Journal of Clinical and Cellular Immunology
Open Access
ISSN: 2155-9899
+44 1223 790975
ISSN: 2155-9899
+44 1223 790975
Djamel Messaoudene, Houda Belguendouz, Mohamed Laid Ahmedi, Malika Terahi, Pierre Youinou4 and Chafia Touil-boukoffa
Accepted Abstracts: J Clin Cell Immunol
Background: Although several immunological abnormalities have been demonstrated in Beh�et's disease (BD), the exact mechanism of the inflammatory changes occurring is still unknown. Monocytes and lymphocytes are now recognized as key effector cells in BD. Objective: To assess effects of Beh�et disease serum on blood peripheral mononuclear cells from healthy donors and to evaluate if complement activation and complex immune were involved. Methods: Monocytes and lymphocytes from a healthy donor were incubated with 33 sera from BD patients in both active and inactive disease. After incubation cells were analyzed by flow cytometry. The apoptosis-inducing effect (AIE) of these sera was monitored with flow cytometry using annexin V and propidium iodide (PI) binding and proliferation cells was assessed by CFSE labeling. Results: Proliferation in monocytes and lymphocytes was significantly higher in sera of patient?s compared to the cells stimulated by serum of healthy donor and staurosporine (P<0.01), the CD25/CD69 and CD64 expression was statistically significant compared to the positive and negative stimulation, this activation correlate with disease activity. Levels of all cytokines [interferon-γ (IFN-γ), tumour necrosis factor-α (TNF-α), interleukin (IL)-6, interleukin (IL)-10 and IL-4] were highest in Beh�et patients. Level of complement, circulating immune complexes and AECA were higher in serum of patients of Beh�et disease. Heat inactivation and complexes immunes? depletion of sera affect significantly CD69 and CD64 expression. Conclusion: Taken together, our results indicate that serum of patients with BD induces activation of lymphocyte and monocytes in vitro . Thus, BD serum factor(s) have a strong and apparently disease-specific activation inducing capacity, which could contribute to the physiopathology of the disease.