Abstract
T cell receptor (TCR) γ δ bearing lymphocytes in peripheral blood and synovial fluid from rheumatoid arthritis (RA) and seronegative spondyloarthritides (SSA) were evaluated by means of double label immunofluorescence and cytofluorographic analysis. Three monoclonal antibodies (MAb) were used. TCR δ-1 against a common δ chain epitope, BB3 directed against the T cell subset whose TCR is encoded by the Vδ2 gene, and A13 directed against the Vδ1 subset. Peripheral blood Tγδ cells were significantly reduced compared to normal control blood in RA patients who had joint effusion but not in other RA patients. The decrease of Tγδ in the RA PB was mainly confined to the A13+ subset. In RA synovial fluid (RA SF) Tγδ cells were significantly increased compared to paired but not normal peripheral blood, the most significant being the increase of A13+ cells. In contrast, in patients with SSA, no change in Tγδ cells was observed on PB or SF. These data suggest that in RA, but not SSA, Tγδ cells migrate from PB to inflamed synovium and thus may be involved in the pathogenesis of RA.
| Original language | English |
|---|---|
| Pages (from-to) | 165-172 |
| Number of pages | 8 |
| Journal | Clinical Immunology and Immunopathology |
| Volume | 59 |
| Issue number | 1 |
| DOIs | |
| Publication status | Published - 1991 |
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ASJC Scopus subject areas
- Immunology
- Immunology and Allergy
- Pathology and Forensic Medicine
Cite this
γ δ T cells and their subpopulations in blood and synovial fluid from rheumatoid arthritis and spondyloarthritis. / Meliconi, R.; Pitzalis, C.; Kingsley, G. H.; Panayi, G. S.
In: Clinical Immunology and Immunopathology, Vol. 59, No. 1, 1991, p. 165-172.Research output: Contribution to journal › Article
}
TY - JOUR
T1 - γ δ T cells and their subpopulations in blood and synovial fluid from rheumatoid arthritis and spondyloarthritis
AU - Meliconi, R.
AU - Pitzalis, C.
AU - Kingsley, G. H.
AU - Panayi, G. S.
PY - 1991
Y1 - 1991
N2 - T cell receptor (TCR) γ δ bearing lymphocytes in peripheral blood and synovial fluid from rheumatoid arthritis (RA) and seronegative spondyloarthritides (SSA) were evaluated by means of double label immunofluorescence and cytofluorographic analysis. Three monoclonal antibodies (MAb) were used. TCR δ-1 against a common δ chain epitope, BB3 directed against the T cell subset whose TCR is encoded by the Vδ2 gene, and A13 directed against the Vδ1 subset. Peripheral blood Tγδ cells were significantly reduced compared to normal control blood in RA patients who had joint effusion but not in other RA patients. The decrease of Tγδ in the RA PB was mainly confined to the A13+ subset. In RA synovial fluid (RA SF) Tγδ cells were significantly increased compared to paired but not normal peripheral blood, the most significant being the increase of A13+ cells. In contrast, in patients with SSA, no change in Tγδ cells was observed on PB or SF. These data suggest that in RA, but not SSA, Tγδ cells migrate from PB to inflamed synovium and thus may be involved in the pathogenesis of RA.
AB - T cell receptor (TCR) γ δ bearing lymphocytes in peripheral blood and synovial fluid from rheumatoid arthritis (RA) and seronegative spondyloarthritides (SSA) were evaluated by means of double label immunofluorescence and cytofluorographic analysis. Three monoclonal antibodies (MAb) were used. TCR δ-1 against a common δ chain epitope, BB3 directed against the T cell subset whose TCR is encoded by the Vδ2 gene, and A13 directed against the Vδ1 subset. Peripheral blood Tγδ cells were significantly reduced compared to normal control blood in RA patients who had joint effusion but not in other RA patients. The decrease of Tγδ in the RA PB was mainly confined to the A13+ subset. In RA synovial fluid (RA SF) Tγδ cells were significantly increased compared to paired but not normal peripheral blood, the most significant being the increase of A13+ cells. In contrast, in patients with SSA, no change in Tγδ cells was observed on PB or SF. These data suggest that in RA, but not SSA, Tγδ cells migrate from PB to inflamed synovium and thus may be involved in the pathogenesis of RA.
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U2 - 10.1016/0090-1229(91)90090-W
DO - 10.1016/0090-1229(91)90090-W
M3 - Article
C2 - 1826866
AN - SCOPUS:0025733221
VL - 59
SP - 165
EP - 172
JO - Clinical Immunology and Immunopathology
JF - Clinical Immunology and Immunopathology
SN - 0090-1229
IS - 1
ER -