TCL1A, B Cell Regulation and Tolerance in Renal Transplantation

Despite much progress in the management of kidney transplantation, the need for life-long immunosuppressive therapies remains a major issue representing many risks for patients. Operational tolerance, defined as allograft acceptance without immunosuppression, has logically been subject to many investigations with the aim of a better understanding of post-transplantation mechanisms and potentially how it would be induced in patients. Among proposed biomarkers, T-cell Leukemia/Lymphoma protein 1A (TCL1A) has been observed as overexpressed in the peripheral blood of operational tolerant patients in several studies. TCL1A expression is restricted to early B cells, also increased in the blood of tolerant patients, and showing regulatory properties, notably through IL-10 secretion for some subsets. TCL1A has first been identified as an oncogene, overexpression of which is associated to the development of T and B cell cancer. TCL1A acts as a coactivator of the serine threonine kinase Akt and through other interactions favoring cell survival, growth, and proliferation. It has also been identified as interacting with others major actors involved in B cells differentiation and regulation, including IL-10 production. Herein, we reviewed known interactions and functions of TCL1A in B cells which could involve its potential role in the set up and maintenance of renal allograft tolerance.

Automated summary

Despite the progress in kidney transplantation, the issue of life-long immunosuppressive therapies remains a concern. Operational tolerance, which refers to allograft acceptance without immunosuppression, has been the focus of research to better understand post-transplantation mechanisms. TCL1A, a potential biomarker for operational tolerance, has been found to be overexpressed in the peripheral blood of tolerant patients and may play a role in the establishment and maintenance of renal allograft tolerance.