NDLI: Role of C3a receptors, C5a receptors, and complement protein C6 deficiency in collagen antibody-induced arthritis in mice.

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Role of C3a receptors, C5a receptors, and complement protein C6 deficiency in collagen antibody-induced arthritis in mice.

Content Provider	World Health Organization (WHO)-Global Index Medicus
Author	Mueller-Ortiz, Stacey Holers, V. Michael Hyatt, Stephanie White, Jason T. Wetsel, Rick Antonioli, Alexandra H. Arend, William P. Takahashi, Kazue Glogowska, Magdalena Stahl, Gregory L. Banda, Nirmal K. Merkel, Tod J.
Description	Country affiliation: United States Author Affiliation: Banda NK ( Division of Rheumatology, Department of Medicine and Immunology, University of Colorado School of Medicine, Aurora, CO 80045, USA.)
Abstract	The complement system, especially the alternative pathway, plays essential roles in the induction of injury in collagen Ab-induced arthritis (CAIA) in mice. The goal of the current study was to directly compare the roles of receptors for C3a and C5a, as well as the membrane attack complex, as effector mechanisms in the pathogenesis of CAIA. Clinical disease activity in C3aR(-/-), C5aR(-/-), and C6-deficient (C6-def) mice was decreased by 52, 94, and 65%, respectively, as compared with wild-type mice. Decreases in histopathologic injury as well as in IgG and C3 deposition paralleled the clinical disease activity. A decrease in the percentage of synovial neutrophils was observed in C3aR(-/-), C5aR(-/-), and C6-def mice, and a decrease in macrophages was observed in C3aR(-/-) and C5aR(-/-), but not in C6-def, mice. Synovial mRNA obtained by laser capture microdissection exhibited a decrease in TNF- in C5aR(-/-) mice and in IL-1ß in both C5aR(-/-) and C6-def mice, whereas C3aR(-/-) mice demonstrated no change in either cytokine. Our findings show that absent C3aR-, C5aR-, or membrane attack complex-initiated effector mechanisms each decrease susceptibility to CAIA, with clinical effects most pronounced in C5aR-deficient mice. Although the absence of C3aR, C5aR, or C6 led to differential deficiencies in effector mechanisms, decreased proximal joint IgG and C3 deposition was common to all three genotypes in comparison with wild-type mice. These data suggest the existence of positive-feedback amplification pathways downstream of all three effectors that promote additional IgG deposition and C3 activation in the joint.
ISSN	00221767
e-ISSN	15506606
DOI	10.4049/jimmunol.1102310
Journal	The Journal of Immunology
Issue Number	3
Volume Number	188
Language	English
Publisher	The American Association of Immunologists
Publisher Date	2012-02-01
Publisher Place	United States
Access Restriction	Open
Subject Keyword	Arthritis, Experimental Etiology Complement C6 Deficiency Receptor, Anaphylatoxin C5a Physiology Receptors, Complement Animals Complement Activation Complement C3a Immunology Cytokines Disease Susceptibility Immunoglobulin G Macrophages Pathology Mice Mice, Knockout Neutrophils Synovial Fluid Research Support, N.i.h., Extramural Discipline Immunology
Content Type	Text
Resource Type	Article
Subject	Immunology and Allergy Immunology

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Role of C3a Receptors, C5a Receptors, and Complement Protein C6 Deficiency in Collagen Antibody-Induced Arthritis in Mice

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