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Tytuł pozycji:

Intercellular adhesion molecule-1/LFA-1 ligation favors human Th1 development

Tytuł :
Intercellular adhesion molecule-1/LFA-1 ligation favors human Th1 development
Autorzy :
Smits, Hermelijn H.
de Jong, Esther C.
Schuitemaker, Joost H. N.
Geijtenbeek, Theo B. H.
van Kooyk, Yvette
Kapsenberg, Martien L.
Wierenga, Eddy A.
Pokaż więcej
Temat :
Dendritic Cells/immunology
Cell Differentiation
Th1 Cells/drug effects
Interleukin-12/pharmacology
Poly I-C/pharmacology
Cytokines/biosynthesis
Lymphocyte Function-Associated Antigen-1/metabolism
Mitogen-Activated Protein Kinases/metabolism
Cells, Cultured
Interleukin-4/pharmacology
Flow Cytometry
Humans
Intercellular Adhesion Molecule-1/metabolism
Antiviral Agents/pharmacology
T-Lymphocytes, Helper-Inducer/immunology
Źródło :
Journal of immunology (Baltimore, Md., 168(4), 1710 - 1716. American Association of Immunologists
Journal of Immunology, 168(4), 1710 - 6. American Association of Immunologists
Rok publikacji :
2002
Język :
English
ISSN :
0022-1767
Numer akcesji :
edsair.dedup.wf.001..1c75df4d5059e50ea86a5dd85fa1e5b6
Th cell polarization toward Th1 or Th2 cells is strongly driven by exogenous cytokines, in particular IL-12 or IL-4, if present during activation by Ag-presenting dendritic cells (DC). However, additional Th cell polarizing mechanisms are induced by the ligation of cell surface molecules on DC and naive Th cells. In the present study, the role of LFA-1/ICAM-1 ligation in human Th cell polarization was investigated. Triggering of LFA-1 on anti-CD3/CD28 stimulated naive Th cells with immobilized Fc-ICAM-1, in the absence of DC and exogenous cytokines, induced a marked shift toward Th1 cell development, accompanied by a dose-dependent decrease in GATA-3 expression and a dose-dependent increase in T-bet expression. Th1 polarization by LFA-1 ligation could be demonstrated only under low cytokine conditions, as it was largely overruled by IL-12 or IL-4. This IL-12-independent Th1-driving mechanism appears to be operated by certain subsets of effector DC. Maturation of DC by poly(I:C), a synthetic dsRNA, used as an in vitro model for viral infections, leads to the generation of Th1-driving effector DC (DC1), which express elevated levels of ICAM-1 but produce only low levels of IL-12p70. Blocking the ICAM-1/LFA-1 interaction in cocultures of these DC with naive Th cells attenuated their Th1-driving capacity. The molecular mechanism by which LFA-1 signaling supports Th1 differentiation is blocked by specific inhibitors of extracellular signal-regulated kinase phosphorylation. The present data indicate the existence of an IL-12-independent, extracellular signal-regulated kinase-mediated mechanism, through which high ICAM-1-expressing DC1 can drive Th1 polarization. This mechanism may be operational during viral infections.

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