Suppressed expression of ICAM-1 and LFA-1 and abrogation of leukocyte collaboration after exposure of human mononuclear leukocytes to respiratory syncytial virus in vitro. Comparison with exposure to influenza virus.

@article{Salkind1991SuppressedEO,
  title={Suppressed expression of ICAM-1 and LFA-1 and abrogation of leukocyte collaboration after exposure of human mononuclear leukocytes to respiratory syncytial virus in vitro. Comparison with exposure to influenza virus.},
  author={A. Salkind and J. Nichols and N. Roberts},
  journal={The Journal of clinical investigation},
  year={1991},
  volume={88 2},
  pages={
          505-11
        }
}
Human mononuclear leukocytes (MNL) exposed to respiratory syncytial virus (RSV) produce net IL-1 inhibitor bioactivity with the anticipated consequences of cell cycle arrest, suppressed virus-specific proliferation, and reduced expression of activation markers. These studies were undertaken to investigate effects of exposure and resultant net IL-1 inhibitor activity on the expression of the intercellular adhesion molecule-1 (ICAM-1), and its ligand the lymphocyte function-associated antigen… Expand
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References

SHOWING 1-10 OF 38 REFERENCES
Interleukin-1-inhibitor activity induced by respiratory syncytial virus: abrogation of virus-specific and alternate human lymphocyte proliferative responses.
TLDR
The possibility that a contributing mechanism for recurrence of RSV infection is early suppression of the clonal expansion of virus-specific lymphocytes due to net IL-1-inhibitor activity is raised. Expand
Interleukin 1 and interleukin 1 inhibitor production by human macrophages exposed to influenza virus or respiratory syncytial virus. Respiratory syncytial virus is a potent inducer of inhibitor activity
TLDR
The data raise the possibility that marked production of IL-1 inhibitor activity in response to RSV plays a role in the clinical recurrence of RSV infection despite the absence of clear evidence for antigenic shift or drift of the virus. Expand
Interleukin‐1 Inhibitor Production by Human Mononuclear Leukocytes and Leukocyte Subpopulations Exposed to Respiratory Syncytial Virus: Analysis and Comparison With the Response to Influenza Virus
TLDR
The results raise the possibility that such antiproliferative activity is mediated, at least in part, by monocytes‐macrophages, and suggest that IL‐1 inhibitors produced by MNL after exposure to RSV may contribute along with other factors to the recurrence of RSV infection in immune individuals. Expand
The function of human intercellular adhesion molecule‐1 (ICAM‐1) in the generation of an immune response
Monoclonal antibody RR1/1 directed against the putative LFA‐1 ligand molecule intracellular adhesion molecule‐1 (ICAM‐1) was found to inhibit the T cell prolifera‐tive response to the antigen PPD.Expand
Induction by IL 1 and interferon-gamma: tissue distribution, biochemistry, and function of a natural adherence molecule (ICAM-1).
ICAM-1 is a cell surface glycoprotein originally defined by a monoclonal antibody (MAb) that inhibits phorbol ester-stimulated leukocyte aggregation. Staining of frozen sections andExpand
Induction of cell‐associated interleukin 1 through stimulation of the adhesion‐promoting proteins LFA‐1 (CD11a/CD18) and CR3 (CD11b/CD18) of human monocytes
Serum‐free culture of human monocytes in the presence of monoclonal antibodies to the LFA‐1 α chain (CD11a), CR3 α chain (CD11b) or β chain (CD18) bound to Sepharose induced the dose‐dependentExpand
Purified intercellular adhesion molecule-1 (ICAM-1) is a ligand for lymphocyte function-associated antigen 1 (LFA-1)
TLDR
The purified ICAM-1 was incorporated into artificial supported lipid membranes and required metabolic energy production, an intact cytoskeleton, and the presence of Mg2+ and was temperature dependent, characteristics of LFA-1- and ICAM -1-dependent cell-cell adhesion. Expand
T cell induction of membrane IL 1 on macrophages.
TLDR
It appears that T cells may induce macrophages to express mIL 1 both by direct cell-cell contact mediated through binding of T cell receptor to the Ia/antigen complex, and through the release of a lymphokine after activation. Expand
The CD2-LFA-3 and LFA-1-ICAM pathways: relevance to T-cell recognition.
TLDR
This review focuses primarily on the two molecular pathways of lymphocyte adhesion that have been shown to play a critical role in facilitation of antigen-specific recognition, namely CD2 and its ligand, lymphocyte function associated antigen-3 (LFA-3), and LFA-1 and itsligand, intercellular adhesion molecule-1 (ICAM-1). Expand
Regulated expression of the Mac-1, LFA-1, p150,95 glycoprotein family during leukocyte differentiation.
TLDR
The regulation of Mac- 1, LFA-1, and p150,95 expression during leukocyte differentiation was examined and resembled hairy cell leukemia, a B cell plasmacytoid leukemia. Expand
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