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Laboratoire d’Immuno-Virologie, EA 3038, Université Paul Sabatier, 31062 Toulouse, France
1Correspondence: Laboratoire d’Immuno-Virologie EA 3038, Université Paul Sabatier 118, route de Narbonne batiment 4R3 31062 Toulouse, France. E-mail: bahraoui{at}cict.fr
In HIV-infected patients, production of interleukin-10 (IL-10), a highly immunosuppressive cytokine, is associated with the disease progression toward AIDS. We have previously shown that HIV-1 Tat induces IL-10 production by human monocytes via a protein kinase C (PKC) -dependent pathway. Here we show that PKC activation by Tat is essential for IL-10 induction. Among the eight PKC isoforms present in human monocytes, we investigated which isoform(s) plays this crucial role in Tat-mediated IL-10 production and show that 1) Tat can activate PKC-
, PKC-ßII, PKC-
, and PKC-
, 2) of these four potential candidates, only PKC-ßII, PKC-, and PKC- are activated by the active domain Tat 1–45, which is responsible for IL-10 production and depleted by long-term exposure to PMA, which abolishes Tat-mediated IL-10 production, 3) whereas selective inhibition of PKC- and PKC- by specific antisense oligonucleotides has no effect on Tat-mediated IL-10 induction, inhibition of either PKC-ßII or PKC- partially inhibits IL-10 production; and 4) the simultaneous inhibition of PKC-ßII and PKC- totally inhibits Tat-mediated IL-10. Altogether, these results suggest that the induction of IL-10 by Tat is strictly dependent on the PKC- and -ßII isoforms.—Bennasser, Y., Bahraoui, E. HIV-1 Tat protein induces interleukin 10 in human peripheral blood monocytes: involvement of protein kinase C-ßII and -.
Key Words: IL-10 • PKC isoforms • uninfected monocytes
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