A role for CD36 in the regulation of dendritic cell function

Dendritic cells (DC) are crucial for the induction of immune responses and thus an inviting target for modulation by pathogens. We have previously sho wn that Plasmodium falciparum-infected erythrocytes inhibit the maturation of DCs. Intact P. falciparum-infected erythrocytes can bind directly to CD3 6 and indirectly to CD51, It is striking that these receptors, at least in part, also mediate the phagocytosis of apoptotic cells. Here we show that a ntibodies against CD36 or CD51, as well as exposure to early apoptotic cell s, profoundly modulate DC maturation and function in response to inflammato ry signals. Although modulated DCs still secrete tumor necrosis factor-alph a, they fail to activate T cells and now secrete IL-10, We therefore propos e that intact P, falciparum-infected erythrocytes and apoptotic cells engag e similar pathways regulating DC function. These findings may have importan t consequences for the treatment of malaria and may suggest strategies for modulating pathological immune responses in autoimmune diseases.