Abstract
Purpose: :
To determine CD85j, CD94, NKG2D and CD158 expression on CD8+CD57+ T cells in patients with pars planitis.
Methods: :
15 pars planitis patients were included. The expression of CD8, CD57, CD85j, CD94, NKG2, and CD158b were assessed by flow cytometry at basal microenvironment. In a second step CD8+ T cells were isolated by positive immunomagnetic selection and stimulated with/without IL-15.
Results: :
We observed that CD8+CD57+ T cells were increased in patients with pars planitis. CD85j expression was 3.2 times increased on CD8+CD57+ T cells subsets compared to CD8+CD57- T cells subsets (p=0.009). We also observed a higher frequency of CD94+ on CD8+CD57+ t cells than on CD8+CD57- T cells subsets (p< 0.0001). CD158b expression was 8.1 times more frequent on CD8+CD57+ T cells than on CD8+CD57- T cells (p= 0.001). After stimulation with IL-15 we observed changes in the expression of CD158b on CD8+CD57+ T cells and CD8+CD57-.
Conclusions: :
CD8+CD57+ T cells were increased in patients with pars planitis as has been reported. CD85j, CD94 and CD158b were preferentially expressed on CD8+CD57+ T cells. IL-15 stimulation apparently down regulates CD158b expression on both CD8+CD57+ T cells and CD8+CD57- T cells. Our findings suggest that chronic inflammatory conditions such as pars planitis may induce the expression of killer cell immunoglobulin-like receptors (KIRs). These receptors have been associated to cellular activation or inhibition functions depending on their associated intracytoplasmic regions. The addition of the proinflammatory cytokine IL-15 found in chronic inflammatory conditions may modify the pattern of the KIR receptors in CD8+ T cells subsets. These properties may be used to design a directed immunotherapy using these cellular surface markers.Acknowledgments: This work was partially supported by a grant from National Council of Science and Technology (CONACYT 71291) and Fundacion Conde de Valenciana.
Keywords: autoimmune disease • immune tolerance/privilege • inflammation