Current concepts of IgE regulation and impact of genetic determinants

Potaczek, Daniel P.; Kabesch, Michael

doi:10.1111/j.1365-2222.2011.03953.x

Cited by 100 publications

(98 citation statements)

References 280 publications

(630 reference statements)

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“…STAT6 function is critical for allergy, because STAT6-deficient mice have impaired Th2 function and B cell class switching to IgE (59). Numerous IL-4 and IL-13 gene variants were associated with elevated IgE levels and atopic conditions, including ocular allergy (6,60). We also observed reduction of Il4 expression in CCL7 2/2 mice with EAC.…”

Section: Discussionsupporting

confidence: 52%

Role of CCL7 in Type I Hypersensitivity Reactions in Murine Experimental Allergic Conjunctivitis

Kuo

Collins

Boettner

et al. 2017

The Journal of Immunology

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Molecules that are necessary for ocular hypersensitivity reactions include the receptors CCR1 and CCR3; CCL7 is a ligand for these receptors. Therefore, we explored the role of CCL7 in mast cell activity and motility in vitro and investigated the requirement for CCL7 in a murine model of IgE-mediated allergic conjunctivitis. For mast cells treated with IgE and Ag, the presence of CCL7 synergistically enhanced degranulation and calcium influx. CCL7 also induced chemotaxis in mast cells. CCL7-deficient bone marrow–derived mast cells showed decreased degranulation following IgE and Ag treatment compared with wild-type bone marrow–derived mast cells, but there was no difference in degranulation when cells were activated via an IgE-independent pathway. In vivo, CCL7 was upregulated in conjunctival tissue during an OVA-induced allergic response. Notably, the early-phase clinical symptoms in the conjunctiva after OVA challenge were significantly higher in OVA-sensitized wild-type mice than in control challenged wild-type mice; the increase was suppressed in CCL7-deficient mice. In the OVA-induced allergic response, the numbers of conjunctival mast cells were lower in CCL7-deficient mice than in wild-type mice. Our results demonstrate that CCL7 is required for maximal OVA-induced ocular anaphylaxis, mast cell recruitment in vivo, and maximal FcεRI-mediated mast cell activation in vitro. A better understanding of the role of CCL7 in mediating ocular hypersensitivity reactions will provide insights into mast cell function and novel treatments for allergic ocular diseases.

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Section: Discussionsupporting

confidence: 52%

Role of CCL7 in Type I Hypersensitivity Reactions in Murine Experimental Allergic Conjunctivitis

Kuo

Collins

Boettner

et al. 2017

The Journal of Immunology

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“…We next focused on the high-affinity receptor for IgE (FceRI) composed of one a chain, one b chain and two identical c chains (21,22). FceRI expression increased in culture (Fig.…”

Section: Resultsmentioning

confidence: 99%

Skin mast cells develop non‐synchronized changes in typical lineage characteristics upon culture

Guhl

Neou

Artuc

et al. 2014

Experimental Dermatology

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Despite their hematopoietic origin, mast cells (MCs) develop exclusively in tissues, hampering their ample use in research. To circumvent this problem, tissue‐derived MCs are typically first expanded in culture, but the changes MCs may undergo in the novel micromilieu are poorly defined. Here, we monitor skin MCs from a number of donors over time, revealing profound yet non‐synchronized modulations in culture. While tryptase and chymase, the most specific markers, strongly decline, FcεRI surface expression, and FcεRI‐mediated histamine release steeply increase (from ≈15.5% to ≈60%), replicated by similar increments in TNF‐α secretion. Interestingly, the modulations are independent of cell cycle progression, as they are comparable in the growth and postgrowth phase, implying they primarily result from microenvironmental conditioning. The data highlight a high degree of MC versatility, but also advise that results based on cultured MCs should be viewed with some caution, as they may not accurately reflect their counterparts in situ.

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“…Interestingly, no increase was observed with the isoform 12.0102, probably because it induced a more Th1-polarized response (as suggested by a lower IgG1/IgG2a ratio). Total and allergen-specific IgE production are supposed to involve common and particular determinants and pathways [46,47]; further studies are needed to elucidate the mechanisms underlying the effect of Blo t 12.0101-chitin on total IgE. Since chitin administration did not modify allergen-specific IgE production, it cannot be regarded as an adjuvant of allergenicity.…”

Section: Discussionmentioning

confidence: 99%

The Influence of Chitin on the Immune Response to the House Dust Mite Allergen Blo t 12

Zakzuk

Benedetti

Fernández-Caldas

et al. 2013

Int Arch Allergy Immunol

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Background: Information about the biological properties of Blomia tropicalis allergens is scarce. It is predicted that Blo t 12, an allergen with two described isoforms, contains a chitin-binding domain, similar to that found in peritrophins. Th2 adjuvant properties have been described for chitin. Therefore, it is feasible that binding to this carbohydrate influences its allergenicity. We aimed to evaluate the chitin-binding activity of Blo t 12 isoallergens and its effect on airway inflammation and antibody responses in a murine model of allergen sensitization. Methods: Chitin-binding assays were conducted with the recombinant isoallergens Blo t 12.0101 and Blo t 12.0102. BALB/c mice were sensitized via i.p. with any of the two isoforms (alone, with chitin or alum) and then challenged intranasally. Methacholine-induced bronchial hyperreactivity was tested by whole-body plethysmography and lung sections were stained with hematoxylin and eosin and periodic-acid Schiff. Total IgE and allergen-specific IgE, IgG1 and IgG2 levels were measured by ELISA. Results: The two isoforms bound chitin, but Blo t 12.0101 showed a stronger binding capacity. Both isoforms induced total and allergen-specific IgE, airway hyperreactivity, bronchial inflammation and mucus secretion without any adjuvant; however, when administered with chitin, Blo t 12.0101 induced higher total IgE levels. The IgG1/IgG2a ratio was significantly higher in mice immunized with Blo t 12.0101 than those immunized with Blo t 12.0102. As peritrophins, Blo t 12 was detected in mite feces. Conclusions: Blo t 12 isoforms are chitin-binding proteins that induce airway inflammation and bronchial hyperreactivity. However, for Blo t 12.0101, chitin reinforces its effects on total IgE production.

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Current concepts of IgE regulation and impact of genetic determinants

Cited by 100 publications

References 280 publications

Role of CCL7 in Type I Hypersensitivity Reactions in Murine Experimental Allergic Conjunctivitis

Role of CCL7 in Type I Hypersensitivity Reactions in Murine Experimental Allergic Conjunctivitis

Skin mast cells develop non‐synchronized changes in typical lineage characteristics upon culture

The Influence of Chitin on the Immune Response to the House Dust Mite Allergen Blo t 12

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