Germinal-centre reactions in allergic inflammation

Gould, Hannah J.; Takhar, Pooja; Harries, Helen E.; Durham, Stephen R.; Corrigan, Christopher

doi:10.1016/j.it.2006.08.007

Cited by 53 publications

(52 citation statements)

References 49 publications

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“…We suspect that the predisposition of IgE + B cells toward a short-lived PC fate may be disrupted in individuals with IgE-mediated diseases, such as allergy. Interestingly, in human patients with allergic rhinitis, several studies have concluded that IgE + PCs are localized within the nasal mucosa and may reside there for long periods of time (Gould et al, 2006).…”

Section: Discussionmentioning

confidence: 99%

Fluorescent In Vivo Detection Reveals that IgE+ B Cells Are Restrained by an Intrinsic Cell Fate Predisposition

2012

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IgE antibodies may be protective in parasite immunity, but their aberrant production can lead to allergic disease and life-threatening anaphylaxis. Despite the importance of IgE regulation, few studies have directly examined the B cells that express IgE, because these cells are rare and difficult to detect. Here, we describe fluorescent IgE reporter mice and validate a flow cytometry procedure to allow sensitive and specific identification of IgE-expressing B cells in vivo. Similar to IgG1(+) cells, IgE(+) B cells differentiated into germinal center (GC) B cells and plasma cells (PCs) during primary immune responses to a T cell-dependent hapten-protein conjugate and the helminth Nippostrongylus brasiliensis. However, the participation of IgE(+) B cells in GCs was transient. IgE(+) B cells had an atypical propensity to upregulate the transcription factor Blimp-1 and undergo PC differentiation. Most IgE(+) PCs were short lived and showed reduced affinity maturation, revealing intrinsic mechanisms that restrict the IgE antibody response.

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Section: Discussionmentioning

confidence: 99%

Fluorescent In Vivo Detection Reveals that IgE+ B Cells Are Restrained by an Intrinsic Cell Fate Predisposition

2012

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“…IgE class-switching recombination in nasal mucosa was observed after ex vivo or in vivo allergen exposure (45,46). Although IgE may be produced in various lymphoid tissue sites, local mucosa offers not only biologic efficiency in countering allergen at its entry site, but also a microenvironment favoring class-switching to IgE (47). McMenamin et al (48) showed that Ag-specific IgE-secreting plasma cells were not found in the bone marrow of rats that were repeatedly exposed to Ag-containing aerosols.…”

Section: Discussionmentioning

confidence: 99%

Unique Epitopes on CεmX in IgE–B Cell Receptors Are Potentially Applicable for Targeting IgE-Committed B Cells

Chen

Hung

et al. 2010

The Journal of Immunology

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“…On the other hand, it has become increasingly clear that IgE class-switching can occur within lymphoid accumulations in the mucosa, as reviewed by Gould et al 48 Several groups have found increased IL-4, signal 1 for IgE-class switching, in the nasal mucosa of patients with allergic rhinitis 49 and bronchial biopsy specimens from asthmatic patients. 50 It is known that mast cells present in airway mucosa can provide CD40L, signal 2 for IgE switching.…”

Section: ''Where'': Where Do Ige-secreting Cells Reside?mentioning

confidence: 99%