TY - JOUR
T1 - A selective defect in tissue factor mRNA expression in monocytes from AIDS patients
AU - Lathey, Janet L.
AU - Agosti, Jan M.
AU - Nelson, Jay A.
AU - Corey, Lawrence
AU - Gregory, Susan A.
AU - Morrissey, James H.
AU - Edgington, Thomas S.
AU - Oldstone, Michael B.A.
N1 - Funding Information:
This is Publication Number 5435IMM from the Department of Immunology, Scripps Clinic and Research Foundation, La Jolla, CA. This work was supported in part by USPHS Grants NS-12428, NIH HL-16411, AI-07007, AI-24178, and University of California Task Force on AIDS (J.A.N.) and a NIH postdoctoral training award (NS-07078) to J.L.L. This work was done during the tenure of an Established Investigatorship (J.H.M.) from the American Heart Association. J.A.N. is the recipient of a faculty award from the American Cancer Society. The authors wish to thank Tom Cook and Jamie Myer for their technical assistance, and Diane Nolin and Gay Schilling for manuscript preparation.
PY - 1990/1
Y1 - 1990/1
N2 - Expression of tumor necrosis factor (TNFα), tissue factor (TF), and interleukin 1-β (IL-1β) mRNA was evaluated in monocytes isolated from patients infected with human immunodeficiency virus (HIV). There was a significant depression (66%) of the induced level of TF mRNA expression in response to lipopolysaccharide. Conversely, the response of TNFα and IL-1β, following LPS induction, was "normal." TF mRNA reduction was also observed to a lesser degree in AIDS-related complex patients (20%) but not in asymptomatic seropositives. TF is necessary for initiation of the coagulation protease cascade, leading to thrombin production and fibrin deposition, which play a role in inflammatory responses. Its selective reduction may be a factor in the diminished resistance to secondary infections observed in AIDS. Further, since the TF defect increases as patients progress toward AIDS, it may serve as a marker for disease progression.
AB - Expression of tumor necrosis factor (TNFα), tissue factor (TF), and interleukin 1-β (IL-1β) mRNA was evaluated in monocytes isolated from patients infected with human immunodeficiency virus (HIV). There was a significant depression (66%) of the induced level of TF mRNA expression in response to lipopolysaccharide. Conversely, the response of TNFα and IL-1β, following LPS induction, was "normal." TF mRNA reduction was also observed to a lesser degree in AIDS-related complex patients (20%) but not in asymptomatic seropositives. TF is necessary for initiation of the coagulation protease cascade, leading to thrombin production and fibrin deposition, which play a role in inflammatory responses. Its selective reduction may be a factor in the diminished resistance to secondary infections observed in AIDS. Further, since the TF defect increases as patients progress toward AIDS, it may serve as a marker for disease progression.
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U2 - 10.1016/0090-1229(90)90001-7
DO - 10.1016/0090-1229(90)90001-7
M3 - Article
C2 - 2293902
AN - SCOPUS:0025099006
SN - 0090-1229
VL - 54
SP - 1
EP - 13
JO - Clinical Immunology and Immunopathology
JF - Clinical Immunology and Immunopathology
IS - 1
ER -