Mast cells as initiators of immunity and host defense

Henz, Beate M.; Maurer, Marcus; Lippert, Undine; Worm, Margitta; Babina, Magda

doi:10.1034/j.1600-0625.2001.100101.x

Cited by 176 publications

(141 citation statements)

References 100 publications

(121 reference statements)

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“…The high production of IL-4 and IL-10 cytokines and serum IgE Abs in anti-CTLA-4-treated mice may have enhanced mast cell proliferation and differentiation as described by Lukacs and colleagues (34). In addition, the CTLA-4 ligands CD80 and CD86 are expressed on mast cells (35). It is unknown whether ligation of CTLA-4 with these molecules may have a direct suppressive effect on mast cells, but it might be another explanation for the observed mast cell degranulation upon anti-CTLA-4 treatment.…”

Section: Discussionmentioning

confidence: 99%

CTLA-4 Signaling Regulates the Intensity of Hypersensitivity Responses to Food Antigens, but is Not Decisive in the Induction of Sensitization

Wijk¹,

Hoeks²,

Nierkens³

et al. 2005

The Journal of Immunology

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Although food allergy has emerged as a major health problem, the mechanisms that are decisive in the development of sensitization to dietary Ag remain largely unknown. CTLA-4 signaling negatively regulates immune activation, and may play a crucial role in preventing induction and/or progression of sensitization to food Ag. To elucidate the role of CTLA-4 signaling in responses to food allergens, a murine model of peanut allergy was used. During oral exposure to peanut protein extract (PPE) together with the mucosal adjuvant cholera toxin (CT), which induces peanut allergy, CTLA-4 ligation was prevented using a CTLA-4 mAb. Additionally, the effect of inhibition of the CTLA-4 pathway on oral exposure to PPE in the absence of CT, which leads to unresponsiveness to peanut Ag, was explored. During sensitization, anti-CTLA-4 treatment considerably enhanced IgE responses to PPE and the peanut allergens, Ara h 1, Ara h 3, and Ara h 6, resulting in elevated mast cell degranulation upon an oral challenge. Remarkably, antagonizing CTLA-4 during exposure to PPE in the absence of CT resulted in significant induction of Th2 cytokines and an elevation in total serum IgE levels, but failed to induce allergen-specific IgE responses and mast cell degranulation upon a PPE challenge. These results indicate that CTLA-4 signaling is not the crucial factor in preventing sensitization to food allergens, but plays a pivotal role in regulating the intensity of a food allergic sensitization response. Furthermore, these data indicate that a profoundly Th2-biased cytokine environment is insufficient to induce allergic responses against dietary Ag.

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Section: Discussionmentioning

confidence: 99%

CTLA-4 Signaling Regulates the Intensity of Hypersensitivity Responses to Food Antigens, but is Not Decisive in the Induction of Sensitization

Wijk¹,

Hoeks²,

Nierkens³

et al. 2005

The Journal of Immunology

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“…OX40L, CD40L, CD28, and ICAM1 are thought to have a critical role in mast cell-T cell communication (33)(34)(35). BMMCs and PCMCs express low levels of OX40L, CD40L, and CD28 (data not shown), and these were not significantly enhanced in the presence of LPS and BP.…”

Section: Icam1 Expression On Mast Cells Is Important In Mast Cell-t Cmentioning

confidence: 96%

Fasciola hepatica Tegumental Coat Impairs Mast Cells’ Ability To Drive Th1 Immune Responses

Vukman

Adams

Metz

et al. 2013

The Journal of Immunology

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The parasitic worm Fasciola hepatica induces strong Th2 and T-regulatory immune responses while simultaneously suppressing Th1-driven immune responses to bystander microbial infections. It also prevents the initiation of Th1-mediated autoimmune disorders in mice through the suppression of Th17 and Th1 immune responses, and this can be mimicked by parasite-derived molecules. We have isolated F. hepatica tegumental coat Ag (FhTeg) and demonstrated its suppressive effect in vivo by directly targeting dendritic cells, impairing their ability to drive Th1 responses. Mast cells are critical in promoting Th1 protective immunity during bacterial infection and in driving Th1-mediated pathological conditions in autoimmune diseases. In this article, we show that FhTeg inhibits the ability of mast cells to drive the Th1 immune response by suppressing cytokine secretion (TNF-α, IL-6, IFN-γ, and IL-10) and ICAM1 expression in mast cells stimulated with LPS or heat-inactivated Bordetella pertussis Ag. These heat-inactivated B. pertussis Ag/LPS–stimulated mast cells fail to promote Th1 immune responses in CD4+ T cells when pretreated with FhTeg, and a role for ICAM1 in this process was demonstrated. FhTeg suppresses the activation of transcription factors in the TLR signaling pathway, which explains the decrease in cytokine production and cell surface marker expression. We demonstrated that FhTeg suppresses MAPK and NF-κB activation and enhances SOCS3 expression, which could explain its negative effect on the TLR pathways. We conclude that FhTeg targets innate immune cells, inhibiting their ability to drive Th1 immune responses.

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“…Since mast cells are located in the superficial dermis close to blood vessels, they are advantageously positioned to react with allergens diffusing through a ruptured epidermis. They are, therefore, recognized as key effector cells during IgE-associated Th2-type immune responses (Galli et al, 2005), and cross-linking of the high-affinity IgE receptor (FcεRI) leads to release of potent inflammatory mediators (Turner & Kinet, 1999) such as histamine, proteases, chemotactic factors, cytokines, and metabolites of arachidonic acid (Henz et al, 2001). Mast cells have a wide variety of cell surface receptors that can interact directly with pathogens, including Toll-like receptors (TLRs), which are involved in innate immune recognition of invading microorganisms (Qiao et al, 2006).…”

Section: Skin Barrier Dysfunctionmentioning

confidence: 99%

Fungus as an Exacerbating Factor of Atopic Dermatitis, and Control of Fungi for the Remission of the Disease

Nakashima¹,

Niwano²

2012

Atopic Dermatitis - Disease Etiology and Clinical Management

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Mast cells as initiators of immunity and host defense

Cited by 176 publications

References 100 publications

CTLA-4 Signaling Regulates the Intensity of Hypersensitivity Responses to Food Antigens, but is Not Decisive in the Induction of Sensitization

CTLA-4 Signaling Regulates the Intensity of Hypersensitivity Responses to Food Antigens, but is Not Decisive in the Induction of Sensitization

Fasciola hepatica Tegumental Coat Impairs Mast Cells’ Ability To Drive Th1 Immune Responses

Fungus as an Exacerbating Factor of Atopic Dermatitis, and Control of Fungi for the Remission of the Disease

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