Table 1.
Cells | Significance in stroke | Host defense | Differentiation cytokine | Transcription factor | Cytokine produced |
---|---|---|---|---|---|
Th1 | Induce inflammation, activation of microglia | Intracellular pathogens | IFN-γ, IL-12 | Tbet | IFN-γ, IL-2 |
Th2 | Induce inflammation | Large worms (helminths) | IL-2, IL-4 | GATA3 | IL-4, IL-5, IL-13 |
Th9 | Neuroprotective | Extracellular parasites | IL-9 | Foxo1 | IL-9 |
Th17 | Activation of MMPs and BBB breakdown | Extracellular pathogens (fungi) | IL-6, IL-23 | RORγt | IL-17A, IL-17F, IL-22 |
Treg | Suppression of inflammation, neuroprotection | Bacteria and parasites | TGF-β | FoxP3 | TGF-β, IL-10, IL-35 |
Tfh | Increase early ischemic tissue injury | Defense against extracellular pathogens | IL-6 | Bcl6 | IL-21 |
CD4+ T-cells polarization in various subtypes like Th1, Th2, Th9, Th17, Treg, and Tfh takes place in the presence of specific combination of cytokines to protect host from pathogens and injuries. For the differentiation and production of cytokines every cell type has their own signature transcription factors. Treg: Regulatory T cells, IFN-γ: Interferon-γ, IL: Interleukin, TGF-β: Transforming growth factor-β, BBB: Blood-brain barrier, MMPs: Matrix metalloproteinases