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Eosinophils continue to be studied intensively, in large part, as a result of their potential role in the pathogenesis of asthma. The concept of the eosinophil as a cell that has protective effects against helminthic parasite infection, but can cause tissue damage when inappropriately activated, remains intact, although the evidence for both these roles is circumstantial. Eosinophil production and function are profoundly influenced by interleukin (IL)-5; and, thus, eosinophilia is associated with diseases characterized by T-helper (Th)2-mediated immune responses, including infections by helminthic parasites and extrinsic asthma. However, eosinophilia also occurs in diseases not obviously associated with Th2 dominance, such as intrinsic asthma, hypereosinophilic syndromes (HESs), and inflammatory bowel disease. Thus, IL-5 and other eosinophil mediators can be generated in various types of inflammatory response.

The eosinophil, like other leukocytes, can generate proinflammatory mediators. Eosinophil-specific granule proteins are toxic for a range of mammalian cells and parasitic larvae. Eosinophils, like mast cells, produce sulfidopeptide leukotrienes, as well as other lipid mediators, such as platelet-activating factor (PAF). Cytokine production by eosinophils broadens their potential functions, for example in wound healing through their generation of transforming growth factor (TGF)-α. Synthesis of TGF-β may explain the propensity of eosinophils to be associated with fibrotic reactions such as endomyocardial fibrosis, characteristic of HES, and fibrosing alveolitis.

Considerable effort has gone into trying to unravel the molecular basis of eosinophil tissue recruitment. The selective accumulation of eosinophils is the result of a concerted and integrated series of events involving their production in the marrow and egress therefrom, adhesion to endothelium, selective chemotaxis, and prolonged survival in tissues. These events are controlled, either directly or indirectly, by production of IL-4, IL-5, and IL-13.

The discovery that a proportion of patients with HES have either a clonal myeloid neoplasm resulting from an acquired mutation that generates a constitutively active, novel tyrosine kinase (FIP1L1-PDGFRα [F/P]) or a T-cell lymphoproliferative disease causing a reactive eosinophilia has offered the prospect of new and more effective treatments for these conditions, as well as giving new insights into the control of eosinophil production. There has long been a debate about the extent to which eosinophils cause tissue damage, are innocent bystanders, or even help to ameliorate the condition. This is now being resolved with data showing that specific reduction in eosinophils using anti–IL-5 monoclonal antibody is beneficial in eosinophilic airway disease and HES.

Acronyms and Abbreviations

AAV, ANCA-associated vasculitides; AHR, airway hyperresponsiveness; ANCA, antineutrophil cytoplasmic antibodies; BAL, bronchoalveolar lavage; BSA, bovine serum albumin; CCL, chemokine (C-C motif) ligand; CCR, chemokine receptor; CEL, chronic eosinophilic leukemia; CLC, Charcot-Leyden crystal; CLM-1, CMRF35-like molecule-1; CMPD, chronic myeloproliferative disease; ECP, eosinophil cationic protein; EDN, eosinophil-derived neurotoxin; EGPA, eosinophilic granulomatosis with polyangiitis; EM, electron microscopic; EMR, mucin-like hormone receptor; FEV1, forced expiratory volume in 1 second; FISH, fluorescence in situ hybridization; GM-CSF, granulocyte-monocyte colony-stimulating growth factor; GPA, granulomatosis with polyangiitis; HES, hypereosinophilic syndrome; HLA, human leukocyte antigen; ICAM, ...

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