Primary Antibodies
Secondary Antibodies
Proteins & Peptides
ELISA Kits
About Us
Contact Us
Antibodies.com Logo Antibodies.com Logo
Sign In/Register
0

Memory T Cell Markers

Lucas Baumard, PhD | 13th June 2025

Memory T cells are specialized CD4+ or CD8+ subsets that are important for giving long term protection from re-infection or cancer. In dysfunction, however, these cells can drive autoimmunity and chronic inflammation.

Memory cells derive from antigen-reactive T cells that remain after the bulk of effector cells die following antigen clearance, albeit at low numbers. Re-exposure to the specific antigen drives these memory cells to quickly proliferate and differentiate into effector cells in order to mount a rapid response.1 Memory cells provide a more robust response to secondary infection/ antigen stimulation because these antigen-specific cells are present at a higher proportion than antigen-naïve T cells, increasing the likelihood and specificity of an immune response.2 Memory T cells require a lower strength of, and lower exposure to, co-stimulatory signals from antigen presenting cells than naïve T cells do. Furthermore, while naïve T cells can only be activated by dendritic cells, a wide variety of antigen-presenting cells (APCs) can activate memory T cells, increasing the speed and strength of the immune response.3,4

Explore allSee Memory T Cell Marker Antibodies

Table of Contents

Memory T Cell Subsets and Core Markers

Memory T cells can be sub-divided by their tissue trophism (central memory T cells (Tcm), tissue-resident memory T cells (Trm)) and by activity (T effector memory T cells (Tem)) (Figure 1). Table 1 shows a summary of these cells’ roles and some common markers.

Schematic showing migration routes of memory T cell subsets.

Figure 1: Memory T cell subsets have distinct migration patterns. Tcm cells and naïve T memory cells migrate between the lymph, blood, and T cell zones (TCZ) within secondary lymphoid organs (SLO). Tem cells circulate between blood, non-lymphoid tissue, and afferent lymphatics (passing transiently through lymph nodes). Trm cells do not circulate, remaining within their non-lymphoid tissue of residence.

Memory T cell subtype CD4+/ CD8+ Surface Markers Cytokine Markers Location Activity Refs
T central memory (Tcm) Both CCR7+
CD44
CD45RO
CCR6
CXCR3
CD18mid
CD62L		 IL-2 Secondary lymphoid organs (e.g. lymph nodes, spleen) Sustained protection against pathogens 1,5
T effector memory (Tem) Both CCR7-
CD44
β1, β2 integrins
CD11b
CCR6
CXCR3
CD18
CLA		 IL-2low
IL-4
IL-5
IFN-γ		 Peripheral organs, lymph nodes Rapid, briefly sustained reaction to pathogen 1
Tissue-resident memory (Trm) Both CD44
CD69
CD103		 Granzyme B
IL-2		 Epithelial barrier tissues Sustained protection against pathogens 5,6

Table 1: Core markers and characteristics of distinct memory T cell subsets.

As indicated in Table 1, high expression of CD44 can be regarded as a pan memory T cell marker, in general distinguishing naïve (CD44low) from antigen-experienced (CD44high) T cells.2 Following antigen activation, T cells upregulate CD44, the receptor for hyaluronate, which may allow activated T cells to enter regions of high inflammation. This expression is maintained on memory T cells. While it cannot be used to distinguish memory T cell subsets from each other nor other activated T cells, CD44 is a classic marker for effector T activation.

CD4 and CD8 Expressing Memory T Cells

In addition to the populations illustrated above, memory T cells can be divided into CD4 or CD8 subsets; generally, Tcm cells are predominantly CD4+ while Tem are CD8+.7 CD4+ memory T cells tend to be less common (and less studied) due to their significantly limited proliferative capacity after activation and their low abundance in blood compared to CD8+ memory T cells.8,9

There are also some differences in the expression of surface markers for CD4+ and CD8+ memory T cells subsets (Table 2); most likely driven by the transient nature of CD4+ memory cells compared to CD8s.9 CD4 and CD8 memory T cells follow a similar response pattern to their non-memory CD4+/CD8+ T cell counterparts: providing helper and cytotoxic responses, respectively.

Classification Subtype Marker Expression Frequency of cells in PBMC populations
CD45RA CD62L CCR7 Healthy Virally infected
CD4+ Naïve + High + ++++ ++/+++
TCM – High + +/++ ++
TEM – Hi/lo – ++ ++
+ Hi/lo – – +
CD8+ Naïve + High + ++ +
TCM – High + ++ +
TEM – Low – + ++
+ Low – ++ +++

Table 2: Difference in frequency and surface marker expression between CD4+ and CD8+ naïve and memory T cell subsets. Data from 9.

Plastic Nature of Memory Cell Marker Expression

Characterization of memory subsets is complicated by their dual natures: non-activated memory T cells are long lived whereas activated memory T cells are relatively transient: after antigen-dependent activation, activated memory T cells rapidly differentiate into non-memory effector sub-types. For instance, upon antigen stimulation, Tem cells re-express CCR7 and CXCR5 (chemokine receptors that drive migration, associated with Tcm cells) and downregulate CCR5, while CD62L is rapidly shed after activation and migration have finished.10,11

The study of memory T cells therefore faces multiple difficulties:

  1. Sensitivity to local conditions of non-activated memory T cells that may lead to activation
  2. Transient state of activated memory T cells, reflected by the transient nature of some markers
  3. Variation in the expression of markers within some subsets (Table 2)

These difficulties can be overcome by the careful management of activation and the use of multiple overlapping markers. Studying multiple parameters simultaneously, such as by examining surface marker expression (e.g. by flow cytometry) and cytokine expression (e.g. by ELISA, intracellular flow cytometry) can improve accuracy.

T Central Memory T (Tcm) Cell Markers

Tcm cells have limited effector function themselves. Instead, upon antigen stimulation, they home to T cell areas in secondary lymphoid organs (spleen, lymph nodes) and proliferate and differentiate into effector cells.7 Tcm cells are enriched in lymph nodes and tonsil tissue.12

Tcm cells are considered CD45RO+ CCR7+ CD62L+ CD44high cells, with CCR7 and CD62L being important for mediating migration through blood vessels to secondary lymphoid organs.13 As part of their support role, and to help drive rapid differentiation and proliferation upon activation, they release IL-2, transitioning to releasing IFN-γ and IL-4 as they differentiate.7

Immunofluorescence - Anti-CCR7 Antibody [ARC0231] (A307143)

Figure 2: IHC of human spleen stained with Anti-CCR7 Antibody [ARC0231] (A307143).

IHC - Anti-CD45RO Antibody [T200/797] (A249812)

Figure 3: IHC of human tonsil stained with Anti-CD45RO Antibody [T200/797] (A249812).

It is posited that Tcm cells are the developed (but not final) form of memory cells and that memory cells can switch between subsets. It was shown in a study - looking at CD8+ memory cells specifically – that whilst the absence of antigen stimulation pushes Tem cells into Tcm cells over time, this process is reversed upon antigen stimulation with Tcm converting back into Tem cells.14 The same study posited that Tcm represent the true form of memory cells, with Tem being a transitionary, effector population: naïve T cells → effector cells → Tem cells → Tcm cells.

CD45RO is an alternative splicing isoform of CD45 (expressed on all leucocytes; Figure 4) and a canonical marker of memory cells shown to respond to recall antigens.15 CD45RO+ cells have been shown to be more long lived and stable than their CD45RA+ counterparts and is considered a marker of activation.16

Schematic showing the alternative splicing forms of CD45.

Figure 4: Alternative Splicing of CD45. A, Alternative splicing of exons 4, 5 and 6 results in various isoforms of CD45 due to the inclusion/exclusion of the heavily glycosylated segments A, B and C, respectively. Following differentiation of naïve T cells into memory T cells, upregulation of hnRNPLL inhibits inclusion of exons 4-6, resulting in characteristic CD45RO expression.17 B, Domains of the full CD45RABC form, including all 3 alternatively spliced exons.

CCR7 is a chemokine receptor and an important marker to identify cells with the ability to home to secondary lymphoid tissues – especially lymph nodes.18 It can be used to distinguish CCR7+CD62L+ Tcm from CCR7-CD62L+ Tem, which home instead to inflamed tissues. Tcm can transition into Tem, switching CCR7 expression for CCR5 in response to cytokine stimulation (IL-7, IL-15, TNF-α, IL-6, IL-10).19 CCR7 is expressed on Tcm, early Tfh cells,20 dendritic cells and B cells.21

CD62L (L-selectin, LECAM-1, LAM1, Leu8 antigen) is a cell adhesion molecule expressed on leucocytes and is important for their trafficking (Figure 5).22 The molecule is shed rapidly as it is expressed on the cell surface and binds to glycoproteins on the surface of blood vessels; this is thought to facilitate adhesion and transmigration.22

Schematic showing the alternative splicing forms.

Figure 5: T cell migration, activation and arrest within high endothelial venules (HEVs) prior to entering lymph nodes from the blood. This is controlled by cell surface molecules such as CD62l, CCR6 and ICAM1 on T cell and endothelial cells.23

IL-2 is a general T cell growth factor which promotes the differentiation and proliferation of memory T cells as well as Th2 cells and CD8+ cytotoxic cells.24-26 High levels of IL-2 drives effector T cell differentiation and increases the expression of cytolytic effectors in these cells whilst low expression increases memory cell maturation.27

T Effector Memory (Tem) Cell Markers

Tem cells are responsible for migrating to inflamed peripheral tissue and providing rapid effector activity in response to antigen stimulation 7. They are the rapid reaction force of the T cell memory compartment, giving time for other memory cells to come to bear, though they are not as long lived as Tcm cells.28 Tem cells are enriched in lung, liver and gastrointestinal tissue.12

CD8+ Tem cells express high amounts of perforin, and CD4 and CD8+ Tem cells both produce IFN-γ, IL-4 and IL-5 within hours of antigenic stimulation. Unlike Tcm, Tem cells have lost CCR7 expression and have a mixed CD62L and CD45RA expression pattern.7 Tem cells are typically described as CCR7- CD62low/high CD45RA+/- CD44high, and they can be further divided by the expression of chemokine receptors that are associated with Th1 and Th2 cells: CCR5 and CXCR5 for Th1, and CCR3 and CRTh2 for Th2 cells (See our T Helper Cell Markers page).

The combination of cytokine expression with that of surface markers (most of which are shared) is likely necessary to accurately distinguish Tem from Tcm. The tissue-specificity of Tem cells can be established by the combination of adhesion molecule and chemokine receptor expression: CLA and CCR4 for skin,29 α4β7 and CCR9 for gut-homing T cells.30

CD45RA is another splice variant of the CD45 gene (Figure 4) found on naïve T cells and re-expressed on Tem and some Tcm cells.31 CD45RA+ Tem (TemRA) probably represent a specific subset of Tem implicated in protective responses to specific pathogens.32

Perforin is a glycoprotein released from CD8+ T cells and natural killer (NK) cells that acts to kill target cells by the formation of pores in their cell membranes, disrupting mineral homeostasis and inducing pro-apoptotic pathways.33,34 CD8+ T cell release of perforin is dependent on MHC antigen presentation.33

Immunofluorescence - Anti-CD45RA Antibody [PTPRC/818] (A249785)

Figure 6: Immunofluorescence of Jurkat cells stained with Anti-CD45RA Antibody [PTPRC/818] (A249785).

IHC - Anti-Perforin Antibody [PRF1/2470] (A249713)

Figure 7: IHC of human spleen stained with Anti-Perforin Antibody [PRF1/2470] (A249713).

Interferon gamma (IFN-γ) is a type II interferon cytokine released by Th1 and NK cells in response to IL-12, IL-18, pattern recognition receptor activation or microbial antigens.35 The receptor, IFN-γR, is expressed on almost all cell types36 - an indication of the importance of the cytokine. IFN-γ activates macrophages, other T helper cells (including Th1) and B cells and downregulates Th2, Th17 responses.35,36

IL-4 is a cytokine important for the development of Th2 cells. IL-4 is also released by eosinophils,37 mast cells and basophils38 in response to parasitic infection, as well as by T follicular helper cells. IL-4 is also important in wound healing, nerve regeneration and allergic disease.39

IL-5 is also released from Tc2 and Th2 cells, mast cells and eosinophils.40 IL-5 specifically activates eosinophils, basophils and B cells as these cells preferentially express IL-5R.41,42 IL-5 is required for proliferation and Ig production in B cells.43

Tissue Resident Memory T (Trm) Cells Markers

Trm cells were more recently discovered than Tcm and Tem. Their main feature is that they occupy tissues and do not circulate. They therefore provide an innate initial response to any infections detected at these locations. However, because these cells do not circulate in blood, they are hard to isolate and therefore characterize. In addition, the body of evidence focuses mostly on CD8+ Trm.

Trm derive from T cells that entered tissues during immune responses and differentiate into memory cells and reside there permanently.44 In the small intestine, newly arrived T cells are kept in situ through the loss of α4β7, which would normally facilitate migration.45 They also gain CD103 and CD69 and maintain granzyme B expression.46 They are associated with expression of IL-2, IFN-γ and IL-17, though expression differs based on tissue and CD4/ CD8 expression.47 Like Tcm and Tem cells, Trm cells express high levels of CD44.

Up or downregulated vs circulating Tems Protein Cellular Localization Effect
Upregulated CD69 Cell surface Identification, tissue retention
CD101 Cell surface Identification (CD8+), immunoregulation
CD49a Cell surface Tissue retention, adhesion
CD103 Cell surface
CRTAM Cell surface
CXCR6 Cell surface Homing
PD-1 Cell surface Inhibition
DUSP6 Cytoplasm
IFNγ Extracellular (cytokine) Rapid response on activation
IL-2 Extracellular (cytokine)
IL-17 Extracellular (cytokine)
IL-10 Extracellular (cytokine) Anti-inflammatory
Downregulated CD62L Cell surface Reduced migratory cues
S1PR1 Cell surface
S1PR5 Cell surface
CX3CR1 Cell surface
KLF2 Nucleus
KLF3 Nucleus
Ki67 Nucleus Decreased turnover

Table 3: Human Trm (CD69+) transcription factors, cytokines and surface markers compared with circulating Tems. Information adapted from 47.

CD103 (αeβ7) is an integrin expressed on T cells, dendritic cells and mast cells whose main ligand is E-cadherin expressed on epithelial cells.48 It is essential to keep migrated T cells within some tissues,49 most likely due to the physical adherence via E-cadherin to tissue epithelial cells, though CD103 expression has also been shown to promote T cell survival.50 However, not all Trm express CD103 and it is not required for retention in some tissues (e.g. small intestine lamina propria).49

The lectin CD69 is induced in Trm after migration to sites of residence.50 Studies in mice have shown that the majority of CD4+ and CD8+ Trm cells express CD69, across multiple sites.46,51-53 CD69 expression is negatively associated with Sphingosine-1 phosphate receptor 1 (S1PR1) expression54 while IFN-γ, IL-33 and TNF-α induce CD69 expression.49,55-57 S1P is a chemotaxis molecule that mediates T cell egress to lymph nodes,54 and the loss of the receptor maintains Trm in tissues (Figure 6). The role and expression of CD69 in human Trm is not fully elucidated.

Granzyme B (GzB) is a serine protease released by activated CD8+ T cells and NK cells.58 GzB enters the target cell’s cytoplasm, where it disrupts various proteins, eventually leading to cell death.58 Some models of its action require perforin to create the pores which allow it to enter the cell, but the exact mechanisms of action are not fully understood.

Flow cytometry - Anti-CD69 Antibody [FN50] (PE) (A86795)

Figure 8: Flow cytometry of human PHA-activated peripheral blood stained with Anti-CD69 Antibody [FN50] (PE) (A86795).

IHC - Recombinant Anti-Integrin alpha E Antibody [ITGAE/3904R] (A249061)

Figure 9: IHC of human spleen stained with Recombinant Anti-Integrin alpha E Antibody [ITGAE/3904R] (A249061).

Memory T Cell Marker Antibodies

CCR6 Antibodies
CCR7 Antibodies
CD45RA Antibodies
CD45RO Antibodies
CD62L Antibodies
CD69 Antibodies
CD103 Antibodies
CXCR3 Antibodies
IL-2 Antibodies

References

Diagrams created with BioRender.com.

  1. Andrian, U. H. v. & Mackay, C. R. T-Cell Function and Migration — Two Sides of the Same Coin. New England Journal of Medicine 343, 1020-1034 (2000).
  2. MacLeod, M. K., Clambey, E. T., Kappler, J. W. & Marrack, P. CD4 memory T cells: what are they and what can they do? Semin Immunol 21, 53-61 (2009).
  3. Inaba, K., Metlay, J. P., Crowley, M. T., Witmer-Pack, M. & Steinman, R. M. Dendritic cells as antigen presenting cells in vivo. International reviews of immunology 6, 197-206 (1990).
  4. Croft, M., Bradley, L. M. & Swain, S. L. Naive versus memory CD4 T cell response to antigen. Memory cells are less dependent on accessory cell costimulation and can respond to many antigen-presenting cell types including resting B cells. Journal of Immunology 152, 2675-2685 (1994).
  5. Schenkel, J. M. & Masopust, D. Tissue-resident memory T cells. Immunity 41, 886-897 (2014).
  6. Pan, Y. et al. Survival of tissue-resident memory T cells requires exogenous lipid uptake and metabolism. Nature 543, 252-256 (2017).
  7. Sallusto, F., Geginat, J. & Lanzavecchia, A. Central Memory and Effector Memory T Cell Subsets: Function, Generation, and Maintenance. Annual Review of Immunology 22, 745-763 (2004).
  8. Foulds, K. E. et al. Cutting Edge: CD4 and CD8 T Cells Are Intrinsically Different in Their Proliferative Responses1. Journal of Immunology 168, 1528-1532 (2002).
  9. Seder, R. A. & Ahmed, R. Similarities and differences in CD4+ and CD8+ effector and memory T cell generation. Nature Immunology 4, 835-842 (2003).
  10. Sallusto, F. et al. Switch in chemokine receptor expression upon TCR stimulation reveals novel homing potential for recently activated T cells. European Journal of Immunology 29, 2037-2045 (1999).
  11. Chao, C.-C., Jensen, R. & Dailey, M. O. Mechanisms of L-selectin regulation by activated T cells. Journal of Immunology 159, 1686-1694 (1997).
  12. Campbell, J. J. et al. CCR7 expression and memory T cell diversity in humans. Journal of Immunology 166, 877-884 (2001).
  13. Campbell, J. J. et al. 6-C-kine (SLC), a lymphocyte adhesion-triggering chemokine expressed by high endothelium, is an agonist for the MIP-3β receptor CCR7. The Journal of Cell Biology 141, 1053-1059 (1998).
  14. Wherry, E. J. et al. Lineage relationship and protective immunity of memory CD8 T cell subsets. Nature Immunology 4, 225-234 (2003).
  15. Beverley, P.C.L., Merkenschlager, M., Wallace, D.L. Identification of Human Naive and Memory T Cells. In: Melchers, F., et al. Progress in Immunology (Springer), 432-438 (1989)
  16. Michie, C. A., McLean, A., Alcock, C. & Beverley, P. C. L. Lifespan of human lymphocyte subsets defined by CD45 isoforms. Nature 360, 264-265 (1992).
  17. Zikherman, J. & Weiss, A. Alternative Splicing of CD45: The Tip of the Iceberg. Immunity 29, 839-841 (2008).
  18. Geginat, J., Lanzavecchia, A. & Sallusto, F. Proliferation and differentiation potential of human CD8+ memory T-cell subsets in response to antigen or homeostatic cytokines. Blood 101, 4260-4266 (2003).
  19. Geginat , J., Sallusto , F. & Lanzavecchia , A. Cytokine-driven Proliferation and Differentiation of Human Naive, Central Memory, and Effector Memory CD4+ T Cells. Journal of Experimental Medicine 194, 1711-1720 (2001).
  20. Förster, R., Schubel, A., Breitfeld, D. & Kremmer, E. Renner-Mü ller I, Wolf E, Lipp M. 1999. CCR7 coordinates the primary immune response by establishing functional microenvironments in secondary lymphoid organs. Cell 99, 23-33
  21. Alrumaihi, F. The Multi-Functional Roles of CCR7 in Human Immunology and as a Promising Therapeutic Target for Cancer Therapeutics. Front Mol Biosci 9, 834149 (2022).
  22. Miyasaka, M. Selectins (CD62-E/L/P). In: Encyclopedia of Immunology (Second Edition) (ed Peter J. Delves) 2158-2161 (Elsevier, 1998).
  23. Masopust, D. & Schenkel, J. M. The integration of T cell migration, differentiation and function. Nature Reviews Immunology 13, 309-320 (2013).
  24. Gattinoni, L. et al. Acquisition of full effector function in vitro paradoxically impairs the in vivo antitumor efficacy of adoptively transferred CD8+ T cells. The Journal of Clinical Investigation 115, 1616-1626 (2005).
  25. Kim, H. P., Imbert, J. & Leonard, W. J. Both integrated and differential regulation of components of the IL-2/IL-2 receptor system. Cytokine & Growth Factor Reviews 17, 349-366 (2006).
  26. Williams, M. A., Tyznik, A. J. & Bevan, M. J. Interleukin-2 signals during priming are required for secondary expansion of CD8+ memory T cells. Nature 441, 890-893 (2006).
  27. Ross, S. H. & Cantrell, D. A. Signaling and Function of Interleukin-2 in T Lymphocytes. Annu Rev Immunol 36, 411-433 (2018).
  28. Nolz, J. C., Rai, D., Badovinac, V. P. & Harty, J. T. Division-linked generation of death-intermediates regulates the numerical stability of memory CD8 T cells. Proceedings of the National Academy of Sciences 109, 6199-6204 (2012).
  29. Campbell, J. et al. The chemokine receptor CCR4 in vascular recognition by cutaneous but not intestinal memory T cells. Nature 400, 776-780 (1999).
  30. Zabel, B. A. et al. Human G protein–coupled receptor GPR-9-6/CC chemokine receptor 9 is selectively expressed on intestinal homing T lymphocytes, mucosal lymphocytes, and thymocytes and is required for thymus-expressed chemokine–mediated chemotaxis. Journal of Experimental Medicine 190, 1241-1256 (1999).
  31. Pulko, V. et al. Human memory T cells with a naive phenotype accumulate with aging and respond to persistent viruses. Nat Immunol 17, 966-975 (2016).
  32. Tian, Y. et al. Unique phenotypes and clonal expansions of human CD4 effector memory T cells re-expressing CD45RA. Nature Communications 8, 1473 (2017).
  33. Osińska, I., Popko, K. & Demkow, U. Perforin: an important player in immune response. Cent Eur J Immunol 39, 109-115 (2014).
  34. Law, R. H. et al. The structural basis for membrane binding and pore formation by lymphocyte perforin. Nature 468, 447-451 (2010).
  35. Ivashkiv, L. B. IFNγ: signalling, epigenetics and roles in immunity, metabolism, disease and cancer immunotherapy. Nature Reviews Immunology 18, 545-558 (2018).
  36. Hu, X. & Ivashkiv, L. B. Cross-regulation of signaling pathways by interferon-γ: implications for immune responses and autoimmune diseases. Immunity 31, 539-550 (2009).
  37. Broide, D. H., Paine, M. M. & Firestein, G. S. Eosinophils express interleukin 5 and granulocyte macrophage-colony-stimulating factor mRNA at sites of allergic inflammation in asthmatics. J Clin Invest 90, 1414-1424 (1992).
  38. Brown, M. A. et al. B cell stimulatory factor-1/interleukin-4 mRNA is expressed by normal and transformed mast cells. Cell 50, 809-818 (1987).
  39. Daines, J. M., Schellhardt, L. & Wood, M. D. The Role of the IL-4 Signaling Pathway in Traumatic Nerve Injuries. Neurorehabil Neural Repair 35, 431-443 (2021).
  40. Blomberg, O. S. et al. IL-5-producing CD4+ T cells and eosinophils cooperate to enhance response to immune checkpoint blockade in breast cancer. Cancer Cell 41, 106-123.e110 (2023).
  41. Resnick, M. B. & Weller, P. F. Mechanisms of eosinophil recruitment. American Journal of Respiratory Cell and Molecular Biology 8, 349-349 (1993).
  42. Takatsu, K. Interleukin-5 and IL-5 receptor in health and diseases. Proc Jpn Acad Ser B Phys Biol Sci 87, 463-485 (2011).
  43. Takatsu, K. et al. Role of IL-5 in the innate immune system and disease control. International Congress Series 1285, 145-154 (2005).
  44. Hofmann, M. & Pircher, H. E-cadherin promotes accumulation of a unique memory CD8 T-cell population in murine salivary glands. Proceedings of the National Academy of Sciences 108, 16741-16746 (2011).
  45. Masopust, D. et al. Dynamic T cell migration program provides resident memory within intestinal epithelium. Journal of Experimental Medicine 207, 553-564 (2010).
  46. Masopust, D., Vezys, V., Wherry, E. J., Barber, D. L. & Ahmed, R. Cutting edge: gut microenvironment promotes differentiation of a unique memory CD8 T cell population. The Journal of Immunology 176, 2079-2083 (2006).
  47. Kumar, B. V. et al. Human Tissue-Resident Memory T Cells Are Defined by Core Transcriptional and Functional Signatures in Lymphoid and Mucosal Sites. Cell Reports 20, 2921-2934 (2017).
  48. Hadley, G. A. & Higgins, J. M. G. in I Domain Integrins (ed Donald Gullberg), 97-110 (Springer, 2014).
  49. Casey, K. A. et al. Antigen-independent differentiation and maintenance of effector-like resident memory T cells in tissues. The Journal of Immunology 188, 4866-4875 (2012).
  50. Mackay, L. K. et al. The developmental pathway for CD103+ CD8+ tissue-resident memory T cells of skin. Nature immunology 14, 1294-1301 (2013).
  51. Jiang, X. et al. Skin infection generates non-migratory memory CD8+ TRM cells providing global skin immunity. Nature 483, 227-231 (2012).
  52. Schenkel, J. M., Fraser, K. A., Vezys, V. & Masopust, D. Sensing and alarm function of resident memory CD8+ T cells. Nature Immunology 14, 509-513 (2013).
  53. Teijaro, J. R. et al. Cutting edge: Tissue-retentive lung memory CD4 T cells mediate optimal protection to respiratory virus infection. The Journal of Immunology 187, 5510-5514 (2011).
  54. Cyster, J. G. & Schwab, S. R. Sphingosine-1-phosphate and lymphocyte egress from lymphoid organs. Annual Review of Immunology 30, 69-94 (2012).
  55. López-Cabrera, M. et al. Transcriptional Regulation of the Gene Encoding the Human C-type Lectin Leukocyte Receptor AIM/CD69 and Functional Characterization of Its Tumor Necrosis Factor-α-responsive Elements (∗). Journal of Biological Chemistry 270, 21545-21551 (1995).
  56. Kohlmeier, J. E., Cookenham, T., Roberts, A. D., Miller, S. C. & Woodland, D. L. Type I interferons regulate cytolytic activity of memory CD8+ T cells in the lung airways during respiratory virus challenge. Immunity 33, 96-105 (2010).
  57. Skon, C. N. et al. Transcriptional downregulation of S1pr1 is required for the establishment of resident memory CD8+ T cells. Nature Immunology 14, 1285-1293 (2013).
  58. Rousalova, I. & Krepela, E. Granzyme B-induced apoptosis in cancer cells and its regulation (review). Int J Oncol 37, 1361-1378 (2010).
Show all