{'fraction_non_alphanumeric': 0.02824207492795389, 'fraction_numerical': 0.006340057636887608, 'mean_word_length': 5.916334661354582, 'pattern_counts': {'":': 0, '<': 0, '<?xml version=': 0, '>': 0, 'https://': 0, 'lorem ipsum': 0, 'www.': 0, 'xml': 0}, 'pii_count': 0, 'substrings_counts': 0, 'word_list_counts': {'cursed_substrings.json': 0, 'profanity_word_list.json': 0, 'sexual_word_list.json': 0, 'zh_pornsignals.json': 0}}
T cells in reactive arthritis

T cells appear to play a major role in the development, maintenance and also resolution of reactive arthritis (ReA). Recent advances in understanding the processes involved in T cell activation now allow us to examine the peripheral blood and synovial fluid T cell responses to given “arthritogenic” microorganisms in terms of antigen specificity, epitope identification, cytokine secretion patterns, HLA restriction and the role of different T cell subsets in ReA. Peripheral blood bulk proliferation and limiting dilution studies provide evidence that the peripheral T cell response against arthritis‐associated gram‐negative bacteria is decreased in patients developing immunological sequelae such as ReA after gastrointestinal infection. Using clonal analysis of synovial fluid CD4+ T cells it has been shown that a polyclonal rather than an oligoclonal response to a variety of bacterial antigens is induced at the site of synovitis and that these CD4+ T cells produce a Thl‐type of cytokine. 65 kD heat shock protein may represent one of the possible linkages of anti‐infectious and autoimmune reactions. Furthermore, a spectrum of killer cells is present in the synovial fluid of patients with ReA. This spectrum of cytotoxic T cells includes antigen‐specific, class I‐restricted αβ‐TCR+CD8+ lymphocytes, antigen‐specific, apparently non‐MHC‐restricted αβ‐TCR+CD8+ lymphocytes and γδ‐TCR+ cells with broad cytolytic activity directed against bacteria‐infected target cells. HLA‐B27‐restricted Yersinia‐ or Salmonella‐specific synovial fluid CD8+ T cells may provide the missing link between genetic disposition (HLA‐B27) and extra‐articular infection with arthritogenic bacteria in these patients.