Sujittra ChaisavaneeyakornJulie M. MooreJuliana OtienoSansanee C. ChaiyarojDouglas J. PerkinsYa Ping ShiBernard L. NahlenAltaf A. LalVenkatachalam UdhayakumarNational Center for Infectious DiseasesThe University of GeorgiaMahidol UniversityNew Nyanza Provincial General HospitalKenya Medical Research InstituteDepartment of Veterans AffairsOrganisation Mondiale de la Sante2018-07-242018-07-242002-01-01Journal of Infectious Diseases. Vol.185, No.1 (2002), 127-131002218992-s2.0-0036138505https://repository.li.mahidol.ac.th/handle/123456789/20591Pregnant 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.Mahidol UniversityMedicineArticleSCOPUS10.1086/338013