TH0T-Helper Type 0
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Th1 cytokines such as interleukin (IL)-12, interferon (IFN)-a, tumor necrosis factor (TNF)-a can promote the differentiation of Th0 cells into Th1 cells, and eliminate aspergillus.[6] However, in immune-compromised patients, AMs and neutrophilic granulocytes cannot kill hyphae and conidia effectively.
Prolonged stimulation of Th0 cells with a specific antigen allows their differentiation into two phenotypes: Th1 or Th2, characterized by different profiles of cytokines.
The acquisition of a distinct cytokine profile by naive [CD4.sup.+] T (Th0) cells and their proliferative capacity is modulated by specific cytokines.
Such positive feedback promotes differentiation of Th0 toward Thl cells.
The balance between naive T-cells (Th0), Th1, Th2,Th17 and regulatory Foxp3 is maintained by pro- and anti-inflammatory drifts.
Interleukin (IL)-12 which is secreted by macrophages and dendritic cells has a key role in differentiation of Th0 cells into Th1 cells 4, and therefore it could theoretically have a role in RAS pathogenesis.
The human liver contains multiple populations of NK cells, T cells, and CD3+ CD56+ natural T cells with distinct cytotoxic activities and Th1, Th2, and Th0 cytokine secretion patterns.
In addition, IL-12p70 is the determinant factor for the differentiation of TH0 cells into Th1 or Th2 cells.
However, subsequent studies have shown that IL-33 can activate murine dendritic cells directly through the polarization of naive T cells (innocent or Th0) to the Th2 phenotype.