TNF-α and IFN-γ reverse IL-4 inhibition of lymphokine-activated killer cell function

Cellular Immunology

Volumn 128, Issue 2, 1990, Pages 450-461

  Swisher, Stephen G ^a   Economou, James S ^a   Holmes, E Carmack ^a   Golub, Sidney H ^a  

^a UNIVERSITY OF CALIFORNIA   (United States)

Author keywords

[No Author keywords available]

Indexed keywords

GAMMA INTERFERON; INTERLEUKIN 4; TUMOR NECROSIS FACTOR ALPHA;

ARTICLE; CELL CULTURE; HUMAN; HUMAN CELL; LYMPHOKINE ACTIVATED KILLER CELL; NATURAL KILLER CELL; NORMAL HUMAN; PRIORITY JOURNAL;

COLONY-STIMULATING FACTORS; CYTOTOXICITY, IMMUNOLOGIC; DRUG SYNERGISM; GRANULOCYTE-MACROPHAGE COLONY-STIMULATING FACTOR; GROWTH SUBSTANCES; HUMAN; IMMUNITY, CELLULAR; IMMUNOSUPPRESSION; IN VITRO; INTERFERON TYPE I, RECOMBINANT; INTERFERON TYPE II; INTERFERON-GAMMA, RECOMBINANT; INTERLEUKIN-2; INTERLEUKIN-4; KILLER CELLS, LYMPHOKINE-ACTIVATED; MACROPHAGE COLONY-STIMULATING FACTOR; SUPPORT, U.S. GOV'T, P.H.S.; TUMOR NECROSIS FACTOR;

EID: 0025297502     PISSN: 00088749     EISSN: 10902163     Source Type: Journal    
DOI: 10.1016/0008-8749(90)90040-X     Document Type: Article

References (44)

1. Obligatory role of IFN-gamma in induction of lymphokine-activated and T lymphocyte killer activity, but not in boosting of natural cytotoxicity.
2. Tumor necrosis factor-alpha and tumor necrosis factor-beta (lymphotoxin) stimulate the production of granulocyte-macrophage colony-stimulating factor, macrophage colony-stimulating factor, and IL-1 in vivo.