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Titolo:
Inability of interleukin-12 to modulate T-helper 0 effectors to T-helper 1effectors: a possible distinct subset of T cells
Autore:
Hu, C; Salgame, P;
Indirizzi:
Temple Univ, Sch Med, Dept Microbiol & Immunol, Philadelphia, PA 19140 USATemple Univ Philadelphia PA USA 19140 Immunol, Philadelphia, PA 19140 USA
Titolo Testata:
IMMUNOLOGY
fascicolo: 1, volume: 97, anno: 1999,
pagine: 84 - 91
SICI:
0019-2805(199905)97:1<84:IOITMT>2.0.ZU;2-#
Fonte:
ISI
Lingua:
ENG
Soggetto:
ANTIGEN-PRESENTING CELLS; IFN-GAMMA; LYMPHOKINE PRODUCTION; IL-4-PRODUCING CELLS; LEISHMANIA-MAJOR; IMMUNE-RESPONSES; TYPE-1 TH1; IL-12; CLONES; MICE;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
37
Recensione:
Indirizzi per estratti:
Indirizzo: Salgame, P TempledUniv, Sch Med, Dept Microbiol & Immunol, Kresge Room 501,3400 N Broa Temple Univ Kresge Room 501,3400 N Broad St Philadelphia PA USA 19140
Citazione:
C. Hu e P. Salgame, "Inability of interleukin-12 to modulate T-helper 0 effectors to T-helper 1effectors: a possible distinct subset of T cells", IMMUNOLOGY, 97(1), 1999, pp. 84-91

Abstract

Interleukin-12 (IL-12) strongly favours the development of T-helper 1 (Th1)-type cells through its ability to induce interferon-gamma (IFN-gamma) production by natural killer cells and T cells. In the present work we analysed the effects of IL-12 on the synthesis and secretion of IFN-gamma and IL-4by human T-cell clones. Several previously described human T-cell clones exhibiting Th1, Th2 or Th0 phenotypes were used for these analyses. We demonstrated, by enzyme-linked immunosorbent assay (ELISA) and intracytoplasmic staining, that, in Th0 clones, IL-12 up-regulated the production of both IFN-gamma and IL-4 and was unable to modulate these cells to Th1-type. The up-regulation of cytokine gene expression was transcriptionally regulated andwas not due to differences in mRNA stability. In Th1 cells. IL-12 up-regulated only IFN-gamma and not IL-4. However, in Th cells, both IFN-gamma and IL-4 were up-regulated by IL-12. This suggests that Th2 cells may be less stable than Th1 cells. We also observed that human Th2 cells expressed the IL-12 beta 2 receptor, in contrast to murine Th2, which lacks this receptor. The observed differences in the effects of IL-12 on the three T-cell subsets may have important ramifications for IL-12-based therapies.

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Documento generato il 03/07/20 alle ore 01:44:38