The role of interleukin-16 in the immunopathogenesis of rheumatoid arthritis

Abstract EN

Objective : We analyzed, interleukin-16 (IL-16), in relation to disease activity to characterize its biologic function in RA.

Methodology : Secreted IL-16 was measured with enzyme immunoassay in the sera from 30 RA patients and 30 apparently healthy controls as well as in synovial fluid (SF) from 16 RA patients and 15 patients with non-RA sinusitis as controls.

IL-16 expression in peripheral blood mononuclear cells (PBMC) was characterized with flow kilometric analysis after intracellular cytokine staining for IL-16.

In synovial tissue specimens, both were done: immunohistochemistry for localization of IL-16, and histopathology, in which the tissue was scored semi quantitatively for synovial hyperplasia and cellular infiltration.

Results : IL-16 was detected at significantly higher levels in sera and SF of RA patients in comparison to apparently healthy controls and non-RA sinusitis (p < 0.001 and p < 0.0001 respectively).

Also, IL-16 was detected significantly higher in SF in comparison to sera in RA patients (p < 0.001).

Flow cytometer of PBMC showed that a great proportion of both CD4+ and CD8+ cells expressed IL-16 protein.

Also, immunohisto-chemistry revealed more CD4+ and less frequency of CD8+ cells in synovial infiltration.

A significant correlation between IL-16 expression and local inflammatory activity could not be established (p > 0.21) with microscopic analysis of the synovial cells infiltrate.

In addition, no significant association was observed between serum, SF, and synovial tissue expression of IL–16 and clinical disease activity in RA (p > 0.

61, p > 0.5 and p > 0.

42 respectively).

Conclusion : IL-16 seems to play a regulatory rather than a proinflammatory role in the immunopathogenesis of RA.