About this Research Topic
Classically, nTregs are identified through several common markers, such as CD4+ CD25+ Foxp3+ CD127–. However, there are several subpopulations within these cells representing their suppressive function. Activated Tregs (aTregs [CD4+ CD25+++ Foxp3hi CD45RA–]), resting Tregs (rTregs [CD4+ CD25++ Foxp3lo CD45RA+]), and non-Tregs (CD4+ CD25++ Foxp3lo CD45RA-) are observed within nTregs. Further, aTregs represent a more suppressive function than rTregs. In contrast, non-Tregs produce a considerable amount of interleukin-2 (IL-2), interferon-gamma (IFN-γ), and IL-17 and tend to differentiate into T helper 17 (Th-17) cells. In addition to the above classification, some other molecules, such as glycoprotein A repetition predominant (GARP), CD147, CD39, and human leukocyte antigen-DR (HLA-DR), are used to discriminate high suppressor Tregs from the low ones.
By using different classifications, some studies reported that transplant recipients with operational tolerance or tolerance under immunosuppressive agents have significantly higher aTregs than patients with both acute and chronic rejections. However, unique and consistent classification is missing information in the literature. Moreover, the kinetics of aTregs and rTregs frequency is poorly understood in the transplant recipients, which could help to better understand the immunological properties in which allograft is stable or rejected. Hence, further investigations are needed to evaluate the kinetics of different subpopulations of Tregs and their association with rejection and tolerance. In addition, we welcome studies evaluating more markers to define unique and consistent aTregs that have a high suppressive function.
In this Research Topic, we welcome the submission of Original Researches, Mini Reviews, Reviews, Perspectives, and Hypothesis articles that address, but are not limited to, the following areas:
1. Identifying different subpopulations of Tregs with more surface markers and transcription factors.
2. Kinetics of different subpopulations of Tregs and total Tregs frequency in the transplant recipients.
3. Association between subpopulations of Tregs and total Tregs with acute rejection., chronic rejection, and tolerance induction
4. Association between different subpopulations of Tregs and different immunosuppressive regimens (induction therapy vs. non-induction therapy).
5. Alloreactive Tregs vs. polyspecific Tregs frequency in transplant recipients with tolerance and rejection.
6. The balance of subpopulations of Tregs and stimulatory T cells.
7. Tregs stability and plasticity in transplant recipients with tolerance and rejection.
8. Mechanisms of regulation by different subsets of Tregs during transplantations.
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