Recombinant human IFN-γ induction of autoimmune disease mechanisms discussed.docVIP

 PAGE \* MERGEFORMAT 16 Recombinant human IFN-γ induction of autoimmune disease mechanisms discussed Of: Ling-Ling Chen, Yu-Chuan Wu, Liu Yulin [Abstract] Objective To observe whether IFN-γ induction in human peripheral blood and cord blood B cells produce antibodies, and the difference between the two antibodies, IFN-γ is of CD5 + B1 cells by affecting the function of inducing autoimmune disease, to further clarify the IFN-γ induced autoimmune disease mechanisms, clinical research prevention and treatment of autoimmune diseases and provide experimental basis. Methods sterile blood collected from healthy people, cord blood, RosetteSepTM separation by B cells, flow cytometry detection of B cell purity, the isolated cord blood B cells and B cells were stimulated by IFN-γ, in culture the first 3,5,7 d ELISA assay changes in antibody levels in the control group did not add any stimulation of B cells in the peripheral blood and cord blood B cells in group group. the use of SAS statistical software to the concentration of antibodies obtained were analyzed statistically. Results by flow cytometry, B cell purity was 81.4%, two sources of B cells by IFN -γ stimulation, in section 3d to start generating IgM. But at the same time, peripheral blood and umbilical cord blood B cells were cultured in the amount of IgM produced no statistically significant difference (Pgt; 0.05); in the blood sources under the same circumstances with time and gradually increase the amount of IgM produced, three time the amount of IgM produced pairwise comparisons were significantly (P lt;0.01); all experimental groups were not detected IgG, the control group did not detect IgM, IgG. Conclusion IFN-γ can stimulate B cells to produce antibodies, and the types of B cells is not selective; only stimulate the production of IgM, no IgG production, but the nature of IgM antibodies need to be further identified, which may be III-type hypersensitivity mechanisms induced by autoimmune diseases.