The effect of homocysteine on CD28 costimulatory receptor exposure and IL-2, TNF-α and INF-γ release from CD4+ T Cells

Samaneh Maskani, Hafez Heydari ©, Zahra Mohammadi Abgarmi, Moslem Lari Najafi, Mitra Kheyrabadi, Marzieh Ramezani Farani

The effect of homocysteine on CD28 costimulatory receptor exposure and IL-2, TNF-α and INF-γ release from CD4+ T Cells

کد: G-58413

نویسندگان: Samaneh Maskani, Hafez Heydari ©, Zahra Mohammadi Abgarmi, Moslem Lari Najafi, Mitra Kheyrabadi, Marzieh Ramezani Farani

زمان بندی: زمان بندی نشده!

برچسب: بیوشیمی

دانلود: دانلود پوستر

خلاصه مقاله:

Background and Aim

There is evidence suggesting that Hyperhomocysteinemia accelerates cardiovascular disease development by modulating CD4+ T cell functions. However, the effects of mild, moderate and sever hyperhomocysteinemia on induction of functional characteristics relevant to the development of cardiovascular disease in CD4+ T cells is not fully understood. Therefore, at the present study, our aim was to examine the direct effects of Hcys on CD4+ T cells.

Methods

Untouched CD4+ T cells were purified from peripheral blood, using a negative selection strategy. The purified CD4+ T cells were treated with different concentrations of Hcys (6.25, 12.5, 25, 50, 75 and 100μM) for 24 hours after activation.

Results

Lactate dehydrogenase assay and caspase-3 activity measurement showed that Hcys at concentrations ≥12.5μM had cytotoxic effects toward CD4+ T cells in a concentration-dependent manner. However, at concentration ≤6.25μM, Hycs promotes CD4+ T cells proliferation via IL-2 independent pathway. Also, at concentrations ≥12.5μM, Hcys significantly enhanced the release of IL-2, INF- and TNF-α from activated CD4+ T cells. Hcys does not have an effect on CD28 exposure in resting CD4+ T cells, however, the down-regulation of CD28 after activation was significantly decreased in Hycs treated CD4+ T cells compared to controls.

Conclusion

Our results indicate that sever hyperhomocysteinemia induced apoptotic cell death in CD4+ T cells, however, mild and moderate hyperhomocysteinemia significantly increase atherogenic cytokines release from activated CD4+ CD28+ T cells possibly by prolonging CD28+ exposure time. This novel finding may improve our undrestanding of the mechanism whereby Hcys impaired pro-inflamatory cytokine release.

Keywords

Homocysteine; CD4+; atherosclerosis; cytokine

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