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- W4313354680 abstract "Abstract Asthma is an inflammatory disease of the airways that affects more than 300 million people worldwide. Clinically, asthma is characterized by acute, intermittent and recurrent episodes of inflammation that can be induced by a specific allergen. CD4+ T cells contribute to this process by producing the Type 2 cytokines IL-4, IL-5, and IL-13 and inducing B cell production of IgE in response to T cell receptor (TCR) recognition of allergen peptides bound to MHCII molecules on host cells. In both murine models of disease and asthmatic patients, quiescent allergen peptide:MHCII (pMHCII)-specific CD4+ memory T cells can persist in lungs and lymphoid organs long after resolution of inflammation. Upon subsequent exposure to allergen, CD4+ memory T cells rapidly drive asthma-induced immunopathology making these cells attractive targets for allergen-specific immune modulation. Little is known, however, about how these cells orchestrate the asthmatic response due to the challenge of tracking small populations of CD4+ T cells that express allergen pMHCII-specific TCRs. To address this lack of knowledge, we have utilized a MHCII tetramer containing a peptide from the Der p1 protein of the house dust mite (HDM), Dermatophagoides pteronyssinus, the most common cause of atopic asthma. Using this tetramer and a novel magnetic bead-based cell enrichment method, we can assess the differentiation and function of Der p1 pMHCII-specific Th2 effector and memory cells in mice responding to HDM." @default.
- W4313354680 created "2023-01-06" @default.
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- W4313354680 date "2013-05-01" @default.
- W4313354680 modified "2023-10-18" @default.
- W4313354680 title "Th2 differentiation during atopic asthma (P1167)" @default.
- W4313354680 doi "https://doi.org/10.4049/jimmunol.190.supp.50.26" @default.
- W4313354680 hasPublicationYear "2013" @default.
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