Modulation of T-cell function by (R)- and (S)-isomers of albuterol: Anti-inflammatory influences of (R)-isomers are negated in the presence of the (S)-isomer

Journal of Allergy and Clinical Immunology

Volumn 109, Issue 3, 2002, Pages 449-454

  Baramki, Dawn ^a   Koester, Jeffrey ^b   Anderson, Andrea J ^b   Borish, Larry ^a  

^a UNIVERSITY OF VIRGINIA HEALTH SYSTEM   (United States)

^b SUNOVION PHARMACEUTICALS INC   (United States)

Author keywords

Albuterol; Apoptosis; Cytokine; Proliferation; Racemic; T lymphocyte; adrenergic receptor

Indexed keywords

BETA ADRENERGIC RECEPTOR; BETA ADRENERGIC RECEPTOR STIMULATING AGENT; DRUG METABOLITE; INTERLEUKIN 13; INTERLEUKIN 2; PHYTOHEMAGGLUTININ; PROPRANOLOL; RECOMBINANT INTERLEUKIN 2; SALBUTAMOL; TETANUS TOXOID;

ADULT; ANTIGEN SPECIFICITY; ANTIINFLAMMATORY ACTIVITY; APOPTOSIS; ARTICLE; BETA ADRENERGIC STIMULATION; CELL PROLIFERATION; CELL VIABILITY; CONCENTRATION RESPONSE; CONTROLLED STUDY; CYTOKINE PRODUCTION; DOSE RESPONSE; DRUG METABOLISM; DRUG RECEPTOR BINDING; HUMAN; HUMAN CELL; INHIBITION KINETICS; ISOMERISM; PRIORITY JOURNAL; RACEMIC MIXTURE; T LYMPHOCYTE ACTIVATION; TETANUS;

EID: 0036128350     PISSN: 00916749     EISSN: None     Source Type: Journal    
DOI: 10.1067/mai.2002.122159     Document Type: Article

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