Immunoglobulin levels in bronchoalveolar lavage fluid of children with chronic chest disease

Kitz, Richard J.; Ahrens, Peter; Zielen, Stefan

doi:10.1002/(sici)1099-0496(200006)29:6<443::aid-ppul6>3.0.co;2-m

Cited by 24 publications

(10 citation statements)

References 24 publications

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“…Moreover, we observed in another study significantly elevated immunoglobulins in bronchoalveolar lining fluid from children with chronic chest disease. 12 Obviously, a healthy immune system responds to mucosal inflammatory processes with an increased immunoglobulin production. This consideration is in favor of high-dose intravenous immunoglobulin substitution or by alternative routes of administration (e.g., nasal).…”

Section: Discussionmentioning

confidence: 99%

Immunoglobulins and Inflammatory Cytokines in Nasal Secretions in Humoral Immunodeficiencies

et al. 2006

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Section: Discussionmentioning

confidence: 99%

Immunoglobulins and Inflammatory Cytokines in Nasal Secretions in Humoral Immunodeficiencies

et al. 2006

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“…Analysis of these populations showed a strong association with HDM-specific IgG, but not cat-specific IgG, for increased risk of asthma [67]. These studies suggesting a role for allergen-specific IgG in the promotion of Th2-mediated allergic disease are further supported by data showing elevated levels of IgG1 and IgG4 in the bronchoalveolar lavage fluid (BALF) of individuals with asthma [68, 69]. Furthermore, the induction of IgG during allergic Th2 responses is not limited to asthma; in other Th2-mediated diseases individuals with allergic bronchopulmonary aspergillosis and allergic alveolitis (e.g., farmer's lung and bird fancier's disease) are associated with increased levels of antigen-specific IgG [70, 71].…”

Section: Fcγr and Igg In Human Allergy And Asthmamentioning

confidence: 99%

The Contribution of Allergen-Specific IgG to the Development of Th2-Mediated Airway Inflammation

2012

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In both human asthmatics and animal models of allergy, allergen-specific IgG can contribute to Th2-mediated allergic inflammation. Mouse models have elucidated an important role for IgG and Fc-gamma receptor (FcγR) signaling on antigen presenting cells (APC) for the induction of airway inflammation. These studies suggest a positive feedback loop between IgG produced by the adaptive B cell response and FcγR signaling on innate immune cells. Studies of IgG and FcγRs in humans with asthma or allergic lung disease have been more controversial. Some reports have identified associations between allergen-specific IgG and severity of allergic responses, while other studies have found associations of IgG subclass IgG4 with allergic tolerance. In this paper, we review the literature to help define the nature of IgG and FcγR signaling on innate immune cells and how it contributes to the development of allergic immune responses.

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“…Taken together with the fact that inhaled allergens can be contaminated with endotoxins, these 2 signals could augment Th2 inflammation in the lung during secondary responses (19). Intriguingly, this hypothesis is supported by clinical studies that have shown increased IgG levels in the bronchoalveolar lavage (BAL) of patients with asthma due to increased leakage from the blood as well as increased local IgG production (20,21). Furthermore, other studies have identified allergen-specific ICs in the sera of allergic individuals (22).…”

Section: Introductionmentioning

confidence: 99%

IL-33–dependent induction of allergic lung inflammation by FcγRIII signaling

Tjota¹,

Williams²,

Lu³

et al. 2013

J. Clin. Invest.

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Atopic asthma is a chronic inflammatory disease of the lungs generally marked by excessive Th2 inflammation. The role of allergen-specific IgG in asthma is still controversial; however, a receptor of IgG-immune complexes (IgG-ICs), FcγRIII, has been shown to promote Th2 responses through an unknown mechanism. Herein, we demonstrate that allergen-specific IgG-ICs, formed upon reexposure to allergen, promoted Th2 responses in two different models of IC-mediated inflammation that were independent of a preformed T cell memory response. Development of Th2-type airway inflammation was shown to be both FcγRIII and TLR4 dependent, and T cells were necessary and sufficient for this process to occur, even in the absence of type 2 innate lymphoid cells. We sought to identify downstream targets of FcγRIII signaling that could contribute to this process and demonstrated that bone marrow-derived DCs, alveolar macrophages, and respiratory DCs significantly upregulated IL-33 when activated through FcγRIII and TLR4. Importantly, IC-induced Th2 inflammation was dependent on the ST2/IL-33 pathway. Our results suggest that allergen-specific IgG can enhance secondary responses by ligating FcγRIII on antigen-presenting cells to augment development of Th2-mediated responses in the lungs via an IL-33-dependent mechanism.

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Immunoglobulin levels in bronchoalveolar lavage fluid of children with chronic chest disease

Cited by 24 publications

References 24 publications

Immunoglobulins and Inflammatory Cytokines in Nasal Secretions in Humoral Immunodeficiencies

Immunoglobulins and Inflammatory Cytokines in Nasal Secretions in Humoral Immunodeficiencies

The Contribution of Allergen-Specific IgG to the Development of Th2-Mediated Airway Inflammation

IL-33–dependent induction of allergic lung inflammation by FcγRIII signaling

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