期刊
JOURNAL OF IMMUNOLOGY
卷 169, 期 11, 页码 6604-6609出版社
AMER ASSOC IMMUNOLOGISTS
DOI: 10.4049/jimmunol.169.11.6604
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- NIAID NIH HHS [AI10682] Funding Source: Medline
- NIAMS NIH HHS [AR44850, AR47360] Funding Source: Medline
Spontaneous arthritis in the KRN transgenic mouse (K/BxN) model is due to the autoreactivity of the transgenic TCR and subsequent induction of autoantibodies directed against glucose-6-phosphate isomerase. These autoantibodies transfer clinically apparent arthritis into most recipient mouse strains and systemic catabolism of the transferred Abs attenuates paw swelling. Although mice deficient in the common gamma-chain of the FcgammaR did not show clinical synovitis after receiving K/BxN sera, erosive lesions in the bone still developed. Further analysis demonstrated that FcgammaRII(-/-) mice manifested accelerated arthritis whereas the FcgammaRIII(-/-) mice had a more slowly progressing arthritis. Paw swelling required FcgammaR expression by bone marrow-derived cells and mast cells substantially contributed to the acute phase of paw swelling. In the K/BxN serum transfer model of arthritis, there is a clinically apparent acute phase, which is modulated by FcgammaRII and FcgammaRIII, and a subacute component, which results in bone erosion, even in the absence of FcgammaR signaling.
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