Differential expression of NK receptors CD94 and NKG2A by T cells in rheumatoid arthritis patients in remission compared to active disease

• Published in: PloS one 2011-11, Vol.6 (11), p.e27182-e27182
• Main Authors: Walsh, Ceara E, Ryan, Elizabeth J, O'Farrelly, Cliona, Golden-Mason, Lucy, FitzGerald, Oliver, Veale, Douglas J, Bresnihan, Barry, Fearon, Ursula
• Format: Article
• Language: English
• Subjects: Antirheumatic agents; Arthritis; Arthritis, Rheumatoid - drug therapy; Arthritis, Rheumatoid - immunology; Arthritis, Rheumatoid - metabolism; Autoimmune diseases; Biochemistry; Biology; Care and treatment; Case-Control Studies; CD3 antigen; CD56 antigen; CD57 antigen; CD69 antigen; Cohort Studies; Comparative analysis; Cytokines; Cytometry; Dendritic cells; Effector cells; Enzymes; Female; Flow cytometry; Follow-Up Studies; Humans; Immunology; Inflammatory bowel disease; Killer cells; Killer Cells, Natural - drug effects; Killer Cells, Natural - metabolism; Laboratories; Leukocytes, Mononuclear; Ligands; Lymphocytes; Lymphocytes T; Male; Medical research; Medicine; Middle Aged; Natural killer cells; Neutropenia; Neutrophils; NK Cell Lectin-Like Receptor Subfamily C - metabolism; NK Cell Lectin-Like Receptor Subfamily D - metabolism; NKG2 antigen; Patients; Peripheral blood mononuclear cells; Psoriasis; Receptors; Remission; Remission (Medicine); Remission Induction; Rheumatoid arthritis; Rheumatoid factor; Rheumatology; Somatotropin; T cell receptors; T cells; T-Lymphocytes - drug effects; T-Lymphocytes - metabolism; Therapy; Tumor Necrosis Factor-alpha - antagonists & inhibitors
• ISSN: 1932-6203; 1932-6203
• DOI: 10.1371/journal.pone.0027182

TNF inhibitors (TNFi) have revolutionised the treatment of rheumatoid arthritis (RA). Natural killer (NK) cells and Natural Killer Cell Receptor+ T (NKT) cells comprise important effector lymphocytes whose activity is tightly regulated through surface NK receptors (NKRs). Dysregulation of NKRs in patients with autoimmune diseases has been shown, however little is known regarding NKRs expression in patients with TNFi-induced remission and in those who maintain remission vs disease flare following TNFi withdrawal. Patients with RA were recruited for this study, (i) RA patients in clinical remission following a minimum of one year of TNFi therapy (n = -15); (2) Active RA patients, not currently or ever receiving TNFi (n = 18); and healthy control volunteers (n = 15). Patients in remission were divided into two groups: those who were maintained on TNFi and those who withdrew from TNFi and maintained on DMARDS. All patients underwent full clinical assessment. Peripheral blood mononuclear cells were isolated and NKR (CD94, NKG2A, CD161, CD69, CD57, CD158a, CD158b) expression on T-(CD3+CD56-), NK-(CD3-CD56+) and NKT-(CD3+CD56+) cells was determined by flow cytometry. Following TNFi withdrawal, percentages and numbers of circulating T cells, NK cells or NKT cell populations were unchanged in patients in remission versus active RA or HCs. Expression of the NKRs CD161, CD57, CD94 and NKG2A was significantly increased on CD3+CD56-T cells from patients in remission compared to active RA (p