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Title: 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
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
National Center for Infectious Diseases
The University of Georgia
Mahidol University
New Nyanza Provincial General Hospital
Kenya Medical Research Institute
Department of Veterans Affairs
Organisation Mondiale de la Sante
Keywords: Medicine
Issue Date: 1-Jan-2002
Citation: Journal of Infectious Diseases. Vol.185, No.1 (2002), 127-131
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.
ISSN: 00221899
Appears in Collections:Scopus 2001-2005

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