Measurement of antibodies to collagen II by inhibition of collagen fibril formation in vitro

Gray, Robyn Elizabeth; Seng, Natalie; Mackay, Ian R.; Rowley, Merrill J.

doi:10.1016/j.jim.2003.11.010

Cited by 25 publications

(19 citation statements)

References 20 publications

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“…Thus, it seems reasonable to hypothesize that the increased concentrations of proinflammatory cytokines and osteoclast activators in a quantitatively nonaltered bacterial environment, such as the maxillae of AIA mice, were triggered by anti-collagen I Abs. Abs can also directly cause the destruction of their target tissue through impairment of tissue formation (35), inhibition of collagen fibrillogenesis (36), and disruption of collagen fibrils in the extracellular matrix (37). Once more, there is evidence of increased matrix metalloproteinases in maxillae of AIA mice (4, 16); however, it remains to be determined whether it is triggered by autoantibodies.…”

Section: Discussionmentioning

confidence: 99%

Experimental Arthritis Triggers Periodontal Disease in Mice: Involvement of TNF-α and the Oral Microbiota

Queiroz-Junior

Madeira

Coelho

et al. 2011

The Journal of Immunology

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Rheumatoid arthritis (RA) and periodontal disease (PD) are prevalent chronic inflammatory disorders that affect bone structures. Individuals with RA are more likely to experience PD, but how disease in joints could induce PD remains unknown. This study aimed to experimentally mimic clinical parameters of RA-induced PD and to provide mechanistic findings to explain this association. Chronic Ag-induced arthritis (AIA) was triggered by injection of methylated BSA in the knee joint of immunized mice. Anti–TNF-α was used to assess the role of this cytokine. Intra-articular challenge induced infiltration of cells, synovial hyperplasia, bone resorption, proteoglycan loss, and increased expression of cytokines exclusively in challenged joints. Simultaneously, AIA resulted in severe alveolar bone loss, migration of osteoclasts, and release of proinflammatory cytokines in maxillae. Anti–TNF-α therapy prevented the development of both AIA and PD. AIA did not modify bacterial counts in the oral cavity. PD, but not AIA, induced by injection of Ag in immunized mice was decreased by local treatment with antiseptic, which decreased the oral microbiota. AIA was associated with an increase in serum C-reactive protein levels and the expression of the transcription factors RORγ and Foxp3 in cervical lymph nodes. There were higher titers of anti-collagen I IgG, and splenocytes were more responsive to collagen I in AIA mice. In conclusion, AIA-induced PD was dependent on TNF-α and the oral microbiota. Moreover, PD was associated with changes in expression of lymphocyte transcription factors, presence of anti-collagen Abs, and increased reactivity to autoantigens.

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Section: Discussionmentioning

confidence: 99%

Experimental Arthritis Triggers Periodontal Disease in Mice: Involvement of TNF-α and the Oral Microbiota

Queiroz-Junior

Madeira

Coelho

et al. 2011

The Journal of Immunology

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“…4) [33,34]. Both of the anti-CII antibodies used, bind both high affinity and low affinity immunecomplex mouse Fc␥R [35].…”

Section: Discussionmentioning

confidence: 99%

Transgenic mice expressing human FcγRIIa have enhanced sensitivity to induced autoimmune arthritis as well as elevated Th17 cells

et al. 2010

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“…Two arthritogenic mAb, CIIC1 and M2139 inhibited fibrillogenesis of CII in vitro, whereas the non-arthritogenic mAb CIIF4 did not [149]. The arthritogenic mAb, CIIC1, M2139 and UL1 also impaired cartilage formation by cultured chondrocytes, causing morphological changes to the cells, or disorganization of the cartilage fibrils that differed according to the mAb [58,59,62], as well as proteoglycan loss and cartilage damage in cartilage explant cultures [60,62].…”

Section: Autoantibodies To Collagenmentioning

confidence: 99%

The Role of Pathogenic Autoantibodies in Autoimmunity

Rowley

Whittingham

2015

Antibodies

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Abstract:The serological presence of autoantibodies is diagnostic of autoimmunity, and these autoantibodies may be present for many years before the presentation of autoimmune disease (AID). Although a pathogenic role has been demonstrated for various autoantibodies reactive with cell surface and extracellular autoantigens, studies using monoclonal antibodies (mAb) show not all antibodies in the polyclonal response are pathogenic. Differences depend on Fab-mediated diversity in epitope specificity, Fc-mediated effects based on immunoglobulin (Ig) class and subclass, activation of complement, and the milieu in which the reaction occurs. These autoantibodies often occur in organ-specific AID and this review illustrates their pathogenic and highly specific effects. The role of autoantibodies associated with intracellular antigens is less clear. In vitro they may inhibit or adversely affect well-defined intracellular biochemical pathways, yet, in vivo they are separated from their autoantigens by multiple cellular barriers. Recent evidence that Ig can traverse cell membranes, interact with intracellular proteins, and induce apoptosis has provided new evidence for a pathogenic role for such autoantibodies. An understanding of how autoantibodies behave in the polyclonal response and their role in pathogenesis of AID may help identify populations of culprit B-cells and selection of treatments that suppress or eliminate them.

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Measurement of antibodies to collagen II by inhibition of collagen fibril formation in vitro

Cited by 25 publications

References 20 publications

Experimental Arthritis Triggers Periodontal Disease in Mice: Involvement of TNF-α and the Oral Microbiota

Experimental Arthritis Triggers Periodontal Disease in Mice: Involvement of TNF-α and the Oral Microbiota

Transgenic mice expressing human FcγRIIa have enhanced sensitivity to induced autoimmune arthritis as well as elevated Th17 cells

The Role of Pathogenic Autoantibodies in Autoimmunity

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