γδ T cell subsets in patients with arthritis and chronic neutropenia

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 RP⁺ 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 nonerosive, suggesting a protective effect of these cells, as opposed to a more pathogenic contribution of Vγ1 ⁺/Vδ¹+ cells.