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Dendritic Cell-Mediated Th2 Immunity and Immune Disorders

Journal

Publisher

MDPI
DOI: 10.3390/ijms20092159

Keywords

dendritic cells; Th2 immunity; genetic factors; environmental factors; Th2 disorders; therapeutic approaches

Funding

  1. National Research Foundation (NRF) grant - Korea Ministry of Science and ICT [SRC-2017R1A5A1014560]
  2. Korea Health Technology R&D Project through the Korea Health Industry Development Institute (KHIDI) - Ministry of Health & Welfare, Republic of Korea [HI16C1074]
  3. Individual Basic Science and Engineering Research Program - Korean National Research Foundation [2018R1D1A1B07048567]
  4. National Research Foundation of Korea [2018R1D1A1B07048567] Funding Source: Korea Institute of Science & Technology Information (KISTI), National Science & Technology Information Service (NTIS)

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Dendritic cells (DCs) are the professional antigen-presenting cells that recognize and present antigens to naive T cells to induce antigen-specific adaptive immunity. Among the T-cell subsets, T helper type 2 (Th2) cells produce the humoral immune responses required for protection against helminthic disease by activating B cells. DCs induce a Th2 immune response at a certain immune environment. Basophil, eosinophil, mast cells, and type 2 innate lymphoid cells also induce Th2 immunity. However, in the case of DCs, controversy remains regarding which subsets of DCs induce Th2 immunity, which genes in DCs are directly or indirectly involved in inducing Th2 immunity, and the detailed mechanisms underlying induction, regulation, or maintenance of the DC-mediated Th2 immunity against allergic environments and parasite infection. A recent study has shown that a genetic defect in DCs causes an enhanced Th2 immunity leading to severe atopic dermatitis. We summarize the Th2 immune-inducing DC subsets, the genetic and environmental factors involved in DC-mediated Th2 immunity, and current therapeutic approaches for Th2-mediated immune disorders. This review is to provide an improved understanding of DC-mediated Th2 immunity and Th1/Th2 immune balancing, leading to control over their adverse consequences.

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