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Dry eye disease (DED) is an inflammatory disorder in which CD4 T cells play a significant role in its pathogenesis. A CD4 T cell subset termed granulocyte-macrophage colony-stimulating factor-producing T helper (ThGM) cells would contribute to DED pathogenesis. However, the mechanisms by which the activity of ThGM cells is modulated are not thoroughly understood.

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Systemic sclerosis (SSc) is an idiopathic systemic connective tissue disorder characterized by fibrosis of the skin and internal organs, with growing interest in the imbalance between Th17 cells and regulatory T cells (Tregs) in the disease's pathogenesis. Heligmosomoides polygyrus (Hp), a natural intestinal parasite of mice, is known to induce Tregs in the host. We aimed to investigate the effects of Hp-induced Tregs on bleomycin-induced dermal fibrosis and clarify the role of the Th17/Treg balance in SSc fibrosis.

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The main goal of this investigation is to find out how solute carrier family 27 member 3 (SLC27A3) is expressed in the lung tissue of mice with chronic obstructive pulmonary disease (COPD), and how it relates to lung function. A model of COPD was established by exposing organisms to cigarette smoke, followed by investigating the role of SLC27A3 in COPD through experiments conducted both in living organisms and in laboratory settings. Knockout mice lacking SLC27A3 were produced through siRNA transfection to investigate lung function and inflammatory response, using methods such as hematoxylin-eosin staining and enzyme-linked immunosorbent assay.

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Allergic airway inflammation is a universal airway disease induced by inhaling allergens. Published data show that RNF128, an E3 ligase, promotes Th2 activation in the OVA-induced asthma model. Recent advances have shown that group 2 innate lymphoid cells (ILC2s) produce the cytokines IL-5 and IL-13 to mediate type 2 immune response.

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CD4 T cell activation induces dramatic changes to cellular metabolism for supporting their growth and differentiation into effector subsets. While the cytokines IL-4, TGF-β and IL-21 promote differentiation into Th9 cells, metabolic factors regulating this process remain poorly understood. To assess the role of lipid metabolism in human Th9 cell differentiation, naïve CD4 T cells were purified from blood of healthy volunteers and cultured in the presence or absence of compounds targeting PPAR-γ, acetyl-CoA-carboxylase 1 (ACC1), and AMP-activated protein kinase (AMPK) for four days.

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