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Some articles that I find useful:

https://www.annualreviews.org/doi/full/10.1146/annurev-immunol-032712-095954

Tissue resident memory T cells: local specialists in immune defense

Immunological memory: lessons from the past and a look to the future

https://bridge.primo.exlibrisgroup.com/discovery/openurl?institution=01BRC_INST&vid=01BRC_INST:CCO&volume=11&date=1993&aulast=Gray&issue=1&issn=0732-0582&spage=49&id=doi:10.1146%2Fannurev.iy.11.040193.000405&auinit=D&title=Annual%20review%20of%20immunology.&atitle=Immunological%20memory&sid=google

https://www.annualreviews.org/doi/full/10.1146/annurev.immunol.16.1.201

Some cell surface markers that have been associated with TRM are CD69 and integrin αeβ7 (CD103). However, it is worth noticing that TRM cells found in different tissues express different sets of cell surface markers. While CD103+ TRM cells are found to be restrictedly localized to epithelial and neuronal tissues, TRM cells localized in salivary glands, pancreas and female reproductive tracts in mice express neither CD69 or CD103.

Lineage debate
Currently, the field is still debating about the lineage relationship between effector and memory T cells. Two competing models exist. One is called the "On-Off-On" model. When naive T cells are activated and actively proliferate, a large clone of effector cells are formed, undergoing active cytokine secretion and other effector activities. After antigen clearance, some of these effector cells form memory T cells, either in a randomly determined manner or are selected based on their superior specificity. These cells would reverse from the active effector role to a state more similar to naive T cells and would be "turned on" again upon the next antigen exposure. This model predicts that effector T cells can transit into memory T cells and survive, retaining the ability to proliferate. It also predicts that certain gene expression profile would follow the on-off-on pattern during naive, effector and memory stages. Evidence supporting this model includes the finding of genes related to survival and homing that follow the on-off-on expression pattern, including interleukin-7 receptor alpha (IL-7Rα), Bcl-2, CD26L and others. The other model is the developmental differentiation model. This model argues that effector cells produced by the highly activated naive T cells would all undergo apoptosis after antigen clearance. Memory T cells are instead produced by naive T cells that are activated, but never entered with full-strength into the effector stage. The progeny of memory T cells are not fully activated because they are not as specific to the antigen as the expanding effector T cells. Studies looking at cell division history found that the length of telomere and activity of telomerase were reduced in effector T cells comparing to memory T cells, which suggests that memory T cells did not undergo as much cell division as effector T cells, which is inconsistent with the "On-Off-On" model. Repeated or chronic antigenic stimulation of T cells, like HIV infection, would induce elevated effector functions but reduce memory. It was also found that massively proliferated T cells are more likely to generate short-lived effector cells, while minimally proliferated T cells would form more long-lived cells.

Due to the motility of memory T cells and lack of distinct cell surface markers, the understanding of memory T cell lineage is still murky. Future research on the topic is needed to clarifying the lineage debate.

Homeostatic Maintenance
Clones of memory T cells expressing a specific T cell receptor can persist for decades in our body. Since memory T cells have shorter half-lives than naive T cells do, continuous replication and replacement of old cells is likely involved in the maintenance process. Currently, the mechanism behind memory T cell maintenance is not fully understood. Activation through T cell receptor may play a role. It is found that memory T cells can sometimes react to novel antigens, potentially caused by intrinsic properties of the T cell receptors. This cross-reactivity provided by environmental or resident antigens in our bodies could stimulate memory T cell division and help maintain its population. The cross-reactivity mechanism may be important for memory T cells at the mucosal tissue. For those resident in blood, bone marrow, lymphoid tissues and spleen, signaling through homeostatic cytokines (including IL-17 and IL-15) or major histocompatibility complex II (MHCII) may be more important.

Lifetime Overview
Memory T cells undergo different changes and play different roles in different life stages for humans. At birth and early childhood, T cells in the peripheral blood are mainly naive T cells. Through frequent antigen exposure, the population of memory T cells accumulates. This is the memory generation stage, which lasts from birth to about 20-25 years old, when our immune system encounter the greatest number of new antigen. During the memory homeostasis stage that comes next, the number of memory T cells plateaus and is stabilized by homeostatic maintenance. At this stage, the immune response shifts more towards maintaining homeostasis since few new antigens are encountered. Tumor surveillance also becomes important at this stage. At later stages of life, at about 65-70 years of age, immunosenescence stage comes, in which stage immune dysregulation, decline in T cell functionality and increased susceptibility to pathogens are observed.