Elsevier

Current Opinion in Immunology

Volume 54, October 2018, Pages 74-79
Current Opinion in Immunology

Mast cells and basophils in allergic inflammation

https://doi.org/10.1016/j.coi.2018.06.006Get rights and content

Highlights

Mast cells and basophils have similar characteristics in terms of their function and development. They both have detrimental functions, being implicated in pro-inflammatory responses to allergens, but can also provide protection against multicellular parasites such as parasitic worms (helminths). Both cell types express the high affinity Fc receptor for IgE, FcεRI, and allergen cross-linking of this receptor triggers degranulation and release a set of cytokines and biochemical mediators. Although mast cells and basophils are similar in many respects, newly developed antibody reagents and genetically modified mouse models that enable cell type-specific deletion have allowed us to appreciate their independent in vivo roles. This review focuses on recent advances in our understanding of the contribution of basophils and mast cells to innate and adaptive allergic responses.

Section snippets

Mast cells and basophils

Mast cells and basophils were first described by Paul Ehrlich more than 130 years ago as blood leukocytes showing similar morphological characteristics using aniline dye staining. In addition to their morphological similarity, they are now known to have similar functions and developmental processes, and to be potent effector cells in innate immune responses, whose normal physiological function is protection from parasitic worms (helminths) and ticks. Both cell types are generally associated

Mast cell function in allergic responses

Mast cells express the receptor tyrosine kinase c-Kit and contain many cytosolic granules. They are generally located in the blood vessels and in tissues that form a barrier, such as the skin, the intestine and the gills [1,2,3]. The granules are strongly stained with basic pigments due to the presence of highly sulfated heparin and also contain biogenic amines (histamine and serotonin), serglycin, proteoglycans, mast cell-derived proteases (chymase and tryptase), and lipid mediators (platelet

Basophil function in allergic responses

Basophils have large granules that stain dark purple with basic pigments such as methylene blue and toluidine rather than the blue color seen with mast cells. The granules contain histamine, heparin, and hyaluronic acid, which are released during an allergic reaction and cause anaphylactic shock and bronchial asthma. Basophils also express cell surface FcεRI, and its cross-linking with allergen causes degranulation to release a set of cytokines and chemical mediators. Basophils of mice and

Allergic asthma induced by cysteine proteases

The dust mite endopeptidase allergen Derp1 and certain plant allergens with cysteine protease activity, e.g., papain, are major causes of allergic asthma. Depletion of basophils in Bas-TRECK mice resulted in resolution of the eosinophilia and mucus production induced by nasal administration of a protease allergen (Figure 1) [59••]. A series of analyses of transcriptional regulatory elements in the Il4 gene indicated that the 3'UTR contains a basophil-specific enhancer and its deletion caused

Concluding remarks

Recent studies demonstrated that mast cells and basophils had different contribution in innate and adaptive allergic responses. Mast cells mainly controlled IgE-dependent acute allergic responses, while basophils controlled IgE-mediated chronic responses and IgE-independent allergic inflammation. Role of basophils in the capacity to induce Th2 responses is long lasting question. This mechanism is now explained by direct regulation as antigen presenting cells and/or by indirect regulation via

References and recommended reading

Papers of particular interest, published within the period of review, have been highlighted as

  • • of special interest

  • •• of outstanding interest

Acknowledgements

We thank Dr. P. Burrows for helpful comments on the manuscript. This work was supported by a Grant-in-Aid for Scientific Research (A) (24249058) to M.K.

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