B-lymphocyte lineage cells and the respiratory system

Kato, Atsushi; Hulse, Kathryn E.; Tan, Bruce K.; Schleimer, Robert P.

doi:10.1016/j.jaci.2013.02.023

Cited by 144 publications

(154 citation statements)

References 253 publications

(246 reference statements)

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“…Nasal polyps also exhibit extensive B cell infiltrates with local IgA, IgE, and IgG production, while some CRS patients, furthermore, express autoreactive antibodies through the regulation of the protein BAFF [103–105]. The presence of these antibodies in proximity to innate effector cells that possess Fc receptors may lead to degranulation and the observed tissue damage and remodeling changes seen in nasal polyposis [106, 107•]. Evidence for specific cytokines or signaling pathways that may address the other phenotypes of CRS is thus far relatively scant.…”

Section: Immune Barrier Hypothesismentioning

confidence: 99%

The Etiology and Pathogenesis of Chronic Rhinosinusitis: a Review of Current Hypotheses

Lam

Schleimer

Kern

2015

Curr Allergy Asthma Rep

185

143

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Chronic rhinosinusitis (CRS) is a broad clinical syndrome that is characterized by prolonged mucosal inflammation of the nose and paranasal sinuses, and is typically divided into two subtypes based on the presence or absence of nasal polyps. The etiology and pathogenesis of both forms remain areas of active research. Over the last 15 years, a number of hypotheses have been proposed to explain all or part of the clinical CRS spectrum. These hypotheses reflect the concept that CRS results from a dysfunctional interplay between individual host characteristics and factors exogenous to the host. Six broad theories on CRS etiology and pathogenesis are discussed as follows: (1) the “fungal hypothesis,” (2) the “superantigen hypothesis,” (3) the “biofilm hypothesis,” and (4) the “microbiome hypothesis,” all of which emphasize key environmental factors, and (5) the “eicosanoid hypothesis” and (6) the “immune barrier hypothesis,” which describe specific host factors. These theories are reviewed, and the evidence supporting them is critically appraised.

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Section: Immune Barrier Hypothesismentioning

confidence: 99%

The Etiology and Pathogenesis of Chronic Rhinosinusitis: a Review of Current Hypotheses

Lam

Schleimer

Kern

2015

Curr Allergy Asthma Rep

185

143

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“…These results need to be repeated in additional studies; however, it is unlikely that many of these subjects will go on to develop RA or even systemic autoimmunity. However, could this high prevalence of RA-related autoantibodies in the lung be related to enhanced production of ‘natural’ autoantibodies at mucosal surfaces that serve as broad protectors against organisms or other environmental factors at the mucosal surface [103,104]? This will need to be explored in future studies.…”

Section: Ongoing Challenges/unmet Needsmentioning

confidence: 99%

The lung may play a role in the pathogenesis of rheumatoid arthritis

Demoruelle

Solomon

Fischer

et al. 2014

International Journal of Clinical Rheumatology

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Multiple studies have identified strong associations between the lung and rheumatoid arthritis (RA). Such studies identify a high prevalence of lung disease, both airways and parenchymal disease, in subjects with clinically classifiable RA. It has been suggested that lung disease in RA results from targeting of the lung from circulating autoimmunity or other factors such as medications. However, findings that lung disease, specifically inflammatory airways disease, and lung generation of autoimmunity can be present before the onset of joint symptoms suggest that immune reactions in the lung may be involved in the initial development of RA-related autoimmunity. Herein we review these issues in detail, as well as outline a potential research agenda to understand the natural history of lung involvement in RA and its relation to the overall pathogenesis of RA.

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“…14 Five isotypes of antibodies, including immunoglobulins M (IgM), IgD, IgG, IgA, and IgE, are encoded in humans and rodents. 15 Of these, IgM, IgG, IgA, and IgE have been described at elevated levels in nasal polyps (NP) from patients with CRSwNP compared to control subjects tissue.…”

Section: Introductionmentioning

confidence: 99%

Evidence for altered levels of IgD in the nasal airway mucosa of patients with chronic rhinosinusitis

Min

Nayak

Hulse

et al. 2017

Journal of Allergy and Clinical Immunology

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Background Immunoglobulin D (IgD) is an enigmatic antibody isotype best known when co-expressed with IgM on naïve B cells. However, elevated soluble IgD (sIgD) and increased IgD+IgM− B cell populations have been described in the human upper respiratory mucosa. Objective We assessed whether levels of sIgD and IgD+ B cells are altered in nasal tissue from patients with chronic rhinosinusitis (CRS). We further characterized IgD+ B cell populations and explored clinical and local inflammatory factors associated with tissue sIgD levels. Methods sIgD levels were measured by ELISA in nasal tissues, nasal lavages, serum, and supernatants of dissociated nasal tissues. IgD+ cells were identified by immunofluorescence and flow cytometry. Inflammatory mediator levels in tissues were assessed by real-time PCR and multiplex immunoassay. Bacterial cultures from the middle meatus were performed. Underlying medical history and medicine use were obtained from medical records. Results sIgD levels and the number of IgD+ cells were significantly increased in uncinate tissue (UT) of CRS without nasal polyps (CRSsNP) compared to control (4-fold, P<.05). IgD+ cells were densely scattered in the periglandular regions of CRSsNP UT. We also found that IgD+CD19+CD38bright plasmablasts were significantly elevated in CRSsNP tissues compared to control (P<.05). Among numerous factors tested, IL-2 levels were increased in CRSsNP UT and were positively correlated with tissue IgD levels. Additionally, the supernatants of IL-2-stimulated dissociated CRSsNP tissue had significantly increased sIgD levels compared to IL-2-stimulated dissociated control tissue ex vivo (P<.05). Tissue from CRS patients with preoperative antibiotic use or those with pathogenic bacteria presence showed higher IgD levels compared to tissue from patients absent these variables (P<.05). Conclusion sIgD levels and IgD+CD19+CD38bright plasmablasts were increased in nasal tissue of CRSsNP. IgD levels were associated with increased IL-2 and the presence of pathogenic bacteria. These findings suggest that IgD might contribute to enhance mucosal immunity, inflammation, or respond to bacterial infections in CRS, especially CRSsNP.

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B-lymphocyte lineage cells and the respiratory system

Cited by 144 publications

References 253 publications

The Etiology and Pathogenesis of Chronic Rhinosinusitis: a Review of Current Hypotheses

The Etiology and Pathogenesis of Chronic Rhinosinusitis: a Review of Current Hypotheses

The lung may play a role in the pathogenesis of rheumatoid arthritis

Evidence for altered levels of IgD in the nasal airway mucosa of patients with chronic rhinosinusitis

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