Histidine Decarboxylase Expression in Human CD4+ T Lymphocytes

Abstract

The early phase of allergic reactions is largely dominated by IgE-mediated degranulation of mast cells and basophils. Mast cells and basophils release mediators which include histamine, prostaglandins, leukotrienes, cytokines, etc. Histamine is a biogenic compound that can directly cause physiological changes that ultimately contribute to allergy and asthma symptoms. The current literature focused on the study of histamine production from “professional histamine producers”, such as mast cells and basophils in allergic diseases. Previous research had shown that activation of allergic specific T cells led to airway narrowing independent of basophil activation 6-hour post exposure. It was therefore possible that the activation of T cells may release histamine which contributed to the airway narrowing observed. This project aimed to determine expression of histidine decarboxylase (HDC) in T lymphocytes, which is the gene encoding the enzyme solely responsible for the production of histamine. We found that HDC is expressed in rare T cell populations by the bioinformatic analysis of publicly available datasets, and we found that the activation of human primary CD4+ T cells by anti-CD3/CD28 did not lead to the upregulation of HDC by qPCR. The activation of CD4+ T cells in non-allergic donors led to a LOG2FC of HDC to B2M housekeeping gene of: -1.0 +/- 0.48 at 6-hour, -1.3 +/- 0.23 at 24-hour, -2.2 +/- 0.32 at 72-hour. The activation of CD4+ T cells in allergic donors led to a LOG2FC of HDC of: -0.48 +/- 0.13 at 6-hour, -2.1 +/- 0.35 at 24-hour, -4.1 +/- 1.1 at 72-hour. In conclusion, HDC expressing T cells were rare and of low expression level. The activation of CD4+ T cells did not upregulate HDC and therefore it was unlikely that T cell derived histamine contribute to allergic manifestations.