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1 es induced by naive and in vivo-primed human T helper 2 cells.
2 ad an impaired ability to differentiate into T helper 2 cells.
3 4, restricted to the appropriately polarized T helper 2 cells.
4 ng the differentiation of naive T cells into T helper 2 cells.
7 endritic cells to promote differentiation of T-helper 2 cells and production of their cytokines (IL4,
9 pment of tolerogenic NKT cells with a marked T helper 2 cell bias that, in turn, regulated the differ
10 e Chemoattractant Receptor Homologous to the T helper 2 cell (CRTH2), a G protein-coupled receptor, p
12 ll as to antigen-experienced T cells, induce T helper 2 cell development, cytokine production or both
18 inflammation, characterized by expansion of T-helper 2 cells in the colon and lung, and infiltration
19 f naive CD4+ T lymphocytes into pro-allergic T-helper 2 cells induces interleukin (IL)4 expression an
21 helper 17 cells distinct from T helper 1 or T helper 2 cells, participates in the pathogenesis of in
23 migratory dendritic cell subset required for T helper 2 cell polarization following cutaneous challen
27 tions but generate stronger canonical CD4(+) T helper 2 cells responses (IL-4, IgE, mast cells, and b
28 munization was developed to produce specific T helper 2 cell (T(H)2)-type antibodies to provide an ef
29 rleukin (IL) 4 and 13 production from CD4(+) T helper 2 cells (T(H)2) and innate lymphoid type 2 cell
33 ted T cells (ATCs) in the lung, particularly T helper 2 cells (Th2), are strongly associated with ind
34 el of allergic asthma, OSPM caused increased T helper 2 cells (Th2), peribronchiolar inflammation, an
36 oduction of cytokines by T-helper 1 cells or T-helper 2 cells, we obtained bone marrow-derived macrop
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