Abstract
While T cells are considered to play a primary role in IgE-mediated atopic diseases, little is known about the systemic variations of T cell subsets from patients with allergic rhinitis (AR). To elucidate the characteristics of peripheral T cells, we analyzed natural killer, B cell, and T cell populations, performed T cell subset construction, and assessed chemokine receptor and associated serum cytokine expression in 25 AR patients and 20 healthy controls. Our results revealed increased levels of CD4+T cells, serum interleukin (IL)-10, IL-6, and interferon (IFN)-γ, and reduced Th1 and Th17 subsets, identified by their chemokine receptors, in AR patients. These results suggest a systemic activation of T cell responses in AR. We further demonstrated that AR patients exhibit significantly reduced CD4+T cell CXCR3 expression, especially in patients with moderate-severe disease severity, demonstrating that CXCR3 is a potential key molecule that hinders the Th1/Th2 balance in AR pathology. Overall, systemic T cell activation occurred in AR patients and CXCR3 dramatically decreased in CD4+T cells, which may ultimately be used as a potential disease and/or therapeutic target.
Highlights
Allergic rhinitis (AR) is a disease characterized by IgE-mediated allergic inflammation of the nasal mucosa after allergen exposure, associated with nasal symptoms including rhinorrhea, sneezing, nasal obstruction, and nasal itchiness
There was no significant difference in T, B, and natural killer (NK) cell counts between AR patients and HCs, but a mild increased trend of T cells was found in AR patients (Figure 2A)
Contrary to the decreased Th1 and Th17 subset defined by surface markers, we found that AR patients in this study had increased levels of IFN-g, IL-10 and IL-6, which suggests an upregulation of both Th1 and Th17 cytokines (Table 2)
Summary
Allergic rhinitis (AR) is a disease characterized by IgE-mediated allergic inflammation of the nasal mucosa after allergen exposure, associated with nasal symptoms including rhinorrhea, sneezing, nasal obstruction, and nasal itchiness. Upon re-exposure to allergens, crosslinking of IgE on mast cells results in the release of mediators of hypersensitivity, such as histamine and immediate nasal symptoms. There is an infiltration of inflammatory cells, notably Th2 T lymphocytes, eosinophils, and basophils, into nasal mucosal tissue that results in the late-phase allergic response. The whole profile of peripheral lymphocytes, such as natural killer (NK), B, and T cell subsets, has not been fully described in AR patients with different disease severity, which will provide a better understanding of the pathophysiology of AR
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