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

• Main Authors: Sujittra Chaisavaneeyakorn, Julie M. Moore, Juliana Otieno, Sansanee C. Chaiyaroj, Douglas J. Perkins, Ya Ping Shi, Bernard L. Nahlen, Altaf A. Lal, Venkatachalam Udhayakumar
• Other Authors: National Center for Infectious Diseases
• Format: Article
• Published: 2018
• Subjects: Medicine
• Online Access: https://repository.li.mahidol.ac.th/handle/123456789/20591
• Institution: Mahidol University

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.