Cγ1 Deficiency Exacerbates Collagen-Induced Arthritis

Arthritis & Rheumatology
Richard T StraitFred D Finkelman

Abstract

IgG antibodies protect by aggregating pathogens and activating complement and stimulatory Fcγ receptors (FcγR). Although IgG1 accounts for a large percentage of murine serum antibodies, it poorly activates complement, binds more avidly to inhibitory FcγRIIb than to stimulatory FcγRIII, and has a relatively low aggregating ability. We previously demonstrated that IgG1 protects against complement- and FcγR-independent renal disease by inhibiting immune complex obstruction of glomerular capillaries. The purpose of this study was to determine whether IgG1 also protects against the complement- and FcγR-dependent disorder, collagen-induced arthritis (CIA). CIA was induced by injecting mice with type II collagen (CII) (active model) or with IgG2a and IgG2b anti-CII monoclonal antibodies (ArthritoMab) (passive model). Arthritis severity was assessed, and CII-specific IgG was titered. Cγ1-deficient C57BL/6 mice lack IgG1 (IgG1(-/-) ); in these mice, arthritis developed at a higher frequency and was more severe compared with IgG1(+/+) mice in the active model. Disease was FcγRIII- and C3-dependent in both the IgG(+/+) and IgG(-/-) mouse strains and was not influenced by interleukin-4 receptor α in either strain. CII-specific IgG2a/c tite...Continue Reading

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May 29, 2016·Journal of Neuroimmunology·Melike KüçükerdenPremkumar Christadoss
Aug 23, 2019·Science Translational Medicine·Andrew R CrowAlan H Lazarus
Apr 4, 2021·International Journal of Molecular Sciences·Alexandra A VitaNicholas A Pullen
Dec 6, 2019·International Archives of Allergy and Immunology·Xinyu TianYue Wang

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