Cited by 832T-cell and B-cell ImmunologyImmunotherapy and Immune ResponsesImmune responses and vaccinations

T CELL MEMORY

Dutton, R. W., Bradley, L. M., Swain, S. L.·1998·Annual Review of Immunology

Abstract

▪ Abstract Immunological memory can be defined as the faster and stronger response of an animal that follows reexposure to the same antigen. By this definition, it is an operational property of the whole animal or the immune system. Memory cells express a different pattern of cell surface markers, and they respond in several ways that are functionally different from those of naive cells. Murine memory cells are CD44 high and low in the expression of activation markers such as CD25 (IL-2R), whereas human memory cells are CD45RA−, CD45RO+. In contrast to naive cells, memory cells secrete a full range of T cell cytokines and can be polarized to secrete particular restricted patterns of secretion for both CD4 and CD8 T cells. The requirements for the activation of memory cells for proliferation and cytokine production are not quite as strict as those of naive cells, but costimulation in the broad sense is required for optimum responses and for responses to suboptimum antigen concentrations. It would appear that memory cells can persist in the absence of antigenic stimulation and persist as nondividing cells. Reencounter with the same antigen can expand the population to a new, stable, higher level and generate a separate population of CD44 high effectors that may be required for protection, while competition from other antigens can drive it down to a lower stable level. It is unclear how or where memory cells arise, but once generated they have different pathways of recirculation and homing.

Integrity signals

Registry

Crossref · 10.1146/annurev.immunol.16.1.201

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119 of 119 references verified0 citation errors · 0 not checkable

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  • Once the pathogen has been cleared, most effector T cells die by apoptosis, but some persist as long-lived memory T cells that provide enhanced responses upon re-exposure to the cognate Ag.

    “Once the pathogen has been cleared most of the effector T cells die by apoptosis, but some of them persist as long-lived memory T cells that can provide enhanced responses upon re-exposure to the cognate Ag [132, 133].”

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Authors
Dutton, R. W., Bradley, L. M., & Swain, S. L.
Affiliations
Scripps Research Institute (US)
Venue
Annual Review of Immunology
Published
1998-04
Volume
16
Issue
1
Pages
201-223
ISSN
  • 0732-0582 (ISSN-L)
  • 1545-3278
OpenAlex
W2149764521
Cited by
832
References
119
Citations by year
2026: 3 · 2025: 5 · 2024: 7 · 2023: 10 · 2022: 7 · 2021: 13 · 2020: 6 · 2019: 8 · 2018: 11 · 2017: 12 · 2016: 10 · 2015: 24 · 2014: 15 · 2013: 15 · 2012: 28
FWCI
6.26
Type
journal article
Language
en
Open access
closed
Locations
  • Annual Review of Immunology (publishedVersion)
  • PubMed (publishedVersion)
Funders
  • National Institutes of Health (5p01ai037935-04)
  • National Institute of Allergy and Infectious Diseases (AI 37935)
Topics
  • Life Sciences › Immunology and Microbiology › Immunology › T-cell and B-cell Immunology
  • Life Sciences › Immunology and Microbiology › Immunology › Immunotherapy and Immune Responses
  • Life Sciences › Immunology and Microbiology › Immunology › Immune responses and vaccinations
Keywords
T cell memory, immunological memory, memory T cells, naive T cells, CD44, CD25, CD45RA, CD45RO, T cell cytokine secretion, T cell polarization, costimulation, secondary immune response
MeSH terms
Animals, Humans, Immunologic Memory, Phenotype, T-Lymphocyte Subsets

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