Autor: |
Rossignol A; Laboratoire d'Immunologie-Immunopathologie, Centre Hospitalier Universitaire La Milétrie, Pôle Biologie Santé Poitiers, France., Barra A, Herbelin A, Preud'homme JL, Gombert JM |
Jazyk: |
angličtina |
Zdroj: |
Clinical and experimental immunology [Clin Exp Immunol] 2007 Jun; Vol. 148 (3), pp. 555-63. Date of Electronic Publication: 2007 Mar 15. |
DOI: |
10.1111/j.1365-2249.2007.03364.x |
Abstrakt: |
CD1d-restricted invariant natural killer T (iNK T) cells activated by their experimental ligand alpha-galactosylceramide (alpha-GC) can produce both T helper 1 (Th1) and Th2 cytokines and display regulatory functions. Recent studies identified CD4(+) and CD4(-) CD8(-) double-negative (DN) iNK T cells as the two major components of the human population and suggest that they display a Th2 and a Th1 profile, respectively. We compared the Th2-promoting activity of freshly isolated human CD4(+) and DN iNK T cells in terms of their capacity to induce Ig production by autologous B cells. Secretion of IgG and IgE but not IgM was enhanced by the CD4(+) T cell subset (including iNK T cells) but not by its DN counterpart. iNK T cells were directly responsible for this pro-Th2 effect, as demonstrated by the requirement for both alpha-GC stimulation and CD1d presentation, as well as by its disappearance upon iNK T cell depletion. Interaction with iNK T cells led to progressive accumulation of isotype-switched and activated B cells. Myeloid dendritic cells (DC) completely block the induction of Ig production in co-culture. This dominant inhibitory effect of myeloid DC was concomitant with a specific loss of interleukin (IL)-4 production by CD4(+) iNK T but not by conventional T cells. These data support the conclusion that, conversely to the interferon (IFN)-gamma-producing DN human iNK T cell population, interleukin (IL)-4-producing CD4(+) iNK T cells can activate and help B cells to produce both IgG and IgE through a CD1d-dependent mechanism, in keeping with a functional Th1/Th2 dichotomy between these subsets. |
Databáze: |
MEDLINE |
Externí odkaz: |
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