In recent decades, the worldwide prevalence of allergic disease has increased considerably. The atopic march is a model aimed at explaining the apparent progression of allergic diseases from atopic dermatitis (AD) to allergic asthma (AA) and to allergic rhinitis (AR). It hypothesizes that allergic disease begins, typically in children, with the development of AD, then AA, and finally progresses to AR. This theory has been widely studied in cross-sectional and long-term longitudinal studies and it has been found that as prevalence of AD declines, prevalence of AA increases. A similar relationship is reported between AA and AR. The legitimacy of the atopic march model is, however, currently debated. Epidemiological evidence and criticism of longitudinal studies point to an overstatement of the atopic march’s prevalence and incorrect mechanisms, opening a discussion for alternative models to better explain the pathophysiological and epidemiological processes that promote this progression of allergic diseases. Albeit, risk factors for the development and progression of allergic disease, particularly AD, are critical in identifying disease progression. Investigating the role of age, severity, family history, phenotype, and genetic traits may give a better indication into the progression of allergic diseases. In addition, studies following patients from infancy into adulthood and a general increase in longitudinal studies would help broaden the knowledge of allergic disease progression and the atopic march.

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Eosinophilic asthma has conventionally been proposed to be a T helper 2 driven disease but emerging evidence supports a central role of type 2 innate lymphoid cells (ILC2s). These are non-T, non-B cells that lack antigen specificity and produce more IL-5 and IL-13 than CD4 + T lymphocytes, on a cell per cell basis, in vitro. Although it is clear that ILC2s and CD4 + T cells work in concert with each other to drive type 2 immune responses, kinetic studies in allergic asthma suggest that ILC2s may act locally within the airways to "initiate" eosinophilic responses, whereas CD4 + T cells act locally and systemically to "perpetuate" eosinophilic inflammatory responses. Importantly, ILC2s are increased within the airways of severe asthmatics, with the greatest number of IL-5 + IL-13 + ILC2s being detected in sputum from severe asthmatics with uncontrolled eosinophilia despite high-dose steroid therapy. Although the precise relationship between ILC2s and steroid sensitivity in asthma remains unclear, controlling the activation of ILC2s within the airways may provide an effective therapeutic target for eosinophilic inflammation in airways diseases. K E Y W O R D Seosinophilic asthma, eosinophilopoiesis, innate lymphoid cells NMU, neuromedin U; NMUR, neuromedin U receptor; PC 20 , concentration required to achieve a 20% decrease in FEV 1 ; PLZF, pro-myelocytic leukemia zinc finger; TOX, thymocyte selection associated HMB boxprotein; TSLP, thymic stromal lymphopoietin; TSLPR, thymic stromal lymphopoietin receptor. this review, we will discuss the role of innate lymphoid cells (ILCs) in eosinophilic asthma and the potential targets that drive persistent airway eosinophilia.

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Spandana is a 4th year Bachelor of Health Sciences (Honours) student at McMaster University. She began working with the McMaster Cardio-Respiratory Lab in September 2015 under Dr. Gail Gauvreau and John-Paul Oliveria. Her work with the lab focuses on the role of IgE and B cells in allergic asthma.