       Document 0642
 DOCN  M9550642
 TI    Cocaine blunts human CD4+ cell activation.
 DT    9505
 AU    Chiappelli F; Frost P; Manfrini E; Lee P; Pham L; Garcia C; Daley S;
       Kung M; Villanueva P; Laboratory of Human Oral and Molecular Immunology,
       Diagnostic; Sciences, UCLA School of Dentistry.
 SO    Immunopharmacology. 1994 Nov-Dec;28(3):233-40. Unique Identifier :
       AIDSLINE MED/95155012
 AB    Cocaine is reported to be immunotoxic. The biochemical mechanisms
       responsible for the immunopharmacological outcomes of cocaine in vivo
       and in vitro remain, however, to be fully elucidated. Our experimental
       data confirm that exposure of normal human T cells to micromolar
       concentrations of cocaine modulates T-cell responses to stimulation by a
       variety of stimuli, and indicate that cocaine impairs early activation
       events during CD4+ but not CD4- T-cell stimulation. Pre-incubation of
       enriched CD4+ T-cell subpopulations that express the homing receptor
       CD62L with nanomolar concentrations of the endogenous opioid peptide
       beta-endorphin leads to a more severe impairment of activation than that
       noted following pre-incubation with micromolar concentrations of cocaine
       alone. These findings begin to elucidate the molecular and cellular
       mechanisms of the immunopathology of cocaine. Our data support the
       proposition that cocaine abuse may place cocaine-abuser HIV-seropositive
       individuals at increased risk of opportunistic infections.
 DE    beta-Endorphin/ADMINISTRATION & DOSAGE  Antigens, CD/METABOLISM
       Antigens, Differentiation, B-Lymphocyte/METABOLISM
       Cocaine/ADMINISTRATION & DOSAGE/*TOXICITY  Concanavalin A/PHARMACOLOGY
       CD4-Positive T-Lymphocytes/*DRUG EFFECTS/IMMUNOLOGY  Drug Synergism
       Human  In Vitro  Interleukin-2/BIOSYNTHESIS  Lymphocyte
       Transformation/DRUG EFFECTS  Phytohemagglutinins/PHARMACOLOGY
       Receptors, Interleukin-2/METABOLISM  Support, Non-U.S. Gov't  Support,
       U.S. Gov't, P.H.S.  JOURNAL ARTICLE

       SOURCE: National Library of Medicine.  NOTICE: This material may be
       protected by Copyright Law (Title 17, U.S.Code).

