NDLI: Type II collagen-specific antibodies induce cartilage damage in mice independent of inflammation.

Content Provider	World Health Organization (WHO)-Global Index Medicus
Author	Croxford, Allyson M. Whittingham, Senga McNaughton, Donald Nandakumar, Kutty Selva Holmdahl, Rikard Rowley, Merrill J.
Description	Country affiliation: Australia Author Affiliation: Croxford AM ( Monash University, Clayton, Victoria, Australia.)
Abstract	OBJECTIVE: Murine collagen antibody-induced arthritis (CAIA), like collagen-induced arthritis, has clinical and immunopathologic features that parallel those in human rheumatoid arthritis (RA). This study was undertaken to examine the effects of autoantibodies to type II collagen (CII) on articular cartilage in the paws of mice, under conditions in which other factors that may influence joint pathology could be excluded. METHODS: Mice of 2 different strains, B10.QC5Î´ and the parental strain B10.Q, were injected intravenously with either saline or arthritogenic monoclonal antibodies (mAb) to CII. B10.QC5Î´ mice lack complement factor C5 and do not develop CAIA when injected with arthritogenic mAb, whereas B10.Q mice have C5 and develop CAIA when administered the mAb and a subsequent injection of lipopolysaccharide. Three days after injection the paws of the mice were examined by standard histologic methods to assess morphologic appearance and proteoglycan loss, and by synchrotron-enhanced Fourier transform infrared microspectroscopy to assess chemical evidence of structural change. RESULTS: No macroscopic or microscopic signs of inflammation were evident in the mice. However, in contrast to the saline-injected controls, all mAb-injected mice exhibited cartilage damage in all joints, with loss of proteoglycans and collagen, chondrocyte hyperplasia and/or loss, and surface damage in the interphalangeal joints. CONCLUSION: The implication of these findings is that an autoimmune response to CII can disrupt articular cartilage, particularly that of the small joints, and the subsequent integrity of the cartilage depends on a balance between breakdown and repair. This has relevance with regard to RA, in which such autoantibodies occur but the inflammatory response may dominate clinically and mask underlying features of the autoimmune response.
File Format	HTM / HTML
ISSN	00043591
e-ISSN	15290131
Journal	Arthritis & Rheumatism
Issue Number	3
Volume Number	65
Language	English
Publisher	Wiley-Blackwell
Publisher Date	2013-03-01
Publisher Place	United States
Access Restriction	Subscribed
Subject Keyword	Antibody Specificity Research Support, Non-u.s. Gov't Species Specificity Spectroscopy, Fourier Transform Infrared Immunology Cartilage, Articular Disease Models, Animal Collagen Type Ii Autoantibodies Proteoglycans Pharmacology Antibodies, Monoclonal Epitopes Metabolism Arthritis, Experimental Arthritis, Rheumatoid Mice, Knockout Pathology Animals Chondrocytes Hybridomas Mice Mice, Congenic Discipline Rheumatic Diseases
Content Type	Text
Resource Type	Article
Subject	Immunology and Allergy Immunology Pharmacology (medical) Rheumatology

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