Collagen-induced arthritis, an animal model of autoimmunity

Myers, Linda K.; Rosloniec, Edward F.; Cremer, Michael A.; Kang, Andrew H.

doi:10.1016/s0024-3205(97)00480-3

Cited by 297 publications

(231 citation statements)

References 117 publications

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“…CIA is a frequently used mouse model of inflammatory rheumatoid arthritis that is both Ab and T cell dependent (35,36). It has been previously demonstrated that mouse strains prone to autoimmune diabetes have an increased number of T cells expressing CD40 that correlates with development of pathology (14).…”

Section: Cd40 Expression On T Cells From Mice With Ciamentioning

confidence: 99%

A Costimulatory Function for T Cell CD40

Munroe

Bishop

2007

The Journal of Immunology

100

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CD40 plays a significant role in the pathogenesis of inflammation and autoimmunity. B cell CD40 directly activates cells, which can result in autoantibody production. T cells can also express CD40, with an increased frequency and amount of expression seen in CD4+ T lymphocytes of autoimmune mice, including T cells from mice with collagen-induced arthritis. However, the mechanisms of T cell CD40 function have not been clearly defined. To test the hypothesis that CD40 can serve as a costimulatory molecule on T lymphocytes, CD40+ T cells from collagen-induced arthritis mice were examined in parallel with mouse and human T cell lines transfected with CD40. CD40 served as effectively as CD28 in costimulating TCR-mediated activation, including induction of kinase and transcription factor activities and production of cytokines. An additional enhancement was seen when both CD40 and CD28 signals were combined with AgR stimulation. These findings reveal potent biologic functions for T cell CD40 and suggest an additional means for amplification of autoimmune responses.

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Section: Cd40 Expression On T Cells From Mice With Ciamentioning

confidence: 99%

A Costimulatory Function for T Cell CD40

Munroe

Bishop

2007

The Journal of Immunology

100

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“…Lta Ϫ/Ϫ mice are susceptible to CIA despite their resistant C57BL/6 background Susceptibility to CIA is profoundly influenced by MHC-II genetics, and in genetically resistant strains, such as C57BL/6, even repeated immunizations fail to produce disease (10). Our Lta Ϫ/Ϫ and Ltbr Ϫ/Ϫ mice, despite their resistant C57BL/6 background and lack of draining LNs, spontaneously elaborate anti-CII Abs and increased T cell response to CII in a manner reminiscent of strains susceptible to CIA, such as DBA/1(10).…”

Section: Breakdown Of Central Tolerance Leads To Spontaneous Anti-colmentioning

confidence: 99%

“…To explore the possibility that, in addition to AIRE, lymphotoxin signaling drives an additional host of parallel pathways for the ectopic expression of peripheral Ags, we investigated self-Ags known to be targeted in autoimmune disease, but not targeted in APECED. Type II collagen (CII) is a prominent target of autoimmune destruction in rheumatoid arthritis (RA) and is the arthritogenic Ag in the mouse model of RA, collagen-induced arthritis (CIA) (10,11). It is unclear whether there is a defect at the level of central or peripheral tolerance in the pathogenesis of disease.…”

mentioning

confidence: 99%

Lymphotoxin Pathway-Directed, Autoimmune Regulator-Independent Central Tolerance to Arthritogenic Collagen

Chin

Zhu

Christiansen

et al. 2006

The Journal of Immunology

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Ectopic expression of peripherally restricted Ags by medullary thymic epithelial cells (mTECs) is associated with negative selection. Autoimmune regulator (AIRE) is considered to be the master regulator of these Ags. We show in this study that the ectopic expression of type II collagen (CII) in mTECs and the corresponding central tolerance to CII are AIRE independent but lymphotoxin dependent. The failure to properly express CII in mTECs of Lta−/− and Ltbr−/− mice leads to overt autoimmunity to CII and exquisite susceptibility to arthritis. These findings define the existence of additional pathways of ectopic peripheral Ag expression, parallel to and independent of AIRE, which may cover an extended spectrum of peripheral Ags in the thymus.

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“…Moreover, CD69 -/-mice, when challenged with antigen, also developed an exacerbated form of collagen-induced arthritis (CIA) [10]. Murine CIA is a T cell-dependent antibody-mediated autoimmune disease directed against cartilage type II collagen (CII) [11]. Mice with CIA show T and B cell reactivity against collagen, and a strong inflammatory cell infiltrate in joints along with the production of pro-inflammatory cytokines.…”

Section: Introductionmentioning

confidence: 99%

The role of CD69 in acute neutrophil‐mediated inflammation

et al. 2006

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The leukocyte activation marker CD69 functions as a negative regulator of the immune response, both in NK-dependent tumor rejection and in the inflammation associated with lymphocyte-dependent collagen-induced arthritis. In contrast, it has been reported that CD69-deficient mice are refractory to the neutrophil-dependent acute inflammatory response associated with anti-type II collagen antibody-induced arthritis (CAIA), suggesting a positive regulatory role for CD69 in neutrophil function during arthritis induction. To clarify this discrepancy, the CAIA response was independently analyzed in our CD69-deficient mice. In these experiments, the inflammatory response was unaffected by CD69 deficiency. Additionally, the in vivo down-regulation of CD69 expression by treatment of wild-type mice with the anti-CD69 mAb 2.2, which mimics the CD69-deficient phenotype, did not affect the course of arthritis in this model. Moreover, down-regulation of CD69 expression increased expression in arthritic joints of key inflammatory mediators, including IL-1b, IL-6 and the chemokine MCP-1. Neutrophil accumulation in zymosan-treated air pouches and in thioglycolate-treated peritoneal cavities was also unaffected in CD69-deficient mice. In addition, CD69 expression was absent in activated neutrophils. Taken together, these results rule out a significant stimulatory role for CD69 in acute inflammatory responses mediated by neutrophils.

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Collagen-induced arthritis, an animal model of autoimmunity

Cited by 297 publications

References 117 publications

A Costimulatory Function for T Cell CD40

A Costimulatory Function for T Cell CD40

Lymphotoxin Pathway-Directed, Autoimmune Regulator-Independent Central Tolerance to Arthritogenic Collagen

The role of CD69 in acute neutrophil‐mediated inflammation

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