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  • 标题:Fetal exposure to HIV-1 alters chemokine receptor expression by CD4+T cells and increases susceptibility to HIV-1
  • 本地全文:下载
  • 作者:Madeleine J. Bunders ; John L. van Hamme ; Machiel H. Jansen
  • 期刊名称:Scientific Reports
  • 电子版ISSN:2045-2322
  • 出版年度:2015
  • 卷号:4
  • 期号:1
  • DOI:10.1038/srep06690
  • 语种:English
  • 出版社:Springer Nature
  • 摘要:Absolute numbers of lymphocytes are decreased in uninfected infants born to HIV-1-infected women (HIV-1-exposed). Although the exact mechanism is unknown, fetal exposure to maternal HIV-1-infection could prime the immune system and affect T cell trafficking. We compared the expression of chemokine receptors on cord blood CD4+ T cells from HIV-1-exposed children and healthy controls. At baseline CD4+ T cells had a largely naïve phenotype. However, stimulation with cytokines resulted in an upregulation of inflammatory response-related chemokine receptors on CD4+ T cells, with HIV-1-exposed infants having a significantly higher frequency of CD4+ T cells expressing, in particularly Th2 associated chemokine receptors (CCR3 p + CD4+ T cells were reduced (p = 0.01) in HIV-1-exposed infants. We further assessed whether the inflammatory phenotype was associated with susceptibility to HIV-1 and detected higher levels of p24 upon in in vitro infection of stimulated CD4+ T cells of HIV-1-exposed infants. In summary, fetal exposure to HIV-1 primes the immune system in the infant leading to an enhanced immune activation and altered T cell homing, with potential ramifications regarding T cell responses and the acquisition of HIV-1 as an infant.
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