Abstract

Abstract The prevalence of Atopic disease has been on a steady increase over the last 20–30 years. Of these diseases, food allergy represents a major proportion of the anaphylaxis mediated deaths, particularly to peanut. While there are presently multiple theories to explain this increase in allergy, it is clear that in food allergic individuals there is a loss of peripheral tolerance to these innocuous antigens. One of the most effective means of generating peripheral tolerance is through the gut which is home to many specialized immune cells, including intra-epithelial lymphocytes (IELs). Of these IELs, γδ-T cells represent nearly 50% of the population. Due to the large representation of the IELs in the gut, we hypothesize that alteration in the γδ-T cell pool plays a role in the loss of tolerance to these innocuous antigens. Here we examined PBMCs from peanut allergic patients and compared them to healthy controls. We find that while there is no difference within the overall frequency of total γδ-T cells between healthy and peanut allergic patients, when separated based upon CD4 and CD8 expression, we find the CD8 population decreased in the peanut allergic population. Additionally, when investigating subsets within the CD8 γδ-T cells we find altered frequencies of cells expressing costimulatory molecules both classically thought of as being expressed on T-cells (CD7 and OX40), and on antigen presenting cells (CD86). Taken together, these data suggest that γδ-T cells may contribute to the pathogenesis of peanut allergy by way of augmenting the costimulatory dynamic taking place in the gut. Further investigation is required to determine whether this observation leads to the development of peanut allergy or is a result of the disease on the individual.

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