NDLI: Roles of adipocytes and fibroblasts in activation of the alternative pathway of complement in inflammatory arthritis in mice.

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Roles of adipocytes and fibroblasts in activation of the alternative pathway of complement in inflammatory arthritis in mice.

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Roles of adipocytes and fibroblasts in activation of the alternative pathway of complement in inflammatory arthritis in mice.

Content Provider	World Health Organization (WHO)-Global Index Medicus
Author	Holers, V. Michael Mehta, Gaurav Arend, William P. Antonioli, Alexandra H. Takahashi, Minoru Takahashi, Kazue Stahl, Gregory L. Banda, Nirmal K.
Description	Country affiliation: United States Author Affiliation: Arend WP ( Division of Rheumatology, Department of Medicine, University of Colorado School of Medicine, Aurora, CO 80045, USA.)
Abstract	The complement system is involved in mediation of joint damage in rheumatoid arthritis, with evidence suggesting activation of both the classical and alternative pathway (AP). The AP is both necessary and sufficient to mediate collagen Ab-induced arthritis, an experimental animal model of immune complex-induced joint disease. The AP in mice is dependent on MASP-1/3 cleavage of pro-factor D (pro-FD) into mature factor D (FD). The objectives of the current study were to determine the cells synthesizing MASP-1/3 and pro-FD in synovial tissue. Collagen Ab-induced arthritis was studied in wild-type C57BL/6 mice, and the localization of mRNA and protein for FD and MASP-1/3 in synovial adipose tissue (SAT) and fibroblast-like synoviocytes (FLS) was determined using various techniques, including laser capture microdissection. SAT was the sole source of mRNA for pro-FD. Cultured differentiated 3T3 adipocytes, a surrogate for SAT, produced pro-FD but no mature FD. FLS were the main source of MASP-1/3 mRNA and protein. Using cartilage microparticles (CMPs) coated with anti-collagen mAb and serum from MASP-1/3(-/-) mice as a source of factor B, pro-FD in 3T3 supernatants was cleaved into mature FD by MASP-1/3 in FLS supernatants. The mature FD was eluted from the CMP, and was not present in the supernatants from the incubation with CMP, indicating that cleavage of pro-FD into mature FD by MASP-1 occurred on the CMP. These results demonstrate that pathogenic activation of the AP can occur in the joint through immune complexes adherent to cartilage and the local production of necessary AP proteins by adipocytes and FLS.
ISSN	00221767
e-ISSN	15506606
DOI	10.4049/jimmunol.1300580
Journal	The Journal of Immunology
Issue Number	12
Volume Number	190
Language	English
Publisher	The American Association of Immunologists
Publisher Date	2013-06-15
Publisher Place	United States
Access Restriction	Open
Subject Keyword	Adipocytes Metabolism Arthritis, Experimental Complement Activation Physiology Complement Pathway, Alternative Fibroblasts Immunology Animals Pathology Arthritis, Rheumatoid Blotting, Western Immunohistochemistry Laser Capture Microdissection Mice Mice, Inbred C57bl Mice, Knockout Reverse Transcriptase Polymerase Chain Reaction Synovial Membrane Research Support, N.i.h., Extramural Discipline Immunology
Content Type	Text
Resource Type	Article
Subject	Immunology and Allergy Immunology

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