Eosinophils and Th2 immunity: contemporary insights

Spencer, Lisa A.; Weller, Peter F.

doi:10.1038/icb.2009.115

Cited by 163 publications

(114 citation statements)

References 80 publications

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“…Eosinophils are also known to contribute to the generation of Th2 immunity. In fact, many studies have shown that eosinophil deficiency inhibits the efficient generation of the Th2 immune response (21,22). In our model, we found that eosinophils were recruited to the vaginal tissues after intravaginal papain immunization (Fig.…”

Section: Basophils and Eosinophils Are Dispensable For The Intravaginalsupporting

confidence: 50%

A mechanism for the induction of type 2 immune responses by a protease allergen in the genital tract

Oh²,

Jung³

et al. 2017

Proc. Natl. Acad. Sci. U.S.A.

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The genital mucosa is a barrier that is constantly exposed to a variety of pathogens, allergens, and external stimuli. Although both allergen exposure and parasite infections frequently occur in the genital area, the mechanism by which immune responses-particularly type 2 immunity-are induced has rarely been studied in the genital mucosa. Here, we demonstrate the induction of T helper type 2 (Th2) immunity in the genital mucosa in response to a model allergen, the protease papain. Intravaginal papain immunization induced type 2 immunity in a manner that was dependent on protease activity and the estrous phase of the mice. In addition, IL-33 was released from the vaginal epithelia after intravaginal papain immunization, leading to the activation of type 2 innate lymphoid cells (ILC2s). Moreover, the IL-33-MyD88 (myeloid differentiation primary response gene 88) signaling pathway was critical for the induction of type 2 immunity. We also found that Th2 differentiation in response to intravaginal papain treatment requires a specific dendritic cell (DC) subset that is controlled by interferon regulatory factor 4 (IRF4). These findings suggest that type 2 immunity is induced by a unique mechanism in the genital tract, which is an important, but often overlooked, barrier surface.A llergic disorders, such as asthma, atopy, and helminth infections, are major concerns across the globe because their prevalence is increasing (1, 2). These inflammatory and infectious diseases are commonly involved in "type 2 immunity." Type 2 immunity is characterized by the induction of T helper type 2 (Th2) cells, which secrete cytokines such as IL-4, -5, and -13, as well as by IgE production. Th1 and Th17 responses, which are induced by viral, bacterial, and fungal infections, are well studied. Pattern recognition receptors recognize pathogen-specific molecules, and dendritic cells (DCs) control Th cell differentiation by acting as antigen-presenting cells and producing cytokines required for Th cell differentiation. However, the mechanisms underlying the recognition of allergens and helminth infections and the subsequent induction of Th2 and IgE responses are much more complex. Although recent studies have demonstrated many aspects of innate and adaptive type 2 immunity (3-7), these results were derived from mouse models by using s.c. needle injections or allergen sensitization and helminth infections of the lungs and intestines.The vaginal tract is a mucosal barrier that is constantly exposed to a variety of pathogens, allergens, and external stimuli. In addition, this mucosal barrier has the unique feature of being under the control of the hormonal cycle. During the estrous cycle, the thickness of the epithelial layers, the immune cell populations within the vagina, and the receptors expressed on the vaginal epithelial cells change. Thus, the host responses to external stimuli within the vaginal tract are also dependent on the estrous cycle. In this context, the vaginal mucosa should be considered distinct from other mucosal barriers,...

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Section: Basophils and Eosinophils Are Dispensable For The Intravaginalsupporting

confidence: 50%

A mechanism for the induction of type 2 immune responses by a protease allergen in the genital tract

Oh²,

Jung³

et al. 2017

Proc. Natl. Acad. Sci. U.S.A.

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“…Unlike neutrophils that are involved in the antibacterial Th1 reactions, eosinophils are important mediators of Th2 immunity, producing a vast array of Th2 cytokines (e.g. IL4, IL10, IL13, and TGFB) that participate in anti-inflammatory immune responses, M2 polarization of macrophages, and differentiation of Th2 cells (Spencer & Weller 2010).…”

Section: Eosinophilsmentioning

confidence: 99%

The role of adipose tissue immune cells in obesity and low-grade inflammation

Mráz

Haluzı́k

2014

Journal of Endocrinology

448

323

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Adipose tissue (AT) lies at the crossroad of nutrition, metabolism, and immunity; AT inflammation was proposed as a central mechanism connecting obesity with its metabolic and vascular complications. Resident immune cells constitute the second largest AT cellular component after adipocytes and as such play important roles in the maintenance of AT homeostasis. Obesity-induced changes in their number and activity result in the activation of local and later systemic inflammatory response, marking the transition from simple adiposity to diseases such as type 2 diabetes mellitus, arterial hypertension, and ischemic heart disease. This review has focused on the various subsets of immune cells in AT and their role in the development of AT inflammation and obesity-induced insulin resistance.

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“…The eosinophils could not only promote naive CD4 + T cells to differentiate into Th2 cells by secreting cytokines such as IL-4 and IL-13, but they also could present Ags to naive CD4 + T cells directly to promote Th2 polarization. Moreover, chemokines such as eotaxin 1 and CXCL1 secreted by the eosinophils could recruit Th2 effector cells to the infected tissue (29). Based on the understanding that a correct Th1 versus Th2 balance is needed, the various prototype vaccines that have been developed are mainly aimed at inducing a strong Th1-type response and avoiding Th2.…”

mentioning

confidence: 99%

A Recombinant G Protein Plus Cyclosporine A–Based Respiratory Syncytial Virus Vaccine Elicits Humoral and Regulatory T Cell Responses against Infection without Vaccine-Enhanced Disease

Zhou

Zhong

et al. 2016

The Journal of Immunology

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Respiratory syncytial virus (RSV) infection can cause severe disease in the lower respiratory tract of infants and older people. Vaccination with a formalin-inactivated RSV vaccine (FI-RSV) and subsequent RSV infection has led to mild to severe pneumonia with two deaths among vaccinees. The vaccine-enhanced disease (VED) was recently demonstrated to be due to an elevated level of Th2 cell responses following loss of regulatory T (Treg) cells from the lungs. To induce high levels of neutralizing Abs and minimize pathogenic T cell responses, we developed a novel strategy of immunizing animals with a recombinant RSV G protein together with cyclosporine A. This novel vaccine induced not only a higher level of neutralizing Abs against RSV infection, but, most importantly, also significantly higher levels of Treg cells that suppressed VED in the lung after RSV infection. The induced responses provided protection against RSV challenge with no sign of pneumonia or bronchitis. Treg cell production of IL-10 was one of the key factors to suppress VED. These finding indicate that G protein plus cyclosporine A could be a promising vaccine against RSV infection in children and older people.

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Eosinophils and Th2 immunity: contemporary insights

Cited by 163 publications

References 80 publications

A mechanism for the induction of type 2 immune responses by a protease allergen in the genital tract

A mechanism for the induction of type 2 immune responses by a protease allergen in the genital tract

The role of adipose tissue immune cells in obesity and low-grade inflammation

A Recombinant G Protein Plus Cyclosporine A–Based Respiratory Syncytial Virus Vaccine Elicits Humoral and Regulatory T Cell Responses against Infection without Vaccine-Enhanced Disease

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