Γδ T cell subsets in patients with arthritis and chronic neutropenia. Issue 5 (1st May 2002)

• Record Type: Journal Article
• Authors: Bank, I; Cohen, L; Mouallem, M; Farfel, Z; Grossman, E; Ben-Nun, A
• Is Part Of: Annals of the rheumatic diseases. Volume 61:Issue 5(2002)
• Page Start: 438
• Page End: 443
• Publication Date: 2002-05-01
• Subjects: gamma delta T cells -- neutropenia -- autoimmunity -- Felty's syndrome; FS, Felty's syndrome -- mAb, monoclonal antibody -- PB, peripheral blood -- PBL, peripheral blood lymphocytes -- PBS, phosphate buffered saline -- PCR, polymerase chain reaction -- PFS, pseudo-Felty's syndrome -- RA, rheumatoid arthritis -- RF, rheumatoid factor -- TCR, T cell receptor -- T-LGLD, large granular T lymphocytic disorder; Rheumatism -- Periodicals; 616.723005
• DOI: 10.1136/ard.61.5.438
• Languages: English
• ISSNs: 0003-4967

Abstract

Abstract : Background: An abnormal distribution of subsets of γδ T cells, which are a component of the inflammatory infiltrate in arthritic synovium, has been demonstrated in the peripheral blood (PB) of patients with arthritis and neutropenia. Objective: To evaluate whether the clinical manifestations of patients with arthritis and neutropenia are related to the specific γδ T cell subset predominant in the PB. Methods: Flow cytometry of PB lymphocytes in six consecutive patients with chronic neutropenia and arthritis was performed. Variable (V) γ and δ gene families were analysed by polymerase chain reaction. cDNA was subjected to direct automated sequencing of T cell receptor (TCR) genes. Results: Three patients had non-deforming and non-erosive rheumatoid factor (RF) + polyarticular rheumatoid arthritis, RF + oligoarticular arthritis, or RF − non-deforming oligoarticular psoriatic arthritis with persistent expansions of Vγ1 + /Vδ2 +, Vγ2 + /Vδ2 +, or Vγ1 + /Vδ undetermined (2− 1−) T cells, respectively. The other three patients, without persistent expansion of γδ T cells, had either non-deforming and non-erosive oligo- or polyarthritis with a balanced distribution of several Vδ and Vγ genes, or severe erosive RF + arthritis with deficiency of all but Vγ1 + /Vδ1 + T cells. Conclusions: γδ T cell lymphoproliferations in chronic neutropenia and arthritis use different Vγ and Vδ gene families, often forming T cell receptor (TCR) structures that are infrequent in normal adult PB. Arthritis with Vγ1 + /Vδ2 +, Vγ2 + /Vδ2 +, or Vγ1 + /Vδ2 − /Vδ1 − γδ T cells in the PB is non-deforming and non-erosive, suggesting a protective effect of these cells, as opposed to a more pathogenic contribution of Vγ1 + /Vδ1 + cells.