Defective TCR-mediated signaling in synovial T cells in rheumatoid arthritis

Maurice, M. M.; Lankester, Arjan C.; Bezemer, Anja C.; Geertsma, M. F.; Tak, Paul‐Peter; Breedveld, F. C.; Lier, René A. W. van; Verweij, CL

doi:10.1016/s0165-2478(97)88138-2

Cited by 78 publications

(67 citation statements)

References 6 publications

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“…Moreover, mutations in different molecules of the TCR/CD3 signaling pathways affect the lineage-commitment decisions during T cell development (25), as well as the development of autoimmunity (26). In line with this, defects in CD3z expression/ function were suggested to have implications for the development of human autoimmune phenotypes (24,35,36). Thus, several groups reported altered expression and function of CD3z in patients with SLE (19,20) or rheumatoid arthritis (21,22).…”

Section: Discussionmentioning

confidence: 94%

Variation in the Cd3ζ (Cd247) Gene Correlates with Altered T Cell Activation and Is Associated with Autoimmune Diabetes

Lundholm

Mayans

Motta

et al. 2010

The Journal of Immunology

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Section: Discussionmentioning

confidence: 94%

Variation in the Cd3ζ (Cd247) Gene Correlates with Altered T Cell Activation and Is Associated with Autoimmune Diabetes

Lundholm

Mayans

Motta

et al. 2010

The Journal of Immunology

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“…Previous studies have demonstrated deficient expression of the TCR chain and aberrant early signaling events in T cells from a majority of SLE patients, suggesting an important role for the defective chain in mediating a pathologic process leading to SLE (3,9). Deficiency in expression of the TCR chain has been observed in synovial and tumor-infiltrating lymphocytes and other pathologic conditions (45)(46)(47)(48)(49)(50)(51)(52)(53). Although multiple forms of the chain have been implicated in different functions of T cells, a complete spectrum of the deficiency of different forms of the TCR chain in SLE T cells or in any other autoimmune disease has not been described.…”

Section: Discussionmentioning

confidence: 99%

Abnormal expression of various molecular forms and distribution of T cell receptor ? chain in patients with systemic lupus erythematosus

Nambiar

Enyedy

Fisher

et al. 2002

Arthritis & Rheumatism

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“…In RA synovial T cells, chronic oxidative stress leads to misfolding of the cysteine-rich signaling proteins required for proliferation, including linker for activated T cells (LAT) and the TCR-associated -chain (15)(16)(17). This effect can be mimicked pharmacologically in normal T lymphocytes (16) and in murine T cell hybridomas after prolonged exposure to TNF␣ (18).…”

Section: Synovial Adherent Cells and This Correlated With T Cell Mitmentioning

confidence: 99%

CTLA‐4IG suppresses reactive oxygen species by preventing synovial adherent cell–induced inactivation of rap1, a ras family GTPASE mediator of oxidative stress in rheumatoid arthritis T cells

Remans¹,

Wijbrandts²,

Sanders³

et al. 2006

Arthritis & Rheumatism

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Objective. Oxidative stress contributes to the inflammatory properties of rheumatoid arthritis (RA) synovial T lymphocytes. This study was undertaken to investigate the mechanisms leading to production of reactive oxygen species (ROS) and oxidative stress in RA synovial T lymphocytes.Methods. ROS production in T lymphocytes from the peripheral blood (PB) of healthy donors and from the PB and synovial fluid (SF) of RA patients was measured by ROS-dependent fluorescence of 6-carboxy-2 ,7 -dichlorofluorescein. Rap1 GTPase activation was assessed by activation-specific probe precipitation. Proliferation of RA PB and SF T lymphocytes was assayed by 3 H-thymidine incorporation. In some experiments, RA PB T cells were preincubated with autologous SF or with PB or SF adherent cells. Experiments were performed in the absence or presence of transwell membranes or CTLA-4Ig fusion proteins. Short-and longterm stimulations of healthy donor PB T lymphocytes were performed with inflammatory cytokines, in the absence or presence of activating anti-CD28 antibodies. Conclusion. Cell-cell contact between T cells and RA synovial adherent cells mediates Rap1 inactivation and subsequent ROS production in T lymphocytes following exposure to inflammatory cytokines. This process can be blocked by CTLA4-Ig fusion protein. Results. T lymphocyte ROS production and

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Defective TCR-mediated signaling in synovial T cells in rheumatoid arthritis

Cited by 78 publications

References 6 publications

Variation in the Cd3ζ (Cd247) Gene Correlates with Altered T Cell Activation and Is Associated with Autoimmune Diabetes

Variation in the Cd3ζ (Cd247) Gene Correlates with Altered T Cell Activation and Is Associated with Autoimmune Diabetes

Abnormal expression of various molecular forms and distribution of T cell receptor ? chain in patients with systemic lupus erythematosus

CTLA‐4IG suppresses reactive oxygen species by preventing synovial adherent cell–induced inactivation of rap1, a ras family GTPASE mediator of oxidative stress in rheumatoid arthritis T cells

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