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COSTIMULATORY SIGNALS CAN SELECTIVELY MODULATE CYTOKINE PRODUCTION BY SUBSETS OF CD4(+) T-CELLS
Tekijät: SHANAFELT MC, SODERBERG C, ALLSUP A, ADELMAN D, PELTZ G, LAHESMAA R
Kustantaja: AMER ASSOC IMMUNOLOGISTS
Julkaisuvuosi: 1995
Journal: Journal of Immunology
Tietokannassa oleva lehden nimi: JOURNAL OF IMMUNOLOGY
Lehden akronyymi: J IMMUNOL
Vuosikerta: 154
Numero: 4
Aloitussivu: 1684
Lopetussivu: 1690
Sivujen määrä: 7
ISSN: 0022-1767
Tiivistelmä
Analysis of experimental animal models and human clinical samples has indicated that the selective activation of CD4(+) T cell subsets with distinct profiles of cytokine production plays an important role in the pathogenesis of human inflammatory and allergic diseases. The possibility that differential activation of costimulatory pathways is a mechanism for selectively modulating cytokine production by CD4(+) T cells was tested. The proliferative response and cytokines secreted by a panel of human CD4(+) T cell clones, representative of Th1 or Th2/0 cells, in response to activation of different costimulatory pathways was measured. CD28-mediated costimulatory signals induced proliferation and lFN-gamma secretion by Th1 cells. Although CD28-ligation induced Th2/0 cells to proliferate, it did not trigger IL-4 production. Ligation of LFA-1 and CD45 isoforms also generated costimulatory signals activating cytokine secretion by the different types of T cell clones. Th1 cells secreted the same profile of cytokines, irrespective of which costimulatory pathway was engaged. However, the cytokines secreted by a subset of Th2/0 cells varied, depending upon which costimulatory pathways were activated. These results suggest that the costimulatory pathways activated by APCs can selectively influence cytokine production by CD4(+) T cell subsets.
Analysis of experimental animal models and human clinical samples has indicated that the selective activation of CD4(+) T cell subsets with distinct profiles of cytokine production plays an important role in the pathogenesis of human inflammatory and allergic diseases. The possibility that differential activation of costimulatory pathways is a mechanism for selectively modulating cytokine production by CD4(+) T cells was tested. The proliferative response and cytokines secreted by a panel of human CD4(+) T cell clones, representative of Th1 or Th2/0 cells, in response to activation of different costimulatory pathways was measured. CD28-mediated costimulatory signals induced proliferation and lFN-gamma secretion by Th1 cells. Although CD28-ligation induced Th2/0 cells to proliferate, it did not trigger IL-4 production. Ligation of LFA-1 and CD45 isoforms also generated costimulatory signals activating cytokine secretion by the different types of T cell clones. Th1 cells secreted the same profile of cytokines, irrespective of which costimulatory pathway was engaged. However, the cytokines secreted by a subset of Th2/0 cells varied, depending upon which costimulatory pathways were activated. These results suggest that the costimulatory pathways activated by APCs can selectively influence cytokine production by CD4(+) T cell subsets.
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