Effector function of type II collagen–stimulated T cells from rheumatoid arthritis patients: Cross‐talk between T cells and synovial fibroblasts

Cho, Mi La; Yoon, Chong Hyun; Hwang, Sue Yun; Park, Mi Kyung; Min, Sung−Wook; Lee, Sang‐Heon; Park, Sung Hwan; Kim, Ho Youn

doi:10.1002/art.20106

Cited by 85 publications

(61 citation statements)

References 20 publications

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“…One study used unstimulated purified T cells [14] and the other used collagen-type II (CII) responsive T cells [15]. Both studies cite the importance of IL-15 expression by FLS and its upregulation after stimulation by T cells [14,15]. The first study utilized unstimulated T cells purified from peripheral blood or RA synovial fluid.…”

Section: Cross-talk Between T Cells and Flsmentioning

confidence: 99%

“…T cell responses were blunted by blocking antibodies towards ICAM-1 and IL-15. When CII-activated T cells were used as the stimulus, FLS displayed production of TNFα, IL-15 and IL18 [15]. These CII-activated T cells were generated by culture of T cells with bovine CII and autologous irradiated APC for extended periods.…”

Section: Cross-talk Between T Cells and Flsmentioning

confidence: 99%

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Synovial biology and T cells in rheumatoid arthritis

2005

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Events that occur in rheumatoid arthritis synovial tissues are responsible for the signs and symptoms of joint inflammation and for the eventual destruction of articular and periarticular structures that lead to joint dysfunction and disability. The three most abundant cell populations in RA synovium are synovial macrophages (type A synoviocytes), synovial fibroblasts (type B synoviocytes) and infiltrating T lymphocytes. Other important cell populations include B lymphocytes, dendritic cells, plasma cells, mast cells and osteoclasts. Our current understanding of rheumatoid arthritis is moving beyond previous concepts that view this disease as the consequence of a specific and focused humoral or cellular autoimmune response to a single autoantigen. Rather, a new view of rheumatoid arthritis is emerging, which seeks to understand this disease as the product of pathologic cell-cell interactions occurring within a unique and defined environment, the synovium. T lymphocytes in rheumatoid arthritis synovium interact closely with dendritic cells, the most potent antigen-presenting cell population in the immune system. T cells also interact with monocytes and macrophages and cytokine-activated T cells may be, especially, suited to trigger production of the important cytokine TNFα by synovial macrophages. Recent evidence also suggests a potent bidirectional interaction between synovial T cells and synovial fibroblasts, which can lead to activation of both cell types. An important role for synovial B lymphocytes has been emphasized recently, both by experimental data and by results of clinical interventions. B cells in synovium can interact with fibroblasts as well as with other cells of the immune system and their potential role as antigen-presenting cells in the joint is as yet underexplored. Rheumatoid arthritis synovium may be one of the most striking examples of pathologic, organ-specific interactions between immune system cells and resident tissue cell populations. This view of rheumatoid arthritis also leads to the prediction that novel approaches to treatment will more logically target the intercellular communication systems that maintain such interactions, rather than attempt to ablate a single cell population.

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Section: Cross-talk Between T Cells and Flsmentioning

confidence: 99%

Section: Cross-talk Between T Cells and Flsmentioning

confidence: 99%

Synovial biology and T cells in rheumatoid arthritis

2005

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“…The products of TH17 cells, such as IL-17 and IL-23, are present in the serum, synovial fluid and synovial tissue of the majority of patients with RA, while they are absent in osteoarthritis (39)(40)(41). Under normal conditions, IL-17 is undetectable or detected at very low levels in the serum of healthy controls.…”

Section: Th17 Cells In Human Autoimmune Diseasesmentioning

confidence: 99%

“…Under normal conditions, IL-17 is undetectable or detected at very low levels in the serum of healthy controls. However, high levels of this cytokine were detected in serum and synovial fluid in two studies evaluating patients with RA (40,42). IL-17-producing clones were recoverable from effector T cells of synovial tissue of patients with RA (43).…”

Section: Th17 Cells In Human Autoimmune Diseasesmentioning

confidence: 99%

Autoimmune diseases in the TH17 era

Mesquita

Cruvinel

Câmara

et al. 2009

Braz J Med Biol Res

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A new subtype of CD4 + T lymphocytes characterized by the production of interleukin 17, i.e., TH17 cells, has been recently described. This novel T cell subset is distinct from type 1 and type 2 T helper cells. The major feature of this subpopulation is to generate significant amounts of pro-inflammatory cytokines, therefore appearing to be critically involved in protection against infection caused by extracellular microorganisms, and in the pathogenesis of autoimmune diseases and allergy. The dynamic balance among subsets of T cells is important for the modulation of several steps of the immune response. Disturbances in this balance may cause a shift from normal immunologic physiology to the development of immune-mediated disorders. In autoimmune diseases, the fine balance between the proportion and degree of activation of the various T lymphocyte subsets can contribute to persistent undesirable inflammatory responses and tissue replacement by fibrosis. This review highlights the importance of TH17 cells in this process by providing an update on the biology of these cells and focusing on their biology and differentiation processes in the context of immune-mediated chronic inflammatory diseases.

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“…IL-17 activates NF-κB and stimulates the production of several inflammatory mediators, including IL-6, IL-8, granulocyte-macrophage colony stimulating factor (GM-CSF), and prostaglandin E2 (PGE 2 ) in synoviocytes (Lubberts et al, 2005;Miossec, 2004;Stamp et al, 2004;Hwang et al, 2004). IL-17 is released mainly by memory T cells and is associated particularly with the severity of synovial inflammation of patients with RA (Cho et al, 2004;Hwang et al, 2004).…”

Section: Introductionmentioning

confidence: 99%