Tag: immune

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Th1/Th2 Immune Balance and Other T Helper Subsets in IgG4-Related Disease.

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Th1/Th2 Immune Balance and Other T Helper Subsets in IgG4-Related Disease.

Curr Top Microbiol Immunol. 2016 Oct 16;

Authors: Moriyama M, Nakamura S

Abstract
IgG4-related disease (IgG4-RD) is a systemic disease characterized by elevated serum IgG4 levels and a strong infiltration of IgG4-positive plasma cells in various organs. IgG4-RD patients also frequently suffer from allergic diseases, including asthma and atopic dermatitis. It is well known that T helper type 2 (Th2) cells have an important role in the initiation of allergic diseases, and Th2 cytokines such as interleukin (IL)-4 and IL-13 promote class switching to IgG4. Therefore, IgG4-RD is considered to be a Th2-predominant disease. However, other Th subsets, including regulatory T cells and T follicular helper cells, have recently received increasing attention with regard to the pathogenesis of IgG4-RD. Exploring the interconnected network of Th subsets in IgG4-RD is a highly promising field of investigation. In this review, we focus on the localization and functions of individual Th subsets to clarify the involvement of these cells in the pathogenesis of IgG4-RD.

PMID: 27744510 [PubMed – as supplied by publisher]

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Humoral immune factors and asthma among American Indian children: a case–control study – BMC Blogs Network

Humoral immune factors and asthma among American Indian children: a case–control study
BMC Blogs Network
Asthma is recognized as intimately related to immunologic factors and inflammation, although there are likely multiple phenotypes and pathophysiologic pathways. Biomarkers of inflammation may shed light on causal factors and have potential clinical …

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Strategy for depleting immune cells implicated in asthma-associated inflammation – Science Daily

Strategy for depleting immune cells implicated in asthma-associated inflammation
Science Daily
Patients with asthma have chronic lung inflammation that results in sporadic narrowing of the airways and difficulty breathing. Symptoms and severity are variable among individuals; however, the cells and inflammatory factors that trigger asthmatic …

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Epigenetic Dysfunction in Turner Syndrome Immune Cells.

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Epigenetic Dysfunction in Turner Syndrome Immune Cells.

Curr Allergy Asthma Rep. 2016 May;16(5):36

Authors: Thrasher BJ, Hong LK, Whitmire JK, Su MA

Abstract
Turner syndrome (TS) is a chromosomal condition associated with partial or complete absence of the X chromosome that involves characteristic findings in multiple organ systems. In addition to well-known clinical characteristics such as short stature and gonadal failure, TS is also associated with T cell immune alterations and chronic otitis media, suggestive of a possible immune deficiency. Recently, ubiquitously transcribed tetratricopeptide repeat on the X chromosome (UTX), a histone H3 lysine 27 (H3K27) demethylase, has been identified as a downregulated gene in TS immune cells. Importantly, UTX is an X-linked gene that escapes X-chromosome inactivation and thus is haploinsufficient in TS. Mice with T cell-specific UTX deficiency have impaired clearance of chronic viral infection due to decreased frequencies of T follicular helper (Tfh) cells, which are critical for B cell antibody generation. In parallel, TS patients have decreased Tfh frequencies in peripheral blood. Together, these findings suggest that haploinsufficiency of the X-linked UTX gene in TS T cells underlies an immune deficit, which may manifest as increased predisposition to chronic otitis media.

PMID: 27039394 [PubMed – in process]

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Rhinovirus-Induced Airway Disease: A Model To Understand the Antiviral and Th2 Epithelial Immune Dysregulation in Childhood Asthma.

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Rhinovirus-Induced Airway Disease: A Model To Understand the Antiviral and Th2 Epithelial Immune Dysregulation in Childhood Asthma.

J Investig Med. 2015 Jun 8;

Authors: Perez GF, Rodriguez-Martinez CE, Nino G

Abstract
Rhinovirus (RV) infections account for most asthma exacerbations among children and adults, yet the fundamental mechanism responsible for why asthmatics are more susceptible to RV than otherwise healthy individuals remains largely unknown. Nonetheless, the use of models to understand the mechanisms of RV-induced airway disease in asthma has dramatically expanded our knowledge about the cellular and molecular pathogenesis of the disease. For instance, ground-breaking studies have recently established that the susceptibility to RV in asthmatic subjects is associated with a dysfunctional airway epithelial inflammatory response generated after innate recognition of viral-related molecules, such as double-stranded RNA. This review summarizes the novel cardinal features of the asthmatic condition identified in the past few years through translational and experimental RV-based approaches. Specifically, we discuss the evidence demonstrating the presence of an abnormal innate antiviral immunity (airway epithelial secretion of types I and III interferons), exaggerated production of the master Th2 molecule thymic stromal lymphopoietin, and altered antimicrobial host defense in the airways of asthmatic individuals with acute RV infection.

PMID: 26057561 [PubMed – as supplied by publisher]

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Bronchial lesions of mouse model of asthma are preceded by immune complex vasculitis and induced bronchial associated lymphoid tissue (iBALT).

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Bronchial lesions of mouse model of asthma are preceded by immune complex vasculitis and induced bronchial associated lymphoid tissue (iBALT).

Lab Invest. 2015 Jun 1;

Authors: Guest IC, Sell S

Abstract
We systematically examined by immune histology the lungs of some widely used mouse models of asthma. These models include sensitization by multiple intraperitoneal injections of soluble ovalbumin (OVA) or of OVA with alum, followed by three intranasal or aerosol challenges 3 days apart. Within 24?h after a single challenge there is fibrinoid necrosis of arterial walls with deposition of immunoglobulin (Ig) and OVA and infiltration of eosinophilic polymorphonuclear cells that lasts for about 3 days followed by peribronchial B-cell infiltration and slight reversible goblet cell hypertrophy (GCHT). After two challenges, severe eosinophilic vasculitis is present at 6?h, increases by 72?h, and then declines; B-cell proliferation and significant GCHT and hyperplasia (GCHTH) and bronchial smooth muscle hypertrophy recur more prominently. After three challenges, there is significantly increased induced bronchus-associated lymphoid tissue (iBALT) formation, GCHTH, and smooth muscle hypertrophy. Elevated levels of Th2 cytokines, IL-4, IL-5, and IL-13, are present in bronchial lavage fluids. Sensitized mice have precipitating antibody and positive Arthus skin reactions but also develop significant levels of IgE antibody to OVA but only 1 week after challenge. We conclude that the asthma like lung lesions induced in these models is preceded by immune complex-mediated eosinophilic vasculitis and iBALT formation. There are elevations of Th2 cytokines that most likely produce bronchial lesions that resemble human asthma. However, it is unlikely that mast cell-activated atopic mechanisms are responsible as we found only a few presumed mast cells by toluidine blue and metachromatic staining limited to the most proximal part of the main stem bronchus, and none in the remaining main stem bronchus or in the lung periphery.Laboratory Investigation advance online publication, 1 June 2015; doi:10.1038/labinvest.2015.72.

PMID: 26006019 [PubMed – as supplied by publisher]

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Bronchial lesions of mouse model of asthma are preceded by immune complex … – Nature.com

Bronchial lesions of mouse model of asthma are preceded by immune complex …
Nature.com
We systematically examined by immune histology the lungs of some widely used mouse models of asthma. These models include sensitization by multiple intraperitoneal injections of soluble ovalbumin (OVA) or of OVA with alum, followed by three intranasal …

View full post on asthma – Google News