Immunity to Placental Malaria. III. Impairment of Interleukin(IL)–12, not IL‐18, and Interferon‐Inducible Protein–10 Responses in the Placental Intervillous Blood of Human Immunodeficiency Virus/Malaria–Coinfected Women

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Abstract
Pregnant women are highly susceptible to malaria, and human immunodeficiency virus (HIV) infection increases this susceptibility. In our previous studies, placental malaria (PM), HIV infection, and HIV/PM coinfection were all associated with decreased interferon (IFN)–γ production by maternal placental (intervillous) blood mononuclear cells (IVBMC). This study investigated whether in vitro production of the IFN-γ regulatory cytokines interleukin (IL)–12 and IL-18 and the chemokine IFN-inducible protein (IP)–10 by IVBMC is altered in women who have been exposed to malaria and are infected with HIV. IL-12 production from IVBMC was significantly lower in HIV-positive women, regardless of PM status, in contrast to HIV-negative, PM-negative women. IL-18 and IP-10 production by IVBMC was reduced in HIV-positive, PM-negative women but elevated in HIV-positive, PM-positive women. These results reveal a substantial impairment of IL-12 production by IVBMC in HIV-positive women, implicating this cytokine as a potentially critical regulator of malaria antigen–specific IFN-γ responses in HIV-infected and HIV/PM-coinfected women

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