ABSTRACT
CD40/CD40 ligand [CD4O/CD4O-L] interaction has pleiotropic effects in a variety of cells and biological processes including immune response. Within the immune system, these molecules represent a critical link between its humoral and cellular arms. Numerous autoimmune diseases are associated with CD40/CD40-L interaction. CD40 is a cell surface receptor that belongs to the tumor necrosis factor-receptor [TNF-R] family, and that was first identified and functionally characterized on B- lymphocytes. CD40 ligand [CD40-L] or [CD154], a member of the TNF superfamily, is a cell membrane molecule expressed on activated CD4+ T-lymphocytes. Therefore, it is now thought that CD40/CD40-L interactions play a more important role in autoimmune disease regulation. The aim of the present work was to measure the level of surface expression of CD40-L and CD40 on PB lymphocytes of rheumatoid arthritis [RA] patients and to correlate it with clinical and laboratory data and with disease activity. To achieve this goal, 30 patients with RA [Group I] who were further subdivided into group IA [15 patients with active RA] and group IB [15 patients with inactive RA], in addition to 20 healthy control volunteers [group II] were studied. All studied groups were subjected to routine laboratory investigations including, complete blood count [CBC], ESR, C-reactive protein [CRP], rheumatoid factor [RF] measured by latex test and by Rose-Waaler test. Surface CD40-L and CD40 expression on lymphocytes was measured by flowcytometry on peripheral blood [PB] of all studied groups. Statistical analysis of the results of the present study showed that surface expression of CD40-L on PB T-lymphocytes was significantly higher in RA compared to the control group. Among RA patients surface expression of CD40-L was significantly higher in active RA patients compared to inactive patients. As regards CD40 expression on PB, no statistical significance was observed among the studied groups. Therefore increased expression of CD40-L on PB T-lymphocytes could be regarded as a marker of disease activity in RA patients and to drive the activation of autoreactive beta-lymphocytes in the disease. These findings are particularly useful for clarifying the pathogenic process in RA patients and for developing a therapeutic approach that blocks pathogenic cytokine and antibody production