TY - JOUR
T1 - The intrinsic migratory capacity of memory T cells contributes to their accumulation in rheumatoid synovium
AU - Cush, John J.
AU - Pietschmann, Peter
AU - Oppenheimer‐Marks, Nancy
AU - Lipsky, Peter E.
PY - 1992/12
Y1 - 1992/12
N2 - Objective. Mechanisms controlling the infiltration of T cells into rheumatoid synovium have not been fully characterized. These studies were undertaken to investigate the relationship between T cell phenotype and migratory capacity, so as to elucidate mechanisms that might contribute to the accumulation of T cells at inflammatory sites. Methods. The characteristics of in vivo migrating cells were studied by dual‐immunofluorescence FACS (fluorescence‐activated cell sorter) analysis of rheumatoid synovial and peripheral blood T cells. Migratory cells were also characterized using a recently developed in vitro assay, wherein peripheral blood T lymphocytes (PBTL) with the capacity to migrate through endothelial cell monolayers were retrieved and assessed. Results. Migratory CD4+ T cells from rheumatoid arthritis (RA) and normal individuals were characterized as being CD45RA‐, CD29bright, CD11abright, L‐selectin‐, CD54+, and CD58+. Migrating RA PBTL (compared with normal PBTL), however, were significantly enriched in activated HLA—DR+ T cells. RA synovial tissue lymphocytes exhibited a similar phenotype, but with decreased surface density of CD4 and an increase in HLA‐DR and VLA‐1. RA synovial lymphocytes exhibited a 2–3‐fold increase in migratory capacity over normal and RA PBTL. Conclusion. These studies demonstrate the inherent migratory proficiency of CD4+ T cells that express a memory phenotype (CD29bright, CD11abright, and CD58+). In addition, enhanced transendothelial migration was observed for CD4+ T cells that were CD54+ and L‐selectin—. These studies demonstrate that the migratory patterns of circulating lymphocytes may be correlated with their surface phenotype and that the intrinsic migratory capacity of memory T cells is one component contributing to their accumulation in the rheumatoid synovium.
AB - Objective. Mechanisms controlling the infiltration of T cells into rheumatoid synovium have not been fully characterized. These studies were undertaken to investigate the relationship between T cell phenotype and migratory capacity, so as to elucidate mechanisms that might contribute to the accumulation of T cells at inflammatory sites. Methods. The characteristics of in vivo migrating cells were studied by dual‐immunofluorescence FACS (fluorescence‐activated cell sorter) analysis of rheumatoid synovial and peripheral blood T cells. Migratory cells were also characterized using a recently developed in vitro assay, wherein peripheral blood T lymphocytes (PBTL) with the capacity to migrate through endothelial cell monolayers were retrieved and assessed. Results. Migratory CD4+ T cells from rheumatoid arthritis (RA) and normal individuals were characterized as being CD45RA‐, CD29bright, CD11abright, L‐selectin‐, CD54+, and CD58+. Migrating RA PBTL (compared with normal PBTL), however, were significantly enriched in activated HLA—DR+ T cells. RA synovial tissue lymphocytes exhibited a similar phenotype, but with decreased surface density of CD4 and an increase in HLA‐DR and VLA‐1. RA synovial lymphocytes exhibited a 2–3‐fold increase in migratory capacity over normal and RA PBTL. Conclusion. These studies demonstrate the inherent migratory proficiency of CD4+ T cells that express a memory phenotype (CD29bright, CD11abright, and CD58+). In addition, enhanced transendothelial migration was observed for CD4+ T cells that were CD54+ and L‐selectin—. These studies demonstrate that the migratory patterns of circulating lymphocytes may be correlated with their surface phenotype and that the intrinsic migratory capacity of memory T cells is one component contributing to their accumulation in the rheumatoid synovium.
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U2 - 10.1002/art.1780351206
DO - 10.1002/art.1780351206
M3 - Article
C2 - 1282007
AN - SCOPUS:0027100467
SN - 0004-3591
VL - 35
SP - 1434
EP - 1444
JO - Arthritis & Rheumatism
JF - Arthritis & Rheumatism
IS - 12
ER -