ارزیابی پرولیفراسیون سلولی و بیان داخل سلولی اینترفرون گاما (IFN-Gamma) در بیماران مبتلا به بروسلوز

T cell proliferation is a standard method to evaluate cellular immune responses&nbsp;against intracellular infectious agents. Recently, intracellular cytokine assay is a&nbsp;valuable procedure for studying of the immune response to various stimuli such as&nbsp;intracellular microbes. The present study was undertaken to assess cell-mediated &nbsp;&nbsp; immune responses in patients with acute and chronic brucellosis. &nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp; Diluted whole blood samples of patients with acute (n=14) and chronic&nbsp;brucellosis (n=13) with age 35.33&plusmn; 21 years, and sex and age-matched healthy&nbsp;volunteers(n=22) were cultured in the presence of either mitogen; heat inactivated&nbsp;bacteria or medium alone. Intracellular IFN-&gamma; expression in CD3+ cells was detected &nbsp;&nbsp; by flow cytometry. Lymphoproliferation was determined by titiated thymidine&nbsp;incorporation using scintillation counter, to evaluate DNA synthesis. &nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp; In all groups, incubation with mitogen induced proliferation of lymphocytes&nbsp;and intracellular IFN-&gamma; expression of CD3+ cells. In contrast, only brucellosis patients&nbsp;responded with cell proliferation and IFN-&gamma; production against heat killedBrucella&nbsp;melitensis. However, blastogenic responses and IFN-&gamma;-producing CD3+ cells were&nbsp;significantly decreased in response to antigen in chronic group compared to&nbsp;patients with acute brucellosis of patients (P<0.001). There was a close correlation&nbsp;between the number IFN-g- producing CD3+ cells only in acute group which shown&nbsp;polarization of immune responses to Th1 type. &nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp; Methods used in this study were useful to evaluate immune responses against&nbsp;specific antigen or polyclonal stimulation. Our data was shown patients with acute&nbsp;infection responded to Brucella antigens by IFN-g expression and proliferation and&nbsp;induced production of T helper 1 (Th1) cytokines, whereas chronically infected&nbsp;patients do not.