Specificity of T cells in synovial fluid: high frequencies of CD8+ T cells that are specific for certain viral epitopes

Tan, Linda; Mowat, A G; Fazou, Chrysoula; Rostron, Tim; Roskell, Helen; Dunbar, P. Rod; Tournay, Claire; Romagné, François; Peyrat, Marie-Alix; Houssaint, Elisabeth; Bonneville, Marc; Rickinson, Alan B.; McMichael, Andrew J.; Callan, Margaret

doi:10.1186/ar80

Cited by 67 publications

(22 citation statements)

References 42 publications

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“…Previously, it has been shown that, in synovial fluid of patients with chronic inflammatory arthritis, Epstein-Barr virus (EBV) peptide-specific CD8+ T cells can be found [29]. Moreover, CD8+ T cells contribute to osteoarthritis progression via cartilage degeneration in an animal model [30].…”

Section: Discussionmentioning

confidence: 99%

Immune Mediators in Osteoarthritis: Infrapatellar Fat Pad-Infiltrating CD8+ T Cells Are Increased in Osteoarthritic Patients with Higher Clinical Radiographic Grading

Apinun

Sengprasert

Yuktanandana

et al. 2016

International Journal of Rheumatology

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Osteoarthritis is a condition of joint failure characterized by many pathologic changes of joint-surrounding tissues. Many evidences suggest the role of both innate and adaptive immunity that interplay, resulting either in initiation or in progression of osteoarthritis. Adaptive immune cells, in particular T cells, have been demonstrated to play a role in the development of OA in animal models. However, the underlying mechanism is yet unclear. Our aim was to correlate the frequency and phenotype of tissue-infiltrating T cells in the synovial tissue and infrapatellar fat pad with radiographic grading. Our results show that CD8+ T cells are increased in osteoarthritic patients with higher radiographic grading. When peripheral blood CD8+ T cells were examined, we show that CD8+ T cells possess a significantly higher level of activation than its CD4+ T cell counterpart (P < 0.0001). Our results suggest a role for CD8+ T cells and recruitment of these activated circulating peripheral blood CD8+ T cells to the knee triggering local inflammation within the knee joint.

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Section: Discussionmentioning

confidence: 99%

Immune Mediators in Osteoarthritis: Infrapatellar Fat Pad-Infiltrating CD8+ T Cells Are Increased in Osteoarthritic Patients with Higher Clinical Radiographic Grading

Apinun

Sengprasert

Yuktanandana

et al. 2016

International Journal of Rheumatology

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“…As gp110 is important in viral entry during infection of B-cells and epithelial cells, a decreased gp110-specific T-cell response could be speculated to reduce the control of EBV and also enhance spreading of the EBV infection in RA patients. Contrarily, CD8+ cytotoxic T-cells specific for the two lytic cycle EBV antigens, BZLF1 and BMLF1, have been detected in synovial fluid and synovial membranes of RA patients, indicating a contribution of infiltrated cytotoxic T-cells specific for EBV lytic cycle antigens in joint inflammation [84, 85]. …”

Section: Ebv In Sadsmentioning

confidence: 99%

“…In RA patients, the EBV-infected cells in the synovial joints are shown to undergo frequent reactivation including EBV-infected plasma cells producing CCP autoantibodies [72, 74–76, 78, 84, 85]. The EBV reactivation results in production of lytic cycle proteins giving rise to host immune responses that presumably contribute to the inflammation and destruction of exocrine glands and synovial joints in SS and RA patients, respectively [72, 74–76, 78, 84–90, 96].…”

Section: Genetic Factors and Possible Mechanisms Associated With Imentioning

confidence: 99%

Epstein-Barr Virus in Systemic Autoimmune Diseases

Draborg

Duus

Houen

2013

Clinical and Developmental Immunology

193

144

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Systemic autoimmune diseases (SADs) are a group of connective tissue diseases with diverse, yet overlapping, symptoms and autoantibody development. The etiology behind SADs is not fully elucidated, but a number of genetic and environmental factors are known to influence the incidence of SADs. Recent findings link dysregulation of Epstein-Barr virus (EBV) with SAD development. EBV causes a persistent infection with a tight latency programme in memory B-cells, which enables evasion of the immune defence. A number of immune escape mechanisms and immune-modulating proteins have been described for EBV. These immune modulating functions make EBV a good candidate for initiation of autoimmune diseases and exacerbation of disease progression. This review focuses on systemic lupus erythematosus (SLE), rheumatoid arthritis (RA), and Sjögren's syndrome (SS) and sum up the existing data linking EBV with these diseases including elevated titres of EBV antibodies, reduced T-cell defence against EBV, and elevated EBV viral load. Together, these data suggest that uncontrolled EBV infection can develop diverse autoreactivities in genetic susceptible individuals with different manifestations depending on the genetic background and the site of reactivation.

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“…Using tetramer staining, one study demonstrated EBV-specific CD8+ T cells in synovial fluid from RA patients. However, these findings were not restricted to RA as there was also an enrichment of these cells in synovial fluid from patients with osteoarthritis and psoriatic arthritis [53]. …”

Section: Pathogenesis Of Lgl Leukemia and Felty’s Syndromementioning

confidence: 99%

The spectrum of large granular lymphocyte leukemia and Feltyʼs syndrome

Liu

Loughran

2011

Current Opinion in Hematology

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Purpose of review Patients with chronic large granular lymphocyte (LGL) leukemia often have rheumatoid arthritis, neutropenia and splenomegaly, thereby resembling the manifestations observed in patients with Felty’s syndrome (FS), which is a rare complication of rheumatoid arthritis (RA) characterized by neutropenia and splenomegaly. Both entities have similar clinical and laboratory presentation, as well as common genetic determinant HLA-DR4, indicating they may be part of the same disease spectrum. This review paper seeks to discuss the underlying pathogenesis and therapeutic algorithm of RA, neutropenia and splenomegaly in the spectrum of LGL leukemia and Felty’s syndrome. Recent findings We hypothesize that there may be a common pathogenic mechanism between LGL leukemia and typical FS. Phenotypic and functional data have strongly suggested that CD3+ LGL leukemia are antigen-activated. Aberrations in the T cell repertoire with the emergence of oligoclonal/clonal lymphoid populations have been found to play a pivotal role in pathogenesis of rheumatoid arthritis. The biologic properties of the pivotal T cell involved in rheumatoid arthritis pathogenesis are remarkably similar to those in leukemic LGL. Summary RA-associated T-LGL leukemia and articular manifestations of typical Felty’s syndrome are not distinguishable. A common pathogenetic link between LGL leukemia and RA is proposed.

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Specificity of T cells in synovial fluid: high frequencies of CD8+ T cells that are specific for certain viral epitopes

Cited by 67 publications

References 42 publications

Immune Mediators in Osteoarthritis: Infrapatellar Fat Pad-Infiltrating CD8+ T Cells Are Increased in Osteoarthritic Patients with Higher Clinical Radiographic Grading

Immune Mediators in Osteoarthritis: Infrapatellar Fat Pad-Infiltrating CD8+ T Cells Are Increased in Osteoarthritic Patients with Higher Clinical Radiographic Grading

Epstein-Barr Virus in Systemic Autoimmune Diseases

The spectrum of large granular lymphocyte leukemia and Feltyʼs syndrome

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