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Title: Impairment of lymphocyte adhesion to cultured fibroblasts and endothelial cells by [gamma]-irradiation

Abstract

A critical component of immune responsiveness is the localization of effector cells at sites of inflammatory lesions. Adhesive molecules that may play a role in this process have been described on the surfaces of both lymphocytes and connective tissue cells. Adhesive interactions of T lymphocytes with fibroblasts or endothelial cells can be inhibited by preincubation of the fibroblasts or endothelial cells with antibody to intercellular adhesion molecule 1 (CD54) or by preincubation of the T cells with antibody to lymphocyte function-associated Ag 1 (CD11a/CD18), molecules shown to be important in several other cell-cell adhesion interactions. Here the authors show that [gamma]-irradiation of human T lymphocytes impaired their ability to adhere to both fibroblasts and endothelial cells. This impairment was not associated with a loss of cell viability or of cell surface lymphocyte function-associated Ag 1 expression. [gamma]-Irradiation of T cells is known to result in the activation of ADP-ribosyltransferase, an enzyme involved in DNA strand-break repair, causing subsequent depletion of cellular nicotinamide adenine dinucleotide (NAD) pools by increasing NAD consumption for poly(ADP-ribose) formation. Preincubation of T cells with either nicotinamide or 3-aminobenzamide, both known inhibitors of ADP-ribosyltransferase, completely reversed the suppressive effects of [gamma]-irradiation on T cell adhesion. The maintenancemore » of adhesion was accompanied by inhibition of irradiation-induced depletion of cellular NAD. These experiments suggest that the impairment of cellular immune function after irradiation in vivo may be caused, in part, by defective T cell emigration and localization at inflammatory sites. 44 refs., 5 figs., 3 tabs.« less

Authors:
; ; ;  [1];  [2]
  1. Univ. of Connecticut School of Medicine, Newington, CT (United States)
  2. Institute of Arthritis and Autoimmunity, West Haven, CT (United States)
Publication Date:
OSTI Identifier:
7199235
Resource Type:
Journal Article
Journal Name:
Journal of Immunology; (United States)
Additional Journal Information:
Journal Volume: 148:1; Journal ID: ISSN 0022-1767
Country of Publication:
United States
Language:
English
Subject:
63 RADIATION, THERMAL, AND OTHER ENVIRON. POLLUTANT EFFECTS ON LIVING ORGS. AND BIOL. MAT.; ENDOTHELIUM; ADHESION; BIOLOGICAL RADIATION EFFECTS; FIBROBLASTS; LYMPHOCYTES; DNA REPAIR; GAMMA RADIATION; STRAND BREAKS; ANIMAL CELLS; ANIMAL TISSUES; BIOLOGICAL EFFECTS; BIOLOGICAL MATERIALS; BIOLOGICAL RECOVERY; BIOLOGICAL REPAIR; BLOOD; BLOOD CELLS; BODY; BODY FLUIDS; CONNECTIVE TISSUE CELLS; ELECTROMAGNETIC RADIATION; IONIZING RADIATIONS; LEUKOCYTES; MATERIALS; RADIATION EFFECTS; RADIATIONS; REPAIR; SOMATIC CELLS; TISSUES; 560120* - Radiation Effects on Biochemicals, Cells, & Tissue Culture

Citation Formats

Piela-Smith, T H, Aneiro, L, Nuveen, E, Korn, J H, and Aune, T. Impairment of lymphocyte adhesion to cultured fibroblasts and endothelial cells by [gamma]-irradiation. United States: N. p., 1992. Web.
Piela-Smith, T H, Aneiro, L, Nuveen, E, Korn, J H, & Aune, T. Impairment of lymphocyte adhesion to cultured fibroblasts and endothelial cells by [gamma]-irradiation. United States.
Piela-Smith, T H, Aneiro, L, Nuveen, E, Korn, J H, and Aune, T. 1992. "Impairment of lymphocyte adhesion to cultured fibroblasts and endothelial cells by [gamma]-irradiation". United States.
@article{osti_7199235,
title = {Impairment of lymphocyte adhesion to cultured fibroblasts and endothelial cells by [gamma]-irradiation},
author = {Piela-Smith, T H and Aneiro, L and Nuveen, E and Korn, J H and Aune, T},
abstractNote = {A critical component of immune responsiveness is the localization of effector cells at sites of inflammatory lesions. Adhesive molecules that may play a role in this process have been described on the surfaces of both lymphocytes and connective tissue cells. Adhesive interactions of T lymphocytes with fibroblasts or endothelial cells can be inhibited by preincubation of the fibroblasts or endothelial cells with antibody to intercellular adhesion molecule 1 (CD54) or by preincubation of the T cells with antibody to lymphocyte function-associated Ag 1 (CD11a/CD18), molecules shown to be important in several other cell-cell adhesion interactions. Here the authors show that [gamma]-irradiation of human T lymphocytes impaired their ability to adhere to both fibroblasts and endothelial cells. This impairment was not associated with a loss of cell viability or of cell surface lymphocyte function-associated Ag 1 expression. [gamma]-Irradiation of T cells is known to result in the activation of ADP-ribosyltransferase, an enzyme involved in DNA strand-break repair, causing subsequent depletion of cellular nicotinamide adenine dinucleotide (NAD) pools by increasing NAD consumption for poly(ADP-ribose) formation. Preincubation of T cells with either nicotinamide or 3-aminobenzamide, both known inhibitors of ADP-ribosyltransferase, completely reversed the suppressive effects of [gamma]-irradiation on T cell adhesion. The maintenance of adhesion was accompanied by inhibition of irradiation-induced depletion of cellular NAD. These experiments suggest that the impairment of cellular immune function after irradiation in vivo may be caused, in part, by defective T cell emigration and localization at inflammatory sites. 44 refs., 5 figs., 3 tabs.},
doi = {},
url = {https://www.osti.gov/biblio/7199235}, journal = {Journal of Immunology; (United States)},
issn = {0022-1767},
number = ,
volume = 148:1,
place = {United States},
year = {Wed Jan 01 00:00:00 EST 1992},
month = {Wed Jan 01 00:00:00 EST 1992}
}