγ RIIB, then the beneficial effect of human CRP is abrogated. Also, subcutaneous administration of purified human CRP stalled progression of ongoing EAE in wild-type mice, but similar treatment failed to impede EAE progression in mice lacking Fcγ RIIB. The results reveal that a CRP → Fc γ RIIB axis is responsible for protection against EAE in the CRPtg model.