Significant IFNγ production by early effector T cells signifies development into memory

Abstract

The mechanism underlying transition of T cells from effector to memory remains largely undefined. It is believed that this transition occurs as a result of exposure to residual suboptimal antigen found in lymphoid tissues as the effector phase wanes. This led to the interpretation that memory arises from slightly activated late effectors producing reduced amounts of IFNγ. Herein, an in vivo model suitable for tracking memory transition was developed and shows that highly activated early effector CD4 T cells transit to memory. Moreover, effector T cells that have undergone 4 divisions expressed significant IL‐7R, produced IFNγ and yielded rapid and robust memory responses. Cells that divided three times which had marginal IL‐7R expression and no IFNγ raised base level homeostatic memory while those which have undergone only two divisions and produced IFNγ yielded conditioned memory despite low IL‐7R expression. These findings indicate that highly activated early effectors generated upon exposure to optimal antigen in vivo develop into memory and such transition is dependent on a significant production of the cell's signature cytokine, IFNγ.Research supported by grant 2RO1AI48541‐08 from the NIH. JSE and JJB were supported by training grant DHHS2T32GM08396‐16A1 from the NIGMS.