Chronicity of Tissue‐Specific Experimental Autoimmune Disease: A Role for B Cells?

Holmdahl, Rikard; Vingsbo, Carina; Mo, John; Michaëlsson, Erik; Malmstrom, V; Jansson, Liselotte; Brunsberg, Ulrica

doi:10.1111/j.1600-065x.1995.tb00067.x

Cited by 33 publications

(21 citation statements)

References 149 publications

(117 reference statements)

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“…Second, B cells might participate in GN pathogenesis as antigen-presenting cells (APCs). This has been documented in a few T cell-mediated autoimmune disease models (29)(30)(31). In general, some believe that B cells may act as APCs in the initial activation of naive autoreactive T cells.…”

Section: Discussionmentioning

confidence: 99%

CD4+ T cells specific to a glomerular basement membrane antigen mediate glomerulonephritis

Wu¹,

Hicks²,

Borillo³

et al. 2002

J. Clin. Invest.

177

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Section: Discussionmentioning

confidence: 99%

CD4+ T cells specific to a glomerular basement membrane antigen mediate glomerulonephritis

Wu¹,

Hicks²,

Borillo³

et al. 2002

J. Clin. Invest.

177

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“…CIA is induced with CII, the major protein component of cartilage and shares many common features with RA [7][8][9]. Both diseases are MHC associated and probably T-cell mediated.…”

Section: Introductionmentioning

confidence: 99%

Arthritis Susceptibility in Mice Expressing Human Type II Collagen in Cartilage

Malmström

Lun

et al. 1997

Scand J Immunol

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Collagen type II (CII) induced arthritis (CIA) in mice is an experimental model for rheumatoid arthritis. Induction with non-self (e.g. human) CII induces severe arthritis whereas the mice are less susceptible to induction with self CII (i.e. mouse). To analyse whether an autoimmune response to human CII can develop and is pathogenic the authors have established transgenic mice expressing human CII in cartilage and backcrossed them into two different gene backgrounds susceptible to CIA (DBA/1 and C3H.Q). The transgenic human CII expression was restricted to cartilage and did not disturb cartilage morphology or lead to chondrodystrophy. In addition, development of stress-induced arthritis was not affected by the transgene. The cartilage specific expression of human CII reduced, but did not eliminate, the susceptibility to CIA irrespective of the species source (human, bovine, chick, rat) of CII used for immunization. A common denominator between these heterologous CII in comparison with mouse CII is the previously defined CII 256-270 epitope. An expression level dependent T-cell tolerance was seen in this epitope as well as to the entire CII. However, all human transgenic mouse lines could still mount significant autoreactive T-and B-cell responses. Approximately 10% of the transgenic mice developed arthritis after immunization with human CII. These findings show, therefore, that cartilage-located human CII induce tolerance but can nevertheless be a target for development of arthritis.

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“…Bovine or rat CII used to immunize animals in the CIA model elicits an antibody response specific for CII. These antibodies against foreign collagen are believed to cross-react with self collagen and become pathogenic (21,33). In the model of arthritis developed in this study, we demonstrated the breach of self tolerance toward collagen and the production of anti-CII and anti-U1 antibodies.…”

Section: Resultsmentioning

confidence: 99%

Characterization of the anticollagen antibody response in a new model of chronic polyarthritis

Conigliaro¹,

Benson²,

Patakas³

et al. 2011

Arthritis & Rheumatism

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Objective. Type II collagen (CII)-specific B cell responses have been recognized in human rheumatoid arthritis (RA) and in collagen-induced arthritis (CIA). An important limitation of the CIA model is that the CII response and the disease are stimulated by exogenously injected collagen. A model of experimental ovalbumin (OVA)-mediated acute arthritis has been established in which autoimmunity is spontaneous and elicited by antigen-specific T cells. This study was undertaken to create a new model of chronic autoimmune polyarthritis and characterize the associated CII-specific B cell response.Methods. Secondary challenge with OVA or CII in adjuvant was used to elicit chronic disease. CII-specific B cell responses against the epitopes U1, J1, C1, and citrullinated C1, together with the antibody affinity, were investigated in OVA-mediated arthritis.Results. Chronic autoimmune polyarthritis was induced and was dependent on the antigen used in the secondary challenge. U1 was the major CII epitope recognized, and antibodies showed the same affinity as those in CIA.Conclusion. Our findings indicate that the development and severity of chronic disease is dependent on the antigen and is associated with an increased autoreactive B cell response directed against a specific CII epitope (U1). OVA-mediated chronic arthritis exhibits anti-CII antibodies (against U1), resembling human RA and murine CIA.

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Chronicity of Tissue‐Specific Experimental Autoimmune Disease: A Role for B Cells?

Cited by 33 publications

References 149 publications

CD4+ T cells specific to a glomerular basement membrane antigen mediate glomerulonephritis

CD4+ T cells specific to a glomerular basement membrane antigen mediate glomerulonephritis

Arthritis Susceptibility in Mice Expressing Human Type II Collagen in Cartilage

Characterization of the anticollagen antibody response in a new model of chronic polyarthritis

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