TY - JOUR
T1 - Acute stress impairs NK cell adhesion and cytotoxicity through CD2, but not LFA-1
AU - Rogers, Connie Jo
AU - Brissette-Storkus, Cynthia S.
AU - Chambers, William H.
AU - Cameron, Judy L.
N1 - Funding Information:
The authors appreciate the technical assistance of Lisa Bench and Dawn McClemens. We also thank Alexis Styche and Robert Lakomy of the UPCI Flow Cytometry Facility for the flow cytometric data collection. In addition, the technical support of the Primate and RIA Core Laboratories of the Center for Research in Reproductive Physiology at the University of Pittsburgh School of Medicine was of great value. These studies were supported by a grant from the Research Network on Determinants and Consequences of Health-Promoting and Health-Damaging Behavior, of the John D. and Catherine T. MacArthur Foundation, and NIH grants (MH50748, HD08610). Dr. Cameron was supported by an NIMH research Scientist Develpment Award (NS09561).
PY - 1999/10/29
Y1 - 1999/10/29
N2 - Using a nonhuman primate model, we examined the mechanisms by which acute social stress inhibits the ability of NK cells to form conjugates with, and lyse target cells. We examined the expression and role of the primary NK cell adhesion molecules, CD2 and LFA-1, in mediating conjugation to target cells. Acute stress induced a decrease in NK cell expression of CD2 (17 ± 3%); and to a lesser degree induced a decrease in expression of LFA-1 (CD11a: 8 ± 3%; CD18: 7 ± 3%). Antibody blocking studies indicated that anti-LFA-1 significantly inhibited NK cell conjugate formation and cytotoxicity in both control (~40% and ~50%, respectively) and stressed (~20% and ~45%, respectively) conditions. However, anti-CD2 blocked conjugation and cytotoxicity in the control condition by ~50%, but had no capacity to further affect the inhibition of conjugation or cytotoxicity of NK cells induced by acute stress. These data indicate that there are differential effects of acute stress on the expression and function of LFA-1 and CD2, and that the stress-induced inhibition of NK cell adhesion and cytotoxicity is dependent upon modulation of adhesion and/or signalling through CD2.
AB - Using a nonhuman primate model, we examined the mechanisms by which acute social stress inhibits the ability of NK cells to form conjugates with, and lyse target cells. We examined the expression and role of the primary NK cell adhesion molecules, CD2 and LFA-1, in mediating conjugation to target cells. Acute stress induced a decrease in NK cell expression of CD2 (17 ± 3%); and to a lesser degree induced a decrease in expression of LFA-1 (CD11a: 8 ± 3%; CD18: 7 ± 3%). Antibody blocking studies indicated that anti-LFA-1 significantly inhibited NK cell conjugate formation and cytotoxicity in both control (~40% and ~50%, respectively) and stressed (~20% and ~45%, respectively) conditions. However, anti-CD2 blocked conjugation and cytotoxicity in the control condition by ~50%, but had no capacity to further affect the inhibition of conjugation or cytotoxicity of NK cells induced by acute stress. These data indicate that there are differential effects of acute stress on the expression and function of LFA-1 and CD2, and that the stress-induced inhibition of NK cell adhesion and cytotoxicity is dependent upon modulation of adhesion and/or signalling through CD2.
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U2 - 10.1016/S0165-5728(99)00125-3
DO - 10.1016/S0165-5728(99)00125-3
M3 - Article
C2 - 10505980
AN - SCOPUS:0032704912
SN - 0165-5728
VL - 99
SP - 230
EP - 241
JO - Journal of Neuroimmunology
JF - Journal of Neuroimmunology
IS - 2
ER -