1. ICAM-3 influences human immunodeficiency virus type 1 replication in CD4+ T cells independent of DC-SIGN-mediated transmission
- Author
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Monica T. Yu Kimata, Reetakshi Arora, Julia E. Biggins, Tasha Biesinger, and Jason T. Kimata
- Subjects
CD4-Positive T-Lymphocytes ,ICAM-3 ,T cell ,Activation ,Receptors, Cell Surface ,Biology ,Lymphocyte Activation ,Virus Replication ,DC-SIGN ,Jurkat cells ,Article ,Cell Line ,Jurkat Cells ,03 medical and health sciences ,Interleukin 21 ,0302 clinical medicine ,Antigens, CD ,Virology ,medicine ,Animals ,Humans ,Cytotoxic T cell ,Lectins, C-Type ,IL-2 receptor ,Antigen-presenting cell ,030304 developmental biology ,0303 health sciences ,CD40 ,ZAP70 ,Recombinant Proteins ,3. Good health ,Cell biology ,medicine.anatomical_structure ,Solubility ,SIV ,HIV-1 ,biology.protein ,Simian Immunodeficiency Virus ,Cell Adhesion Molecules ,030215 immunology - Abstract
We investigated the role of ICAM-3 in DC-SIGN-mediated human immunodeficiency virus (HIV) infection of CD4 + T cells. Our results demonstrate that ICAM-3 does not appear to play a role in DC-SIGN-mediated infection of CD4 + T cells as virus is transmitted equally to ICAM-3 + or ICAM-3 − Jurkat T cells. However, HIV-1 replication is enhanced in ICAM-3 − cells, suggesting that ICAM-3 may limit HIV-1 replication. Similar results were obtained when SIV replication was examined in ICAM-3 + and ICAM-3 − CEMx174 cells. Furthermore, while ICAM-3 has been proposed to play a co-stimulatory role in T cell activation, DC-SIGN expression on antigen presenting cells did not enhance antigen-dependent activation of T cells. Together, these data indicate that while ICAM-3 may influence HIV-1 replication, it does so independent of DC-SIGN-mediated virus transmission or activation of CD4 + T cells.
- Published
- 2007