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(Journal of Leukocyte Biology. 2002;71:531-537.)
© 2002 by Society for Leukocyte Biology

ß3-Mediated engulfment of apoptotic tumor cells by dendritic cells is dependent on CAMKII: inhibition by HIV-1 Tat

Alessandro Poggi*, Roberta Carosio*, Anna Rubartelli{ddagger} and Maria Raffaella Zocchi{dagger},{ddagger}

* Laboratory of Immunology and
{ddagger} Unit of Protein Biology, National Cancer Research Institute, Genoa, Italy; and
{dagger} Laboratory of Tumor Immunology, Scientific Institute San Raffaele, Milan, Italy

Correspondence: Maria Raffaella Zocchi, Laboratory of Tumor Immunology, Scientific Institute San Raffaele, Via Olgettina 60 Milan, Italy. E-mail: zocchi.maria{at}hsr.it

In this paper, we show that the engulfment of apoptotic tumor cells by DC requires the activation of the calcium-calmodulin kinase II (CAMKII). Indeed, DC phagocytosis of apoptotic lymphoma cells is consistently inhibited by KN62 and KN93, two blockers of CAMKII, but not by the inactive compound KN92. Wortmannin and LY294002, two inhibitors of the phosphatidyl-inositol-3 kinase, slightly decrease the phagocytosis of apoptotic cells, at variance with PD98059, an inhibitor of the mitogen-activated protein kinase. It is interesting that the addition of synthetic HIV-1 Tat, which we demonstrated to inhibit phagocytosis and calcium influx in DC, blocks the activation of CAMKII elicited via ß3 integrin, which is involved in apoptotic body engulfment by DC. Experiments performed with Tat-derived peptides showed that this inhibition is mediated by the C-terminal domain of Tat. Finally, pertussis toxin can prevent HIV-1 Tat-mediated inhibition, suggesting the involvement of a guanosine triphosphate-binding (G) protein in DC-mediated phagocytosis.

Key Words: AIDS • antigen-presenting cells • calcium • G proteins • phagocytosis




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