Ribonuclease T2 from Aspergillus fumigatus promotes T helper type 2 responses through M2 polarization of macrophages

Hyperglycemia in critical illness is a common complication and a strong independent risk factor for morbidity and death. Intensive insulin therapy decreases this risk by up to 50%. It is unclear to what extent this benefit is due to reversal of glucotoxicity or to a direct effect of insulin, because antiinflammatory effects of insulin have already been described, but the underlying mechanisms are still poorly understood. The insulin receptor is expressed on resting neutrophils, monocytes, and B cells, but is not detectable on T cells. However, significant up-regulation of insulin receptor expression is observed on activated T cells, which suggests an important role during T cell activation. Exogenous insulin in vitro induced a shift in T cell differentiation toward a T helper type 2 (Th2)-type response, decreasing the T helper type 1 to Th2 ratio by 36%. This result correlated with a corresponding change in cytokine secretion, with the interferon-γ to IL-4 ratio being decreased by 33%. These changes were associated with increased Th2-promoting ERK phosphorylation in the presence of insulin. Thus, we demonstrate for the first time that insulin treatment influences T cell differentiation promoting a shift toward a Th2-type response. This effect of insulin in changing T cell polarization may contribute to its antiinflammatory role not only in sepsis, but also in chronic inflammation associated with obesity and type 2 diabetes.

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Glucocorticoids Inhibit Proliferation and Interleukin-4 and Interleukin-5 Secretion by Aeroallergen-Specific T-Helper Type 2 Cell Lines

Annals of Allergy Asthma & Immunology ◽

10.1016/s1081-1206(10)63075-x ◽

1998 ◽

Vol 80 (6) ◽

pp. 509-516 ◽

Cited By ~ 28

Author(s):

I Caroline Crocker ◽

Martin K Church ◽

Sean Newton ◽

Robert G Townley

Keyword(s):

Cell Lines ◽

Interleukin 4 ◽

T Helper ◽

Interleukin 5 ◽

Helper Type

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The roles of immune cells in atherosclerotic calcification

Vascular ◽

10.1177/17085381211032756 ◽

2021 ◽

pp. 170853812110327

Author(s):

Jingsong Cao ◽

Xuyu Zu ◽

Jianghua Liu

Keyword(s):

B Cells ◽

Immune Cells ◽

Cardiovascular Events ◽

Th2 Cells ◽

Regulatory B Cells ◽

T Helper ◽

Relationship Of ◽

The Relationship ◽

Helper Type

Atherosclerosis is the leading cause of acute cardiovascular events, and vascular calcification is an important pathological phenomenon in atherosclerosis. Recently, many studies have shown that immune cells are closely associated with the development of atherosclerosis and calcification, but there are many conflicting viewpoints because of immune system complications, such as the pro-atherosclerotic and atheroprotective effects of regulatory B cells (Bregs), T helper type 2 (Th2) cells and T helper type 17 (Th17) cells. In this review, we summarize the studies on the roles of immune cells, especially lymphocytes and macrophages, in atherosclerotic calcification. Furthermore, we prepared graphs showing the relationship between T cells, B cells and macrophages and atherosclerotic calcification. Finally, we highlight some potential issues that are closely associated with the function of immune cells in atherosclerotic calcification. Based on current research results, this review summarizes the relationship between immune cells and atherosclerotic calcification, and it will be beneficial to understand the relationship of immune cells and atherosclerotic calcification.

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