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Written by | Snow Moon
T cells are localized within tissues, called tissue-resident memory T (TRM), and are acyclic cells
.
TRM provides optimal protection
against specific or viral infections by localizing near target cells.
TRM can also play other important roles in tissues, participating in tissue protection and homeostasis maintenance
by responding to homologous antigens or inflammatory signals.
Compared to circulating memory T cells, TRM has a unique transcriptional profile that expresses integrins and homing receptors
that promote tissue residency.
CD103 can bind to E-cadherin in epithelial cells, and most CD8+ TRM cells at the barrier site express CD103, which resides in
tissues.
With its unique phenotype and importance for body protection, TRM is an ideal target for vaccines and immunotherapies
.
However, it is unclear
whether TRM is irreversible in tissues and the effect of secondary infection on TRM migration and longevity.
Questions about TRM stability and function are difficult to answer due to the difficulty of distinguishing between truly resident TRMs in tissues and foreign-infiltrated non-resident cells
.
Recently, Science Immunology published two articles on the production of intestinal TRM cells and the changes in the fate of TRM cells after secondary infection: Tessa Bergsbaken's team from the Medical College of New Jersey published a paper titled CD103 fate mapping reveals that intestinal CD103−tissue-resident memory T cells are the primary responders to secondary infection
.
The Dietmar Zehn team from the Technical University of Munich has published a report entitled Secondary infections rejuvenate the intestinal CD103+ tissue-resident memory T cell Pool's article
.
Both articles analyze the heterogeneity and functional characteristics of CD8+TRM in the gut after secondary infection and the source of expansion of the memory cell bank
.
Both studies used CD103-CreERT2/flox-STOP-flox fluorescent reporters/OT-1 mice
.
The authors infected mice with LCMV or Yptb and then adopted CD8+ T cells into uninfected mice
.
Mice infected with adoptive cells undergo LM-OVA, LCMV or Yptb infection
.
Analysis of cells in the gut revealed no significant change in the number of TRMs tracked by lineages, nor did they expand or migrate out of the gut
.
However, CD103-CD8+ T cells in the intestine are significantly expanded and new CD103+ TRMs
are produced.
This suggests that CD103+ TRM cells do not promote the expansion of the T cell pool in the event of secondary infection
.
The authors also used CD103-CreERT2-DTR-floxed mice to remove CD103-T cells, while CD103+TRM remained intact
.
The analysis found that CD103+TRM still did not amplify
after secondary infection.
This suggests that the lack of amplification effect of CD103+TRM is intrinsic and independent
of competition with other cells.
Next, the authors explored whether CD103- cells were different from
the original CD103+ cells.
The authors first analyzed reactivity to antigens as well as differences
in cytokine expression.
The results showed that CD103-T cells had obvious TCR-antigen interaction after infection, while CD103+TRM was not obvious
.
CD103+TRM showed high expression of GzmA and high expression of IFN-g
in CD103-T cells.
Before secondary infection, CD103+TRM expressed known markers homing receptor CCR9 and ITGAE CTLA4 GzmA, while CD103-TRM expressed migration markers CCR7 CCR2 and S1PR1, indicating higher proliferation and migration
.
After secondary infection, the transcription response of CD103-TRM was higher overall, and the expression levels of cytokines and chemokines were high, indicating that CD103+TRM cells were more limited in response to stimuli
.
The authors suggest that CD103+CD8+TRM can monitor
tissue infections in a TCR and antigen-independent manner.
At the same time, CD103+CD8+TRM compositionally expressed GzmA, which was ready
for lysis of target cells.
CD103+CD8+TRM promotes the formation of immune synapses and the release of lytic cell mediators through integratin-mediated adhesion epithelial cells to target infected cells
in tissues.
These results suggest that cell localization and interaction of TRM require different mechanisms to mediate immune surveillance and tissue protection
.
Secondary infection T cell response pattern mapThese
two studies reveal new insights
into TRM cell heterogeneity, function, and cell maintenance.
CD103+CD8+TRM is more closely related to resident tissues to better act on target cells, and CD103-TRM can contribute to
supplementing and increasing the pool of mature TRM cells.
Understanding the different functional response subsets of TRM provides a more comprehensive cellular basis
for vaccination strategies and immunomodulatory therapies.
Isaac J.
Jensen and Donna L.
Farber from Columbia University collaborated on the two articles titled Gutsy memory T cells stand their ground against pathogens Reviews of the article
.
Original link:
1.
http://doi.
org/ 10.
1126/sciimmunol.
abl9925
2.
http://doi.
org/10.
1126/sciimmunol.
abp9553
Platemaker: Eleven
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