PMID- 1707641
OWN - NLM
STAT- MEDLINE
DCOM- 19910521
LR  - 20081121
IS  - 0889-2229 (Print)
IS  - 0889-2229 (Linking)
VI  - 7
IP  - 1
DP  - 1991 Jan
TI  - Re-evaluation of the involvement of the adhesion molecules ICAM-1/LFA-1 in 
      syncytia formation of HIV-1-infected subclones of a CEM T-cell leukemic line.
PG  - 45-53
AB  - The role of the adhesion molecules intercellular adhesion molecule-1 (ICAM-1) and 
      LFA-1 in human immunodeficiency virus type 1 (HIV-1)-induced cell fusion was 
      investigated in subclones of a T-cell leukemic cell line (CEM) with differing 
      abilities to form syncytia. Addition of monoclonal antibodies 84H10 directed 
      against ICAM-1 and MHM23 directed against the common beta subunit of LFA-1 (CD18) 
      resulted in greater than 50% suppression of syncytia formation in cultures of 
      these clones infected with cell-free virus. Two subclones, 2G5-144-84 and 2G5-1, 
      were deficient in their ability to form syncytia and expressed reduced amounts of 
      LFA-1 compared with the parental line. The expression of ICAM-1 but not LFA-1 was 
      upregulated on the clones following treatment with interferon-gamma (IFN gamma); 
      however, this did not overcome the delay in syncytia formation observed in these 
      cells. The syncytia-positive subclones 1B11-39 and 17D-9 expressed high levels of 
      LFA-1. Basal expression of ICAM-1 was upregulated on these cells by treatment 
      with tumor necrosis factor-alpha (TNF alpha), which also accelerated and enhanced 
      syncytia formation. However, anti-ICAM-1 and anti-LFA-1 (CD18) antibodies did not 
      reverse the TNF alpha-induced enhancement of syncytia formation of HIV-1-infected 
      clones 1B11-39 and 17D-9. Under conditions of low viral expression, adhesion 
      molecules may contribute to syncytia formation if adequate levels of both 
      receptor and ligand in the ICAM-1/LFA-1 complex are expressed.(ABSTRACT TRUNCATED 
      AT 250 WORDS)
FAU - Gruber, M F
AU  - Gruber MF
AD  - Division of Cytokine Biology and Virology, Food and Drug Administration, National 
      Institutes of Health, Bethesda, MD 20892.
FAU - Webb, D S
AU  - Webb DS
FAU - Gerrard, T L
AU  - Gerrard TL
FAU - Mostowski, H S
AU  - Mostowski HS
FAU - Vujcic, L
AU  - Vujcic L
FAU - Golding, H
AU  - Golding H
LA  - eng
PT  - Journal Article
PL  - United States
TA  - AIDS Res Hum Retroviruses
JT  - AIDS research and human retroviruses
JID - 8709376
RN  - 0 (Antibodies, Monoclonal)
RN  - 0 (Cell Adhesion Molecules)
RN  - 0 (Lymphocyte Function-Associated Antigen-1)
RN  - 0 (Tumor Necrosis Factor-alpha)
RN  - 126547-89-5 (Intercellular Adhesion Molecule-1)
RN  - 82115-62-6 (Interferon-gamma)
RN  - EC 2.7.7.49 (RNA-Directed DNA Polymerase)
SB  - IM
MH  - Antibodies, Monoclonal/immunology
MH  - Cell Adhesion Molecules/biosynthesis/immunology/*physiology
MH  - Cell Fusion
MH  - Clone Cells
MH  - Giant Cells/*microbiology
MH  - HIV-1/*physiology
MH  - Humans
MH  - Intercellular Adhesion Molecule-1
MH  - Interferon-gamma/pharmacology
MH  - Lymphocyte Function-Associated Antigen-1/biosynthesis/immunology/*physiology
MH  - RNA-Directed DNA Polymerase/metabolism
MH  - Tumor Cells, Cultured
MH  - Tumor Necrosis Factor-alpha/pharmacology
EDAT- 1991/01/01 00:00
MHDA- 1991/01/01 00:01
CRDT- 1991/01/01 00:00
PHST- 1991/01/01 00:00 [pubmed]
PHST- 1991/01/01 00:01 [medline]
PHST- 1991/01/01 00:00 [entrez]
AID - 10.1089/aid.1991.7.45 [doi]
PST - ppublish
SO  - AIDS Res Hum Retroviruses. 1991 Jan;7(1):45-53. doi: 10.1089/aid.1991.7.45.