ENGAGEMGNT OF ADHESION MOLECULES (CD18, CD11A, CD45, CD44, AND CD58) ENHANCES HUMAN-IMMUNODEFICIENCY-VIRUS TYPE-1 REPLICATION IN MONOCYTIC CELLS THROUGH A TUMOR NECROSIS FACTOR-MODULATED PATHWAY

Citation
Rj. Shattock et al., ENGAGEMGNT OF ADHESION MOLECULES (CD18, CD11A, CD45, CD44, AND CD58) ENHANCES HUMAN-IMMUNODEFICIENCY-VIRUS TYPE-1 REPLICATION IN MONOCYTIC CELLS THROUGH A TUMOR NECROSIS FACTOR-MODULATED PATHWAY, The Journal of infectious diseases, 174(1), 1996, pp. 54-62
Citations number
42
Categorie Soggetti
Infectious Diseases
ISSN journal
00221899
Volume
174
Issue
1
Year of publication
1996
Pages
54 - 62
Database
ISI
SICI code
0022-1899(1996)174:1<54:EOAM(C>2.0.ZU;2-6
Abstract
Engagement of monocytic cell membrane proteins was shown to enhance hu man immunodeficiency virus type 1 (HIV-1) replication in monocytic cel ls. Cross-linking of CD18, CD11a, or CD45 by immobilized antibodies pr oduced up to an 11-fold enhancement of HIV-1 release in the OM10.1 mon ocytic cell Line in a tumor necrosis factor-alpha (TNF-alpha)-dependen t manner. In addition, adhesion of OM10.1 cells to immobilized interce llular adhesion molecule-1 (ligand for CD18/CD11a) induced similar TNF -alpha-dependent enhancement of HIV-1 replication. After phenotypic di fferentiation of OM10.1 cells, engagement of cell membrane proteins CD 18, CD11a, CD44, CD45, or CD58 by soluble antibodies enhanced HIV-1 re plication in a TNF-alpha-dependent manner. These data suggest that cro ss-linkage of monocytic cell membrane proteins during cell-cell intera ction and specifically during antigen presentation to CD4 T cells may enhance HIV-1 replication, facilitating infection of adjacent cells.