We can determine how your therapeutic candidate affects Treg function
- In our assay formats, the T cell population to be suppressed can be selected from PBMCs, pan-T cells, CD4+ or CD8+ T cells as required
- We can use natural Tregs, isolated directly from PBMCs, in vitro expanded or induced Tregs
- Our expert immunologists will work closely with you to design the most appropraite system for your specific needs
What are regulatory
Tregs have the ability to the suppress the function of other lymphocytes by releasing immunosuppressive cytokines: IL-10 and TGFβ. These cytokines also act to promote polarization of CD4+ T cells in the periphery to create more Tregs. Tregs can inhibit the activities of CD4+ and CD8+ effector T cells, NK cells, NKT cells, and APCs through multiple mechanisms.
Tregs are defined by functional and phenotypic markers, most notably the expression of the transcription factor FoxP3.
An imbalance in the number of Tregs is associated with various disease states. Too many Tregs can lead to reduced immunosurveillance, creating an environment which favors the survival of tumor cells. Conversely, too few Tregs are associated with a number of autoimmune disorders as the immune system is left unchecked.
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WHAT IS A TREG
When combined in vitro, CD4+ Tregs inhibit the proliferation and activation status of T cells in response to antigen
Tregs isolated from PBMCs are combined with CD4+ or CD8+ T cells and a source of stimulation e.g. anti-CD28/anti-CD3
Proliferation and activation of the T cells is determined in the presence and absence of Tregs
The degree of suppression caused by the Tregs can be expressed in terms of inhibition of proliferation
We can also provide cytokine release measurements (ELISA, Luminex) and phenotyping for activation markers to provide you with more information.
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WHEN TO USE TREG
A number of therapeutics are under development which aim to target Treg function in an attempt to ameliorate drug efficacy. An example of this are anti-CTLA-4 antibodies, which bind to and inhibit CTLA-4 expressed on the surface of Tregs. Anti-CTLA4 binding to Tregs can simultaneously mark them for ADCC-mediated destruction.
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