ICOS Regulate Survivin Expression and Sustain T Cell Survival / 生物化学与生物物理进展

To study whether the late-acting co-stimulatory molecules ICOS can suppress the apoptosis and sustain the survival and proliferation of T cells through the survivin pathway, ICOS signals deficient T-cells were infected with adenovirus carried survivin gene, other T-cells were given ICOS co-stimulatory signals, then infected with adenovirus carried dominant-negative mutant survivin gene. Apoptosis and proliferation were determined by TUNEL and CCK-8 respectively. The results show that engagement of ICOS signal increased the expression level of survivin significantly. Survivin can sustain co-stimulatory deficient T cells survival and suppress the apoptosis. Mutant survivin inhibits ICOS signal positive T cells survival and increase its apoptosis. Late-acting co-stimulatory molecules ICOS can suppress the apoptosis and sustain the survival of T cells through the survivin pathway.

Expression of CD46, CD55, and CD59 on primary murine astrocytes and effect of inflammation factors on it / 第三军医大学学报

Objective To identify the expression of complement regulatory protein CD46, CD55, and CD59 on primary murine pallium astrocytes and the effect of inflammatory factors on it in order to lay the foundation for studying the complement system in AD. Methods The primary murine astrocytes were cultured and purified. The expression of CD46, CD55, and CD59 on the levels of mRNA and protein was assayed by immunofluorescence before and after the stimulation of LPS and IFN-?. Results The expression of CD59 mRNA was confirmed, but the expression of CD46 and CD55 was indefinite. There was no significant difference between stimulation and non-stimulation groups. Immunofluorescence results indicated that CD59 was positive, while CD46 and CD55 were weakly positive. Conclusion Protectin CD59 expresses copiously on primary murine astrocytes, which presumably protects astrocytes from the lysis of complement.