Patients With Hemorrhagic Fever With Renal Syndrome In Cellular Immunity And Cytokine Levels Change

Objective To study the changes of T-lymphocyte subsets in peripheral blood and serum IL-6, IL-10 levels in patients with HFRS and to fine out the relationship among them, in order to explore the role of them in the pathogenesis of HFRS.Methods T-lymphocyte CD 3, subsets CD4, CD8 cells in peripheral blood of the 41 patients with HFRS were detected by flow cytometry; the IL-6, IL-10 levels in serum of 41 patients were detected by double antibody sandwich ELISA method.Results In the course of HFRS,CD3 , CD4, CD8 cells increased at different level, CD3, CD8 cells increased significantly in fever phase(p<0.05 or p<0.01),peaked in hypotensive phase(p<0.01) and were also higher in diuretic phase compared with normal controls(p<0.05); the increase degree of CD4 cells was lower, CD4 cells didn't increase significantly in fever phase(p>0.05),increased progressively in hypotensive phase(p<0.01),peaked in oliguric phase(p<0.01) and decreased in diuretic phase(p>0.05); CD4/CD8 ratio decreased or deversed,it decreased significantly in fever phase(P<0.05),was lowest in hypotensive phase,was also obviously lower in oliguric phase(p<0.01) and wasn't significant in diuretic phase(p>0.05); serum IL-6> IL-10 levels increased significantly in fever phase(p<0.01), peaked in oliguric phase and was also higher in diuretic phase compared with normal controls (P<0.01). In different types of HFRS patients, along with the severity of disease, CD3, CD8 cells increased significantly, but the increase degree of CD4 cells was lower relatively ,CD4 cells peaked in severe type of HFRS patients and were higher than those in gravis type; CD4/CD8 ratio decreased significantly; serum IL-6, IL-10 levels increased significantly; the decrease of CD4/CD8 ratio was consistent with the increase of serum IL-6, IL-10levels, an obvious negative correlation was observed between them, the coefficients(r) were-0.9278 and -0.8787 (P<0.01) .Conclusions The immune disturbance of cellular immune function and enhanced humoral immune function interposed by interleukins plays an important role in the pathogenesis of HFRS.