The contact between T cell receptors (TCR), expressed by CD4 T lymphocytes, and the MHC on the surface of antigen presenting cells is crucial in leading the differentiation of naive T cells into effector cells that are required in the adaptive response against microbes. On the other hand, long-lasting immunity is guaranteed, in the aftermath of the fight against invading organisms, by memory T cells that emerge from a small population of effector T cells that survives the initial clonal expansion.
Although this mechanism is pivotal in a number of immune processes, such as development of immunity after infections and vaccine administration, the molecular machinery behind it is largely unknown. Since TCR activation represents an early and crucial stimulus in the clonal expansion of T cells, Jeremy P Snook, Chulwoo Kim and Matthew A. Williams sought to investigate whether and how TCR signaling is involved in determining which portion of the effector T cell repertoire is committed to being part of the memory pool after the infection.
By using monoclonal populations of lymphocytes expressing TCRs that were previously characterised for their contribution to memory T cell repertoire, the authors determined that TCR signal strength inversely correlates with the possibility of a specific TCR-expressing clone of becoming a memory T cell. In particular, interclonal TCR signal strength and CD25 expression, were predictive of the “memory potential” of each lymphocyte.Leave a reply