IgA, IgG and IgM quantification in bronchoalveolar lavage fluids from allergic rhinitics, allergic asthmatics, and normal subjects by monoclonal antibody-based immunoenzymetric assays

Rs, Peebles; Mc, Liu; Lichtenstein, L M; Rg, Hamilton

doi:10.1016/0022-1759(94)00275-2

Cited by 54 publications

(16 citation statements)

References 13 publications

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“…In non-transplanted patients without lung dysfunction or infection, mean IgA levels in BAL were 23 mg/mL (16,17). These results are comparable with our own results from 10 healthy control patients.…”

Section: Discussionsupporting

confidence: 89%

Immunoglobulin A and secretory immunoglobulin A in the bronchoalveolar lavage from patients after lung transplantation

Bastian

Tunkel

Lins

et al. 2000

Clinical Transplantation

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Secretory immunoglobulin A (sIgA) is the most important Ig on mucosal surfaces. In bronchoalveolar lavage (BAL) fluid, sIgA is mainly produced by bronchus-associated lymphoid tissue (BALT). The presence of pre-formed antibodies against donor tissue in kidney transplantation is associated with hyperacute rejection, indicating a humoral (antibody-mediated) reaction. In heart and liver transplantation, humoral rejection has also been documented. The goal of this study was to evaluate the role of IgA in patients after lung transplantation. An enzyme-linked immunosorbent assay was established to determine the levels of sIgA, IgA, and total protein in the lavage. IgA and sIgA were both detectable in BAL from transplanted lungs. IgA and sIgA levels were both higher during episodes of infection than during episodes of rejection or during the control episodes. The level of IgA during episodes of rejection equaled the level of IgA during the control episodes. The level of sIgA was significantly decreased during episodes of acute rejection (1.8 +/- 1.0 microg/mL) when compared with the control (7.2 +/- 1.0 microg/mL; p = 0.013). This study demonstrates that BALT retains the ability to produce Ig even after lung transplantation. The levels of IgA and sIgA and their ratio do not contribute to the differentiation between rejection and infection in lung-transplanted patients.

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Section: Discussionsupporting

confidence: 89%

Immunoglobulin A and secretory immunoglobulin A in the bronchoalveolar lavage from patients after lung transplantation

Bastian

Tunkel

Lins

et al. 2000

Clinical Transplantation

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“…AMs express high levels of Fcγ-receptors I (CD64), II (CD32) and III (CD16) that recognize the Fc region of IgG. Biologically relevant concentrations IgG can be found in the alveolar lining fluid of healthy humans (126). To trigger phagocytosis, Fcγ-receptors bind multiple IgG molecules within an immune complex.…”

Section: Macrophage Ontogeny and Clearance Mechanismsmentioning

confidence: 99%

“…In comparison, FcγRII and FcγRIII may also promote phagocytosis but have low binding affinity. Respiratory epithelial cells secrete IgA by transcytosis, and IgA can easily be detected in the lumens of both the proximal airways and alveoli (126, 127). AMs express low levels of both FcαRI (CD89) and Fcα/µR that bind IgA and drive phagocytosis (128).…”

Section: Macrophage Ontogeny and Clearance Mechanismsmentioning

confidence: 99%

Control of lung defence by mucins and macrophages: ancient defence mechanisms with modern functions

et al. 2016

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Due to the need to balance the requirement for efficient respiration in the face of tremendous levels of exposure to endogenous and environmental challenges, it is crucial for the lungs to maintain sustainable defense that minimizes damage caused by exposures and the detrimental effects of inflammation to delicate gas exchange surfaces. Accordingly, epithelial and macrophage defenses constitute essential 1st and 2nd lines of protection that prevent the accumulation of potentially harmful agents in the lungs, and under homeostatic conditions do so effectively without inducing inflammation. Though seemingly distinct, recent data show that epithelial and macrophage mediated defenses are linked through their shared reliance on airway mucins, in particular the polymeric mucin MUC5B. This review highlights our understanding of novel mechanisms that link mucus and macrophage defenses. The roles of phagocytosis and the effects of factors that are contained within mucus on phagocytosis, as well as newly identified roles for mucin glycoproteins in the direct regulation of leukocyte functions are discussed. The emergence of this nascent field of glycoimmunobiology sets forth a new paradigm for considering how homeostasis is maintained under healthy conditions and how it is restored in disease.

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“…A prolonged effect of IL-3 versus IL-5 or GM-CSF on eosinophil degranulation has not been reported. High amounts of IgG are present in human BAL fluid [29], and allergen-specific IgG correlates with EDN in sputum of asthmatic patients [30]. Therefore, antigen-bound or aggregated IgG has been used as a relevant model to investigate eosinophil degranulation [31, 32].…”

Section: Introductionmentioning

confidence: 99%

IL‐3 up‐regulates and activates human eosinophil CD32 and αMβ2 integrin causing degranulation

Esnault

Johansson

Kelly

et al. 2017

Clin Experimental Allergy

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Background Eosinophils contribute to the pathogenesis of multiple diseases, including asthma. Treatment with antibodies targeting IL-5 or IL-5 receptor α reduces the frequency of asthma exacerbations. Eosinophil receptors for IL-5 share a common ß-chain with IL-3 and GM-CSF receptors. We recently reported that IL-3 is more potent than IL-5 or GM-CSF in maintaining the ERK/p90S6K/RPS6 ribosome-directed signaling pathway, leading to increased protein translation. Objective We aimed to determine disease-relevant consequences of prolonged eosinophil stimulation with IL-3. Methods Human blood eosinophils were used to establish the impact of activation with IL-3 on IgG-driven eosinophil degranulation, which was then compared to IgG-mediated degranulation of freshly isolated (unstimulated) airway eosinophils activated in vivo by segmental allergen challenge. Results When compared to IL-5, continuing exposure to IL-3 further induced degranulation of eosinophils on aggregated IgG via increased production and activation of both CD32 (low affinity IgG receptor) and αMß2 integrin. In addition, unlike IL-5 or GM-CSF, IL-3 induced expression of CD32B/C (FCGRIIB/C) subtype proteins, without changing CD32A (FCGRIIA) protein and CD32B/C mRNA expression levels. Importantly, these in vitro IL-3-induced modifications were recapitulated in vivo on airway eosinophils. Conclusions We observed for the first time upregulation of CD32B/C on eosinophils, and identified IL-3 as a potent inducer of CD32- and αMß2-mediated eosinophil degranulation.

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IgA, IgG and IgM quantification in bronchoalveolar lavage fluids from allergic rhinitics, allergic asthmatics, and normal subjects by monoclonal antibody-based immunoenzymetric assays

Cited by 54 publications

References 13 publications

Immunoglobulin A and secretory immunoglobulin A in the bronchoalveolar lavage from patients after lung transplantation

Immunoglobulin A and secretory immunoglobulin A in the bronchoalveolar lavage from patients after lung transplantation

Control of lung defence by mucins and macrophages: ancient defence mechanisms with modern functions

IL‐3 up‐regulates and activates human eosinophil CD32 and αMβ2 integrin causing degranulation

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