Abstract
A large body of research supports a pathogenic role for T helper 2 cells in asthma, although T helper 1 cell-type responses may also contribute. Using the principle of T helper cell cross-regulation, investigators have attempted to regulate the pathological effects of T helper 2 cells using regimens that may promote T helper 1 cell-type inflammation. In this review, we propose that the use of factors that promote T helper 1 cell differentiation and activation to treat asthma may be counterproductive, and that alternate regulatory approaches should be explored.
Publication types
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Research Support, Non-U.S. Gov't
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Research Support, U.S. Gov't, P.H.S.
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Review
MeSH terms
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Animals
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Antigens, Bacterial / immunology
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Antigens, Bacterial / metabolism
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Asthma / etiology*
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Asthma / immunology
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Cytokines / metabolism*
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Dendritic Cells / immunology
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Down-Regulation
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Humans
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Inflammation / complications
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Inflammation / immunology
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Interleukins / therapeutic use
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Lymphocyte Activation
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Mice
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Models, Biological
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Th1 Cells / immunology*
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Th1 Cells / metabolism
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Th2 Cells / immunology
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Th2 Cells / metabolism
Substances
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Antigens, Bacterial
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Cytokines
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Interleukins