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The dysregulation of T h 17 and switch to Th17 pathogenic phenotype cells have been associated with autoimmune disorders and inflammation. In the case of autoimmune disorders, T h 17 cell over activation can cause an inappropriate amount of inflammation, like in the case of rheumatoid arthritis.
Cytokines released from DCs stimulate dying keratinocytes to secrete TNF-alpha, IL-1 and IL-6 leading to the chemotaxis of T cells, natural killer cells and monocytes to the epidermis. [23] These cells release IL-23 which induce Th17 cells to produce IL-17. [24]
T h cells contain and release cytokines to aid other immune cells. Cytokines are small protein mediators that alter the behavior of target cells that express receptors for those cytokines. These cells help polarize the immune response depending on the nature of the immunological insult (for example; virus vs. extracellular bacterium vs ...
Th17 cells gain the pathogenic phenotype by induction with pro-inflammatory cytokines IL-1β, IL-6 and IL-23 during their maturation. On the other hand, regulation of the Th17 immune response by TGFβ1 and IL-10 is known to inhibit Th17 pathogenicity.
The Th17-type immune response is directed primarily against extracellular bacteria. IL-17F as an effector cytokine of Th17 cells is involved in host defense against bacterial infections. It has many mechanisms by which it helps resist bacteria .
Polarisation to a Th17 phenotype is triggered by IL-6 and TGF-β, which activate the Th17 transcription factor RORγt. IL-23 stabilises RORγt and thus enables Th17 cells to release their effector cytokines, such as IL-17, IL-21, IL-22 and GM-CSF, which mediate protection against extracellular fungi and bacteria and participate in barrier ...
In murine models, treatment with dexamethasone inhibits the release of Th2-related cytokines but does not affect IL-17A production. [44] Furthermore, Th17 cell-mediated airway inflammation and airway hyperresponsiveness are steroid resistant, indicating a potential role for Th17 cells in steroid-resistant asthma. [44]
All T cells derive from progenitor cells in the bone marrow, which become committed to their lineage in the thymus.All T cells begin as CD4-CD8-TCR- cells at the DN (double-negative) stage, where an individual cell will rearrange its T cell receptor genes to form a unique, functional molecule, which they, in turn, test against cells in the thymic cortex for a minimal level of interaction with ...