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pubmed: 0091-6749



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Early-onset childhood atopic dermatitis is related to NLRP2 repression.
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Early-onset childhood atopic dermatitis is related to NLRP2 repression.

J Allergy Clin Immunol. 2017 Dec 09;:

Authors: Thürmann L, Grützmann K, Klös M, Bieg M, Winter M, Polte T, Bauer T, Schick M, Bewerunge-Hudler M, Roeder S, Bauer M, Wissenbach DK, Sack U, Weichenhan D, Mücke O, Plass C, Borte M, von Bergen M, Lehmann I, Eils R, Trump S

Abstract
Early-onset atopic dermatitis (AD) related repression of the immune regulatory NLRP2 is driven by promoter hypermethylation starting already at time of birth providing an early opportunity to modulate innate immunity to potentially mitigate AD development.

PMID: 29233739 [PubMed - as supplied by publisher]




Circulating allergen-specific Th2 lymphocytes: CCR4+ rather than CLA+ is the predominant phenotype in peanut allergic subjects.
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Circulating allergen-specific Th2 lymphocytes: CCR4+ rather than CLA+ is the predominant phenotype in peanut allergic subjects.

J Allergy Clin Immunol. 2017 Dec 07;:

Authors: Blom LH, Juel-Berg N, Larsen LF, Hansen KS, Poulsen LK

Abstract
The skin and airway homing chemokine CCR4, but not CLA, emerged as the primary discriminating homing factor, of Th2 lymphocytes, suggesting that peanut sensitization occurs both via the skin and airways.

PMID: 29225086 [PubMed - as supplied by publisher]




Anti-cytokine autoantibodies in a patient with a heterozygous NFKB2 mutation.
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Anti-cytokine autoantibodies in a patient with a heterozygous NFKB2 mutation.

J Allergy Clin Immunol. 2017 Dec 07;:

Authors: Ramakrishnan KA, Rae W, Barcenas-Morales G, Gao Y, Pengelly RJ, Patel SV, Kumararatne DS, Ennis S, Döffinger R, Faust SN, Williams AP

Abstract
We report a family with a heterozygous NFKB2 mutation in which anti-cytokine autoantibodies were identified in one individual. Rituximab therapy for autoantibodies led to a reduction in anti-cytokine autoantibodies and a marked improvement in infectious susceptibility.

PMID: 29225085 [PubMed - as supplied by publisher]




Autophagy deficiency in myeloid cells exacerbates eosinophilic inflammation in chronic rhinosinusitis.
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Autophagy deficiency in myeloid cells exacerbates eosinophilic inflammation in chronic rhinosinusitis.

J Allergy Clin Immunol. 2017 Dec 07;:

Authors: Choi GE, Yoon SY, Kim JY, Kang DY, Jang YJ, Kim HS

Abstract
BACKGROUND: Eosinophilic inflammation is a major pathologic feature of chronic rhinosinusitis and is frequently associated with severe refractory disease. Prostaglandin D2 level is elevated in chronic rhinosinusitis and is an important contributing factor to eosinophilic inflammation. Autophagy has a pleiotropic effect on immune responses and disease pathogenesis. Recent studies suggest the potential involvement of autophagy in chronic rhinosinusitis and the prostaglandin pathway.
OBJECTIVE: To investigate whether altered function of autophagy is associated with eosinophilic inflammation and dysregulated production of prostaglandin D2 in chronic rhinosinusitis.
METHODS: We used myeloid cell-specific deletion of Atg7, which is vital for autophagy, and investigated the effects of impaired autophagy on eosinophilic inflammation in a murine model of eosinophilic chronic rhinosinusitis. The effect of autophagy on prostaglandin D2 production and gene expression profiles associated with allergy and the prostaglandin pathway were assessed.
RESULTS: We found that impaired autophagy in myeloid cells aggravated eosinophilia, epithelial hyperplasia, and mucosal thickening in eosinophilic chronic rhinosinusitis mice. This aggravation was associated with gene expression profiles that favor eosinophilic inflammation, Th2 response, mast cell infiltration, and prostaglandin D2 dysregulation. Supporting this, prostaglandin D2 production was also significantly increased by impaired autophagy. Among other myeloid cells, macrophages were associated with autophagy deficiency, leading to elevated IL-1β levels. Macrophage depletion or blockade of IL-1 receptor led to alleviation of eosinophilic inflammation and sinonasal anatomic abnormalities associated with autophagy deficiency.
CONCLUSION: Our results suggest that impaired autophagy in myeloid cells, particularly macrophages, has a causal role in eosinophilic inflammation and eosinophilic chronic rhinosinusitis pathogenesis.

PMID: 29225084 [PubMed - as supplied by publisher]