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Important and specific role for basophils in acute allergic reactions - PubMed

Review

. 2018 May;48(5):502-512.

doi: 10.1111/cea.13117. Epub 2018 Mar 23.

Affiliations

Review

Important and specific role for basophils in acute allergic reactions

P Korošec et al. Clin Exp Allergy. 2018 May.

Abstract

IgE-mediated allergic reactions involve the activation of effector cells, predominantly through the high-affinity IgE receptor (FcεRI) on mast cells and basophils. Although the mast cell is considered the major effector cell during acute allergic reactions, more recent studies indicate a potentially important and specific role for basophils and their migration which occurs rapidly upon allergen challenge in humans undergoing anaphylaxis. We review the evidence for a role of basophils in contributing to clinical symptoms of anaphylaxis and discuss the possibility that basophil trafficking during anaphylaxis might be a pathogenic (to target organs) or protective (preventing degranulation in circulation) response. Finally, we examine the potential role of basophils in asthma exacerbations. Understanding the factors that regulate basophil trafficking and activation might lead to new diagnostic and therapeutic strategies in anaphylaxis and asthma.

© 2018 The Authors. Clinical & Experimental Allergy Published by John Wiley & Sons Ltd.

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Figures

Figure 1
Figure 1

Basophil activation without evidence of degranulation following oral challenge in peanut‐allergic subjects (n = 4). Blood samples were collected prior to, during and 24 h after objective allergic reaction at oral food challenge, as previously described.50 Surface expression of

CD

63 (A) on basophils was evaluated (without further ex vivo stimulation) by flow cytometry.50 Basophils were isolated by Ficoll‐density centrifugation and purified to over 90% purity by immunomagnetic cell sorting, using a negative selection technique which we have previously described.111 Cells were incubated for 15 min at 37°C before stimulation with crude peanut extract (

CPE

) or anti‐IgE for 8 min after which histamine release was assessed by spectrofluorometric autoanalysis according to Shore et al 112 (B). Data are shown as mean percentage histamine releases ±

SEM

. Despite increased surface

CD

63 expression on ex vivo, unstimulated basophils (A), there was no difference in IgE‐mediated histamine release in the same basophils compared with baseline (B). This implies that circulating basophils have become “activated”—or rather, have increased surface expression of

CD

63, an activation marker—but with no evidence of degranulation, at least in terms of histamine release. These data presented at the 45th annual meeting of the European Histamine Research Society (

EHRS

) in Florence, 2016

Figure 2
Figure 2

Hypothetical role of basophil migration in anaphylaxis. Upon allergen challenge, basophil‐directed chemokine

CCL

2 (possibly secreted from mast cells) induces a rapid migration of basophils out of the circulation. This may reactogenic, with migration to target organs resulting in activation and degranulation. Alternatively, the migration may be a protective response, removing basophils from the circulation so that they are unable to degranulate in response to circulating allergen.

CCL

2, chemokine (C‐C motif) ligand 2;

CCR

2, C‐C chemokine receptor type 2; IgE, Immunoglobulin E; IgE receptor, high‐affinity IgE receptor (Fcε

RI

)

Figure 3
Figure 3

Hypothetical role of basophil migration in asthma exacerbation. Following exposure to allergen or respiratory viral infection, basophil chemotactic factors are released in lungs leading to recruitment of basophils from the circulation to the airways where they may contribute to the early asthmatic response. In some patients, a Th2‐type immune response orchestrated by basophils, mast cells and infiltration of eosinophils can cause late asthmatic response, resulting in prolonged swelling of the airway mucosa and aggravating the airway obstruction.

CCL

2, chemokine (C‐C motif) ligand 2;

CCR

2, C‐C chemokine receptor type 2; IgE, Immunoglobulin E; IgE receptor, high‐affinity IgE receptor (Fcε

RI

);

IL

‐4, interleukin 4

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