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Dendritic Cell-Mediated Th2 Immunity and Immune Disorders

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International Journal of Molecular Sciences Review Dendritic Cell-Mediated Th2 Immunity and Immune Disorders 1, 1,2, 1,2 1,2, Sunil Kumar y , Yideul Jeong y , Muhammad Umer Ashraf and Yong-Soo Bae * 1 Science Research Center (SRC) for Immune Research on Non-Lymphoid Organ (CIRNO), Sungkyunkwan University, Jangan-gu, Suwon, Gyeonggi-do 16419, Korea; [email protected] (S.K.); [email protected] (Y.J.); [email protected] (M.U.A.) 2 Department of Biological Science, Sungkyunkwan University, Jangan-gu, Suwon, Gyeonggi-do 16419, Korea * Correspondence: [email protected]; Tel.: +82-31-299-4149; Fax: +82-31-290-7087 These authors contributed equally to this work. y Received: 30 March 2019; Accepted: 29 April 2019; Published: 1 May 2019 Abstract: Dendritic cells (DCs) are the professional antigen-presenting cells that recognize and present antigens to naïve 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. Keywords: dendritic cells; Th2 immunity; genetic factors; environmental factors; Th2 disorders; therapeutic approaches 1. Introduction Dendritic cells (DCs) are the professional antigen-presenting cells (APCs) that play an important role in immune defense by activating the adaptive immune system. DCs were first discovered by Steinman and Cohn in 1973 [1], and extensive studies have since been conducted related to the various DC subsets in humans and mice and their characteristics [2]. Different DC subsets or the same DC subset in different environments can induce different T-cell immunity [3–5]. T helper type 2 (Th2) immunity mainly performs two important interconnected functions, i.e., providing direct protection against the extracellular parasites (helminths), but this protective immunity occasionally leads to adverse reactions, such as an allergic response [6–8]. The protective functions of Th2 immunity for pathogen clearance are mediated by the induction of Th2 cytokines (interleukin 4 (IL-4), 5 (IL-5), 6 (IL-6), 10 (IL-10), and 13 (IL-13)) and the recruitment of B cells and eosinophils, while allergic responses are mediated by hypersecretion of IgE from B cells and histamines from mast cells and basophils. Genetic and environmental factors have also been considered to influence the Th2 immune response. Environmental factors include pathogens (bacteria, viruses, fungi, and parasites), foods, and allergens (house dust mites (HDMs), pollens, etc.), whereas genetic factors include the specific genes of DCs Int. J. Mol. Sci. 2019, 20, 2159; doi:10.3390/ijms20092159 www.mdpi.com/journal/ijms Int. J. Mol. Sci. 2019, 20, 2159 2 of 28 essential for induction of Th2 immunity. Other factors, such as hormones and lipids, also affect Th2 immunity, but details on these subjects are beyond the scope of this review. This review mainly covers DC-mediatedInt. J. Mol. Th2 Sci. 2018 immunity., 19, 2159 2 of 28 DCs are the first lines of immune defense that come into play once encountered with a foreign antigen(bacteria, and decide viruses, whether fungi, toand tolerate parasites), or elicitfoods, a and strong allergens immune (house response dust mites against (HDMs), it. Ifpollens, the response has alreadyetc.), intensified,whereas genetic the immunefactors include system the must specific decide genes what of DCs kind essential of response for induction is appropriate of Th2 to clear immunity. Other factors, such as hormones and lipids, also affect Th2 immunity, but details on these the pathogens. To accomplish this task, DCs engulf and present these antigens via cross-presentation subjects are beyond the scope of this review. This review mainly covers DC-mediated Th2 + + machineryimmunity. to CD4 naïve T or CD8 T cells (Figure1), leading to the birth of a specific T-cell subset, like T helperDCs types are the 1 (Th1),first lines 2 (Th2),of immune and defense 17 (Th17), that co andme into T regulatory play once enco (Treg)untered subsets with a orforeign cytotoxic T lymphocytesantigen (CTLs) and decide to orchestrate whether to immunetolerate or responses elicit a strong in both immune humans response and against mice [it.9]. If Athe pool response of cytokines releasedhas during already this intensified, process actuallythe immune governs system the must fates decide of these what T kind cells of to response acquire is specific appropriate T-cell to polarity. Differentiationclear the ofpathogens. Th1 cells To is triggeredaccomplish bythis interleukin task, DCs 12engulf (IL-12) and andpresent characterized these antigens by high-levelvia cross-presentation machinery to CD4+ naïve T or CD8+ T cells (Figure 1), leading to the birth of a γ secretionspecific of cytokines: T-cell subset, Interferon like T helper gamma types (IFN- 1 (Th1),), interleukin 2 (Th2), and 2 (IL-2), 17 (Th17), and and lymphotoxin, T regulatory which (Treg) recruits + macrophages,subsets or B-lymphocytes, cytotoxic T lymphocytes CD8 T (CTLs) cells, naturalto orchestrate killer immune (NK) cells,responses and in neutrophils both humans to and the site of infectionmice to impart[9]. A pool protective of cytokines Th1 rele immunityased during in this both process humans actually and governs mice [the10]. fates Conversely, of these T cells Th2 to cells are triggeredacquire by IL-4 specific and T-cell characterized polarity. Differentiation by high-level of Th1 secretion cells is triggered of IL-4, by IL-5, interleukin and IL-13, 12 (IL-12) which and activate B cells tocharacterized produce immunoglobulinby high-level secretion E (IgE) of cytokines: and recruit Interferon basophils gamma to (IFN- mediateγ), interleukin Th2-specific 2 (IL-2), immune and lymphotoxin, which recruits macrophages, B-lymphocytes, CD8+ T cells, natural killer (NK) responses in both humans and mice [11]. Despite the crucial role of T-cell subsets in host defense, cells, and neutrophils to the site of infection to impart protective Th1 immunity in both humans and they aremice also [10]. associated Conversely, with Th2 severe cells are immune triggered pathologies, by IL-4 and includingcharacterized hypersensitivity, by high-level secretion tumorigenesis, of and autoimmunityIL-4, IL-5, and [IL-13,12]. The which mechanisms activate B cells controlling to produce immunoglobulin the differentiation E (IgE) of and Th1, recruit Th17, basophils and Treg cells are wellto described. mediate Th2-specific However, immune the detailsresponses of in Th2 both di humansfferentiation and mice by [11]. specific Despite subsets the crucial of role DCs of remain controversial.T-cell subsets Gao in et host al. (2013)defense, investigated they are also associated the role ofwith the severe IRF4 immune+ DC subset pathologies, in initiating including the Th2 responsehypersensitivity, in mice [13]. Murphytumorigenesis, et al. (2015)and autoimmu suggestednity that[12]. a Klf4-expressingThe mechanisms DCcontrolling subset isthe required differentiation of Th1, Th17, and Treg cells are well described. However, the details of Th2 for Th2 responses in mice [14]. A recent study by Ahmed et al. (2017) has shown that a DC subset differentiation by specific subsets of DCs remain controversial. Gao et al. (2013) investigated the role expressingof the SH2 IRF4 domain-containing+ DC subset in initiating adaptor the Th2 response protein in B mice (SHB) [13]. ensures Murphy Th2 et al. homeostasis (2015) suggested by that regulating DC-mediateda Klf4-expressing Th2 immunity DC subset in an is atopicrequired dermatitis for Th2 responses (AD) mouse in mice model [14]. A [recent15]. These study findingsby Ahmed prompted et us to investigateal. (2017) has the shown role of that these a DC genes subset in expressing DC-mediated SH2 domain-containing Th2 immunity. Inadaptor this review, protein weB (SHB) discuss DC subsetsensures and genes Th2 ofhomeostasis interest in by DCs regulating essential DC-mediated for induction Th2 ofimmunity Th2 immune in an atopic responses dermatitis in the (AD) context of mouse model [15]. These findings prompted us to investigate the role of these genes in DC-mediated allergic diseases and illustrate the well-coordinated interplay of different signaling pathways, such as Th2 immunity. In this review, we discuss DC subsets and genes of interest in DCs essential for transcriptioninduction factors, of Th2 cytokines, immune epigenetics, responses in and the microRNAs, context of allergic which arediseases essential and toillustrate obtain anthe optimal Th2 response.well-coordinated interplay of different signaling pathways, such as transcription factors, cytokines, epigenetics, and microRNAs, which are essential to obtain an optimal Th2 response. Figure 1.FigureSchematic 1. Schematic diagram diagram for for the the cross-presentation cross-presentation ma machinerychinery of ofDCs. DCs. DCs DCstake up take extracellular up extracellular antigen, process it to antigenic peptides, and present these peptides not only with MHC II through antigen, process it to antigenic peptides, and present these peptides not only with MHC II through the MIIC to CD4+ T cells (left), but also with MHC I through proteasome and the TAP/ER pathway to CD8+ T cells (right). Int. J. Mol.
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