K J Murray1, L Luyrink, A A Grom, M H Passo, H Emery, D Witte, D N Glass. 1. William S. Rowe Division of Rheumatology, Department of Pediatrics, Children's Hospital Medical Center, University of Cincinnati, College of Medicine, OH, USA.
Abstract
OBJECTIVE: To characterize synovial T cell infiltrate, in terms of CD4/CD8 ratio and level of activation of T cells, in juvenile rheumatoid arthritis (JRA) and juvenile spondyloarthropathy(JSpA), to correlate these findings with clinical outcomes of the different forms of disease, and to compare them with findings in adult RA synovium. METHODS: We studied synovial tissue specimens from 22 individuals with childhood onset of chronic arthritis (12 polyarticular JRA, 5 pauciarticular JRA, 5 JSpA) and 4 with adult RA. Specimens were selected from an initial bank from 40 patients on the basis of significant inflammation on hematoxylin and eosin and CD3 and CD68 monoclonal antibody staining (T cells and macrophages, respectively). Indirect immunohistochemistry was used with monoclonal antibodies to CD3, CD4, CD8, and interleukin 2 receptor alpha to determine CD4/CD8 ratios and the levels of activation within the T cell subsets. The distribution of gamma delta T cells was also studied. RESULTS: Two patterns of T cell infiltration were seen. The majority of patients had lymphocytic aggregates associated with diffuse infiltrates; a few tissue specimens had diffuse infiltrates without aggregates. The CD4/CD8 ratio was significantly lower in pauciarticular course JRA than polyarticular JRA (p < 0.01) and RA (p < 0.05). Similarly patients with JSpA had a significantly lower CD4/CD8 ratio than patients with polyarticular JRA (P < 0.05). The level of T cell activation (CD3+IL-2R+) was significantly higher in pauciarticular compared with both polyarticular JRA (P < 0.01) and RA (p < 0.05). In general, higher levels of activation of CD8 cells than CD4 cells were seen, particularly in the pauciarticular JRA and JSpA groups. gamma delta T cells were prominent in 2 patients. CONCLUSION: Demonstrated differences in T cell subset distribution between types of childhood chronic arthritis at a histopathological level may reflect different pathogenic mechanisms.
OBJECTIVE: To characterize synovial T cell infiltrate, in terms of CD4/CD8 ratio and level of activation of T cells, in juvenile rheumatoid arthritis (JRA) and juvenile spondyloarthropathy(JSpA), to correlate these findings with clinical outcomes of the different forms of disease, and to compare them with findings in adult RA synovium. METHODS: We studied synovial tissue specimens from 22 individuals with childhood onset of chronic arthritis (12 polyarticular JRA, 5 pauciarticular JRA, 5 JSpA) and 4 with adult RA. Specimens were selected from an initial bank from 40 patients on the basis of significant inflammation on hematoxylin and eosin and CD3 and CD68 monoclonal antibody staining (T cells and macrophages, respectively). Indirect immunohistochemistry was used with monoclonal antibodies to CD3, CD4, CD8, and interleukin 2 receptor alpha to determine CD4/CD8 ratios and the levels of activation within the T cell subsets. The distribution of gamma delta T cells was also studied. RESULTS: Two patterns of T cell infiltration were seen. The majority of patients had lymphocytic aggregates associated with diffuse infiltrates; a few tissue specimens had diffuse infiltrates without aggregates. The CD4/CD8 ratio was significantly lower in pauciarticular course JRA than polyarticular JRA (p < 0.01) and RA (p < 0.05). Similarly patients with JSpA had a significantly lower CD4/CD8 ratio than patients with polyarticular JRA (P < 0.05). The level of T cell activation (CD3+IL-2R+) was significantly higher in pauciarticular compared with both polyarticular JRA (P < 0.01) and RA (p < 0.05). In general, higher levels of activation of CD8 cells than CD4 cells were seen, particularly in the pauciarticular JRA and JSpA groups. gamma delta T cells were prominent in 2 patients. CONCLUSION: Demonstrated differences in T cell subset distribution between types of childhood chronic arthritis at a histopathological level may reflect different pathogenic mechanisms.