Recent advances in understanding basophil‐mediated Th2 immune responses

  • Yoshinori Yamanishi
    Department of Immune Regulation Tokyo Medical and Dental University (TMDU) Graduate School of Medical and Dental Sciences Tokyo Japan
  • Kensuke Miyake
    Department of Immune Regulation Tokyo Medical and Dental University (TMDU) Graduate School of Medical and Dental Sciences Tokyo Japan
  • Misako Iki
    Department of Immune Regulation Tokyo Medical and Dental University (TMDU) Graduate School of Medical and Dental Sciences Tokyo Japan
  • Hidemitsu Tsutsui
    Department of Immune Regulation Tokyo Medical and Dental University (TMDU) Graduate School of Medical and Dental Sciences Tokyo Japan
  • Hajime Karasuyama
    Department of Immune Regulation Tokyo Medical and Dental University (TMDU) Graduate School of Medical and Dental Sciences Tokyo Japan

書誌事項

公開日
2017-06-28
資源種別
journal article
権利情報
  • http://onlinelibrary.wiley.com/termsAndConditions#vor
DOI
  • 10.1111/imr.12548
公開者
Wiley

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説明

<jats:title>Summary</jats:title><jats:p>Basophils, the least common granulocytes, represent only ~0.5% of peripheral blood leukocytes. Because of the small number and some similarity with mast cells, the functional significance of basophils remained questionable for a long time. Recent studies using newly‐developed analytical tools have revealed crucial and non‐redundant roles for basophils in various immune responses, particularly Th2 immunity including allergy and protective immunity against parasitic infections. In this review, we discuss the mechanisms how basophils mediate Th2 immune responses and the nature of basophil‐derived factors involved in them. Activated basophils release serine proteases, mouse mast cell protease 8 (<jats:styled-content style="fixed-case">mMCP</jats:styled-content>‐8), and <jats:styled-content style="fixed-case">mMCP</jats:styled-content>‐11, that are preferentially expressed by basophils rather than mast cells in spite of their names. These proteases elicit microvascular hyperpermeability and leukocyte infiltration in affected tissues, leading to inflammation. Basophil‐derived <jats:styled-content style="fixed-case">IL</jats:styled-content>‐4 also contributes to eosinophil infiltration while it acts on tissue‐infiltrating inflammatory monocytes to promote their differentiation into M2 macrophages that in turn dampen inflammation. Although basophils produce little or no <jats:styled-content style="fixed-case">MHC</jats:styled-content> class <jats:styled-content style="fixed-case">II</jats:styled-content> (<jats:styled-content style="fixed-case">MHC</jats:styled-content>‐<jats:styled-content style="fixed-case">II</jats:styled-content>) proteins, they can acquire peptide‐<jats:styled-content style="fixed-case">MHC</jats:styled-content>‐<jats:styled-content style="fixed-case">II</jats:styled-content> complexes from dendritic cells via trogocytosis and present them together with <jats:styled-content style="fixed-case">IL</jats:styled-content>‐4 to naive <jats:styled-content style="fixed-case">CD</jats:styled-content>4 T cells, leading to Th2 cell differentiation. Thus, basophils contribute to Th2 immunity at various levels.</jats:p>

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