Th1T Helper Cell Type 1
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Th1 and Th2 cells are two of the most important CD4+ T lymphocyte subsets.
Since they are antagonistic to Th1, the Th1 cells are driven to lower levels, which increases the risk of infections.
By producing various cytokines including IFN-[gamma], tumor necrosis factor (TNF)-[beta], and interleukin (IL)-2, Th1 cells show a strong effect in repressing tumor growth, and IFN-[gamma] possesses capabilities for anti-tumor effects and immunomodulation (15).
These cytokines, particularly interleukin (IL)-12 and IL-8 subsequently elicit an interferon gamma (IFN-g) response from NK and T cells, thereby establishing Th1 cell-mediated immunity.
The new findings show that IRF-5 leads Th1 cells to self-destruction.
In addition, RC byproducts activated the mRNA expression of galectin-9 in the MLN and spleen with increased T-bet and Foxp3 as a reflection of Th1 and Treg cells, respectively.
Immune response involving Th1 cells has the tendency to produce interferon-gamma (IFN-gamma) and interleukin-2 (IL-2) cytokines and participate in delayed-type hypersensitivity (DTH) and macrophage activation [4].
T-bet is a critical transcription factor that controls differentiation of Th1 cells; it specifically binds to the promoter of the IFN-[gamma] gene and activates its transcription [17-19].
To identify that EGCG can improve the Th1/Th2 balance, flow cytometry was utilized to analyze Th1 cells and Th2 cells in the rat colon.
BMP6 Impaired Immunomodulatory Properties of BMMSCs by Downregulating PGE2 and Upregulating Th1 and Th17 Cells.
Th1 cells are differentiated CD4+ T cells characterized by the production of proinflammatory interferon-[gamma] (IFN-[gamma]) [12].