Eosinophils and allergic airway disease: There is more to the story

Center for Molecular Immunology & Infectious Disease and Department of Veterinary & Biomedical Sciences, The Pennsylvania State University, University Park, PA 16802, USA.
Trends in Immunology (Impact Factor: 10.4). 11/2009; 31(1):39-44. DOI: 10.1016/
Source: PubMed


The eosinophil has been perceived as a terminal effector cell in allergic airway diseases. However, recent work has shown that this multifunctional cell could be more involved in the initial stages of allergic disease development than was previously thought, particularly with regard to the ability of the eosinophil to modulate T-cell responses. In this review, we discuss recent advances that suggest that eosinophils can present antigen to naïve as well as to antigen-experienced T cells, induce T helper 2 cell development, cytokine production or both, and affect T-cell migration to sites of inflammation. These findings are changing the way that eosinophil function in disease is perceived, and represent a shift in the dogma of allergic disease development.

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    • "Blood eosinophilia is usually absent at the disease presentation [1], suggesting that the initial pathological stimulus originates at alveolar or pleural level. Both basic and applied research studies have demonstrated [10] that the selective activation of eosinophils is induced by several mediators, all of them sometimes categorized for simplicity with the most relevant of which, interleukin-5 (IL-5), i.e. with the name of the cytokine that exhibits the most specific and critical control of eosinophilic functions, including the regulation of eosinophilopoiesis in the bone marrow, the recruitment of these granulocytes to tissues, the lengthening of their survival by inhibiting apoptosis, and the differential activation and release of toxic products through their degranulation [11]. The local secretion of IL-5 and its enhanced concentration within restricted regions, detected in the broncho-alveolar lavage (BAL) fluid of patients with AEP, apparently reflects the presence of eosinophil-rich exudates in the alveoli andpleural cavity [12]. "
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    • "These contribute to airway inflammation and lung tissue remodeling that includes epithelial cell damage and loss, airway thickening, fibrosis and angiogenesis.7 More recent evidence suggests that in addition to their role as degranulating effector cells, eosinophils have the capacity to act as antigen-presenting, cells resulting in T cell proliferation and activation, thereby propagating inflammatory responses.8,9 "
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    • "Eosinophils have generally been regarded as terminal effector cells in allergic airway diseases; however, recent studies demonstrate their involvement in the initial stages of allergic disease development, as well [100]. Murine studies suggest eosinophils may actually drive T-cell responses as opposed to merely being driven by them. "
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    ABSTRACT: There is a growing list of viruses and bacteria associated with wheezing illness and asthma. It is well known that a few of these pathogens are strongly associated with wheezing illness and asthma exacerbations. What is not known is if early childhood infections with these pathogens cause asthma, and, if so, exactly what are the pathophysiologic mechanisms behind its development. The current consensus is respiratory infection works together with allergy to produce the immune and physiologic conditions necessary for asthma diasthesis. One link between respiratory infection and asthma may be the eosinophil, a cell that plays prominently in asthma and allergy, but can also be found in the body in response to infection. In turn, the eosinophil and its associated products may be novel therapeutic targets, or at the very least used to elucidate the complex pathophysiologic pathways of asthma and other respiratory illnesses. Together or separately, they can also be used for diagnosis, treatment and monitoring. The optimal care of a patient must take into consideration not only symptoms, but also the underlying disease mechanisms.
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