Normal mast cell numbers in the tissues of AhR‐deficient mice

Pilz, Anna Caroline; Feyerabend, Thorsten B.; Sonner, Jana K.; Redaelli, Chiara; Peter, Katharina; Kunze, Anja; Haas, Katharina; Esser, Charlotte; Schäkel, Knut; Wick, Wolfgang; Rodewald, Hans Reimer; Lanz, Tobias V.; Platten, Michael

doi:10.1111/exd.12864

Cited by 6 publications

(8 citation statements)

References 9 publications

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“…In our hands, growth and differentiation of MCs from bone marrow cultures were impaired in AhR-deficient mice as compared to WT mice, in agreement with Zhou et al [ 18 ]. However, we could not find a reduction of MCs in lymph nodes, as reported by Pilz et al [ 60 ] (Zelante T., personal communication). Despite the contrasting results in AhR-deficient mice, which require further investigations to define the exact contribution of AhR in the growth and differentiation of MCs, AhR is known to regulate many functions of MCs [ 19 ].…”

Section: Mast Cells and Microbes: The Ahr Linkcontrasting

confidence: 49%

“…As said, an important link between MCs and the microbiota involves the AhR, a ligand-activated transcription factor that links environmental stimuli to different functions including detoxification and immune homeostasis [ 14 ], although opposing findings were obtained in AhR-deficient mice—in which MCs were both decreased [ 18 ] or not [ 60 ]. In our hands, growth and differentiation of MCs from bone marrow cultures were impaired in AhR-deficient mice as compared to WT mice, in agreement with Zhou et al [ 18 ].…”

Section: Mast Cells and Microbes: The Ahr Linkmentioning

confidence: 99%

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The Mast Cell-Aryl Hydrocarbon Receptor Interplay at the Host-Microbe Interface

Costantini

Renga

Oikonomou

et al. 2018

Mediators of Inflammation

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Mast cells are increasingly being recognized as crucial cells in the response of the organism to environmental agents. Interestingly, the ability of mast cells to sense and respond to external cues is modulated by the microenvironment that surrounds mast cells and influences their differentiation. The scenario that is emerging unveils a delicate equilibrium that balances the effector functions of mast cells to guarantee host protection without compromising tissue homeostasis. Among the environmental components able to mold mast cells and fine-tune their effector functions, the microorganisms that colonize the human body, collectively known as microbiome, certainly play a key role. Indeed, microorganisms can regulate not only the survival, recruitment, and maturation of mast cells but also their activity by setting the threshold required for the exploitation of their different effector functions. Herein, we summarize the current knowledge about the mechanisms underlying the ability of the microorganisms to regulate mast cell physiology and discuss potential deviations that result in pathological consequences. We will discuss the pivotal role of the aryl hydrocarbon receptor in sensing the environment and shaping mast cell adaptation at the host-microbe interface.

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Section: Mast Cells and Microbes: The Ahr Linkcontrasting

confidence: 49%

Section: Mast Cells and Microbes: The Ahr Linkmentioning

confidence: 99%

The Mast Cell-Aryl Hydrocarbon Receptor Interplay at the Host-Microbe Interface

Costantini

Renga

Oikonomou

et al. 2018

Mediators of Inflammation

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“…Prolonged exposure was reported to induce a shift to IL‐17 production and impaired degranulation indicating that the associated inflammatory response can change with time of exposure. The effect on MC proliferation and differentiation reported in AhR‐null mice was disputed by others albeit studies in an inflammatory model have not been investigated. Therefore, it will be important to study the role of this receptor in various MC‐driven diseases.…”

Section: Nuclear Receptorsmentioning

confidence: 98%

Non‐IgE mediated mast cell activation

Redegeld

Kumari

et al. 2018

Immunological Reviews

160

105

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Mast cells (MCs) are innate immune cells that are scattered in tissues throughout the organism being particularly abundant at sites exposed to the environment such as the skin and mucosal surfaces. Generally known for their role in IgE-mediated allergies, they have also important functions in the maintenance of tissue integrity by constantly sensing their microenvironment for signals by inflammatory triggers that can comprise infectious agents, toxins, hormones, alarmins, metabolic states, etc. When triggered their main function is to release a whole set of inflammatory mediators, cytokines, chemokines, and lipid products. This allows them to organize the ensuing innate immune and inflammatory response in tight coordination with resident tissue cells, other rapidly recruited immune effector cells as well as the endocrine and exocrine systems of the body. To complete these tasks, MCs are endowed with a large repertoire of receptors allowing them to respond to multiple stimuli or directly interact with other cells. Here we review some of the receptors expressed on MCs (ie, receptors for Immunoglobulins, pattern recognition receptors, nuclear receptors, receptors for alarmins, and a variety of other receptors) and discuss their functional implication in the immune and inflammatory response focusing on non-IgE-mediated activation mechanisms.

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“…Mast cells (MCs), which regulate murine and human mucosal innate immunity and allergic and anaphylactic responses by releasing pro-inflammatory mediators (including histamine, mast cell proteases, and pro-inflammatory cytokines) were recently found to express the AHR constitutively (Maaetoft-Udsen et al 2012;Sibilano et al 2012) as well as to be highly responsive to FICZ (Sibilano et al 2012;Zhou et al 2013). Another study did, however, not confirm any role of the AHR in mast cell homeostasis (Pilz et al 2016). In their studies on the degranulation (i.e.…”

Section: Differentiation Of Immune Cells and Immune Responsesmentioning

confidence: 99%

The tryptophan derivative 6-formylindolo[3,2-b]carbazole, FICZ, a dynamic mediator of endogenous aryl hydrocarbon receptor signaling, balances cell growth and differentiation

Rannug

2018

Critical Reviews in Toxicology

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The aryl hydrocarbon receptor (AHR) is not essential to survival, but does act as a key regulator of many normal physiological events. The role of this receptor in toxicological processes has been studied extensively, primarily employing the high-affinity ligand 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD). However, regulation of physiological responses by endogenous AHR ligands remains to be elucidated. Here, we review developments in this field, with a focus on 6-formylindolo[3,2-b]carbazole (FICZ), the endogenous ligand with the highest affinity to the receptor reported to date. The binding of FICZ to different isoforms of the AHR seems to be evolutionarily well conserved and there is a feedback loop that controls AHR activity through metabolic degradation of FICZ via the highly inducible cytochrome P450 1A1. Several investigations provide strong evidence that FICZ plays a critical role in normal physiological processes and can ameliorate immune diseases with remarkable efficiency. Low levels of FICZ are pro-inflammatory, providing resistance to pathogenic bacteria, stimulating the anti-tumor functions, and promoting the differentiation of cancer cells by repressing genes in cancer stem cells. In contrast, at high concentrations FICZ behaves in a manner similar to TCDD, exhibiting toxicity toward fish and bird embryos, immune suppression, and activation of cancer progression. The findings are indicative of a dual role for endogenously activated AHR in barrier tissues, aiding clearance of infections and suppressing immunity to terminate a vicious cycle that might otherwise lead to disease. There is not much support for the AHR ligand-specific immune responses proposed, the differences between FICZ and TCDD in this context appear to be explained by the rapid metabolism of FICZ.

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Normal mast cell numbers in the tissues of AhR‐deficient mice

Cited by 6 publications

References 9 publications

The Mast Cell-Aryl Hydrocarbon Receptor Interplay at the Host-Microbe Interface

The Mast Cell-Aryl Hydrocarbon Receptor Interplay at the Host-Microbe Interface

Non‐IgE mediated mast cell activation

The tryptophan derivative 6-formylindolo[3,2-b]carbazole, FICZ, a dynamic mediator of endogenous aryl hydrocarbon receptor signaling, balances cell growth and differentiation

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