VLDL binds to T-helper lymphocytes and arrest T-cells on G0-G1 phase of cell cycle

SAMPEDRO, MARÍA CECILIA; MOTRÁN, CRISTINA; GRUPPI, ADRIANA; KIVATINITZ, SILVIA CLARA

Carlos Paz, Córdoba, Argentina

Congreso; XXXVII Reunión Anual de la Sociedad Argentina de Investigación en Bioquímica y Biología Molecular; 2001

Sociedad Argentina de Investigación en Bioquímica y Biología Molecular

Human very-low density lipoprotein (VLDL) inhibits DNA synthesis in lymphocytes activated by Concanavalin A (ConA) reducing the population of cells bearing IL-2 receptor and modulating the cytokine secretion profile to a predominantly pro-inflammatory response. We study if the cause under this effect was a change in the proportion of T-helper lymphocytes (CD3+-CD4+) in the entire T-cell population using flow-cytometry. Cells cultured in the presence of ConA and VLDL had the same levels of T-lymphocytes than the cells cultured without VLDL. VLDL inhibits more drastically the proliferative effect of ConA on CD4+ cells than on other CD3+ cells suggesting that the effect of VLDL is specific of T-helper cells. VLDL, labeled in its protein portion with a green fluorescence die (Alexa 488) and with a red fluorescence die (DiI) in its lipid portion, bind mainly on CD4+ cells. It wasalso determined that VLDL binds to activated cells and decreased the population of T-cells that progress thruogh the cell cycle, increasing the population of T-cells in G0/G1. These results show tha VLDL modulates T-helper cells response and support the knowledge that CD4+ cells play a pivotal role in atherogenesis.