Ying and yang of immunological memory in controlling infections: Overriding self defence mechanisms

Immunological memory is critical for host immunity and decisive for individual to respond exponentially to previously encountered infection. Both T and B cell memory are known to orchestrate immunological memory with their central and effector memory arms contributing in prolonged immunity/defence mechanisms of host. While central memory helps in maintaining prolonged immunity for a particular infection, effector memory helps in keeping local/seasonal infection in control. In addition to this, generation of long-lived plasma cells is pivotal for generating neutralizing antibodies which can enhance recall and B cell memory to control re-infection. In view of this, scaling up memory response is one of the major objectives for the expected outcome of vaccination. In this line, this review deals with the significance of memory cells, molecular pathways of their development, maintenance, epigenetic regulation and negative regulation in various infections. We have also highlighted the significance of both T and B cell memory responses in the vaccination approaches against range of infections which is not fully explored so far. Highlights Pathogens induce IL-10R, PD-1, T-reg; and downregulate IL7R and IL15R for hijacking memory response IL-7, 15, Tcf-1 (Wnt5/7A), and CD28 signaling is decisive for T-CM/T-EM and T-RM recall. Bach2 expression suppress Bim and Puma and promotes memory B cell activities VCAM1, IFN-gamma, and GM-CSF pathways are critical for local activation of memory cells Multi-epitope vaccines/adjuvants are potent for inducing specific memory response

Automated summary

Immunological memory is essential for prolonged immunity, with central memory maintaining immunity for specific infections and effector memory controlling local infections. The generation of long-lived plasma cells is crucial for producing neutralizing antibodies to enhance immune recall.