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T Cell Related Products

Study the balance of T cell dynamics in autoimmunity, inflammation and cancer
Tregs and Th17 cells
Regulatory T cells (Tregs) and T helper 17 cells (Th17) are CD4+ lymphocyte subtypes with opposing functions. The shift in the balance of the reciprocal partner populations of these two T cell subtypes is a checkpoint in autoimmunity versus inflammation. When the shift in T cell differentiation is biased towards Treg cells, this leads to dominant immunologic tolerance. When differentiation is shifted towards Th17 cells, this tips the balance toward inflammation.

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Tregs
CD4+ lymphocytes with immune suppressor properties by secreting abundant amounts of immunosuppressant lymphokines such as IL-9, IL-10 and TGF-a upon activation. These lymphokines then inhibit the activation of Th1, Th2 cells and Cytotoxic T Lymphocytes (CTLs) that are required for cell- mediated immunity, inflammation and antibody production. Tregs are characterized by the unique expression the forkhead box P3 transcription factor Foxp3 (also known as scurfin). Alterations in the numbers of Foxp3+ regulatory T cells are found in a number of disease states. Patients with tumors have a local relative excess of Foxp3+ T cells that in turn inhibits the body´s ability to suppress the growth and formation of cancerous cells where self-tolerance is unfavorable. However, Foxp3+ T regs are also critical in the transfer of immune tolerance that can aid to prevent transplant graft rejection, and reduce inflammatory bowl disease, autoimmune disease like rheumatoid arthritis and allergy conditions

Th17 cells
Th17 cells are a distinct T cell lineage that are IL-17-secreting CD4+ T cells. Th17 cells are essential for lymphoid organogenesis and have been shown to have a natural role in immunity to extracellular pathogens. However, it is their potential roles in autoimmune diseases that has gained more attention. An abundabnce of Th17 cells has been associated with autoimmune conditions such as psoriasis, autoimmune uveitis, juvenile diabetes, rheumatoid arthritis, and Crohn´s disease. Th17 cells have a characteristic overexpression of the RAR-related orphan receptor gamma t (RORC/RORgt) nuclear receptor transcription factor. RORC/RORgt is the transcription factor that drives Th17-specific differentiation.


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