Definition and research guide
This page combines a MeSH definition, publication statistics and selected research abstracts. It is a starting point for reading the literature, not a medical textbook or a systematic evidence review.
Content available: 4 complete abstracts (703 words), 10 references. Full article text is not stored or reproduced here; follow the PMID, DOI or PMC links to read the original sources and their access terms.
Definition
The altered state of immunologic responsiveness resulting from initial contact with antigen, which enables the individual to produce antibodies more rapidly and in greater quantity in response to secondary antigenic stimulus.
Definition: NLM Medical Subject Headings (MeSH) scope note (Public domain (U.S. National Library of Medicine); attribution requested). View the MeSH record.
Also known as: Immunologic Memories; Immune Memory; Immune Memories; Memory, Immune; Memory, Immunologic; Immunological Memory; Immunological Memories; Memory, Immunological.
Where it fits in the MeSH classification
- Broader topics
- Adaptive Immunity
Research landscape
PubMed indexes 20,621 records tagged with the MeSH heading “Immunologic Memory” (counts retrieved 2026-10-29). 3,671 of them (17.8%) were published from 2020 onward, and the busiest period so far is 2010-2019 with 6,901 records.
Reviews account for 3,210 records (15.6%) and meta-analyses for 13. Randomized controlled trials number 243 (1.2%) as a share of all records on the topic. Randomized trials make up only a small share of this literature, so much of what is known comes from laboratory, observational or descriptive work.
Show the data
| Period | Records |
|---|---|
| through 1999 | 4,851 |
| 2000-2009 | 5,198 |
| 2010-2019 | 6,901 |
| 2020 onward | 3,671 |
Publication-type chart data
| Type | Records | Share |
|---|---|---|
| Reviews | 3,210 | 15.6% |
| Meta-analyses | 13 | 0.1% |
| Randomized controlled trials | 243 | 1.2% |
Method: PubMed query "Immunologic Memory"[MeSH Terms] with publication-type and date filters, retrieved 2026-10-29.
Reading the evidence in immunology
Immune responses are studied in model organisms, in cells from donors and in patients, and the same pathway can behave differently across these settings. Mouse immune systems differ from human ones in important ways, and blood measurements may not reflect what happens in tissues. Clinical conclusions about immune-mediated disease or immunotherapy come mainly from controlled trials and long-term cohorts. Check the species and tissue studied, whether markers were linked to outcomes patients notice, and the follow-up time.
Evidence from open-access studies
These open-access studies come from PubMed’s best-match results for this heading (papers whose main topic it is), ranked here by citation count, with one recent addition. Each abstract is reproduced in full under its recorded open licence so that you can read the authors’ own words. They illustrate the literature; they are not a systematic summary of it. Citation counts measure attention, not reliability or clinical benefit.
| Study / authors | Year | Source label / design | Europe PMC citations | Licence / source |
|---|---|---|---|---|
| Tissue-resident memory CD8 T cell diversity is spatiotemporally imprinted | 2025 | Research article Design not recorded in structured metadata | 90 | cc by PMID 39843748 · DOI · PMC11903307 |
| Metabolic Regulation in the Induction of Trained Immunity | 2024 | Review article Design not recorded in structured metadata | 67 | cc by PMID 39060761 · DOI · PMC11282170 |
| Trained immunity: induction of an inflammatory memory in disease | 2025 | Review article Design not recorded in structured metadata | 63 | cc by PMID 41083592 · DOI · PMC12589594 |
| Antigen reactivity defines tissue-resident memory and exhausted T cells in tumors | 2026 | Research article Design not recorded in structured metadata | 23 | cc by PMID 41461987 · DOI · PMC12764432 |
Tissue-resident memory CD8 T cell diversity is spatiotemporally imprinted [1]
Abstract reading summary — source excerpts
- Opening excerpt
- Tissue-resident memory CD8 T (TRM) cells provide protection from infection at barrier sites.
- Closing excerpt
- Ultimately, our framework for the study of tissue immune networks reveals that T cell location and functional state are fundamentally intertwined.
- Interpretation limits
- Verbatim excerpts from the authors’ abstract; the closing excerpt may describe a finding, limitation or recommendation. Design, population, effect size and uncertainty have not been independently extracted or appraised. Read the complete abstract and linked paper before interpreting the findings.
Read complete abstract (224 words)
Tissue-resident memory CD8 T (TRM) cells provide protection from infection at barrier sites. In the small intestine, TRM cells are found in at least two distinct subpopulations: one with higher expression of effector molecules and another with greater memory potential1. However, the origins of this diversity remain unknown. Here we proposed that distinct tissue niches drive the phenotypic heterogeneity of TRM cells. To test this, we leveraged spatial transcriptomics of human samples, a mouse model of acute systemic viral infection and a newly established strategy for pooled optically encoded gene perturbations to profile the locations, interactions and transcriptomes of pathogen-specific TRM cell differentiation at single-transcript resolution. We developed computational approaches to capture cellular locations along three anatomical axes of the small intestine and to visualize the spatiotemporal distribution of cell types and gene expression. Our study reveals that the regionalized signalling of the intestinal architecture supports two distinct TRM cell states: differentiated TRM cells and progenitor-like TRM cells, located in the upper villus and lower villus, respectively. This diversity is mediated by distinct ligand-receptor activities, cytokine gradients and specialized cellular contacts. Blocking TGFβ or CXCL9 and CXCL10 sensing by antigen-specific CD8 T cells revealed a model consistent with anatomically delineated, early fate specification. Ultimately, our framework for the study of tissue immune networks reveals that T cell location and functional state are fundamentally intertwined.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 39843748 · DOI · PMC11903307
Metabolic Regulation in the Induction of Trained Immunity [2]
Abstract reading summary — source excerpts
- Opening excerpt
- The innate immune system exhibits features of memory, termed trained immunity, which promote faster and more robust responsiveness to heterologous challenges.
- Closing excerpt
- Specifically, targeting the metabolic programs of innate immune cells is an emerging strategy for clinical interventions, either to boost immune responses in immunosuppressed conditions or to mitigate maladaptive activation in hyperinflammatory diseases.
- Interpretation limits
- Verbatim excerpts from the authors’ abstract; the closing excerpt may describe a finding, limitation or recommendation. Design, population, effect size and uncertainty have not been independently extracted or appraised. Read the complete abstract and linked paper before interpreting the findings.
Read complete abstract (157 words)
The innate immune system exhibits features of memory, termed trained immunity, which promote faster and more robust responsiveness to heterologous challenges. Innate immune memory is sustained through epigenetic modifications, affecting gene accessibility, and promoting a tailored gene transcription for an enhanced immune response. Alterations in the epigenetic landscape are intertwined with metabolic rewiring. Here, we review the metabolic pathways that underscore the induction and maintenance of trained immunity, including glycolysis, oxidative phosphorylation, the tricarboxylic acid cycle, and amino acid and lipid metabolism. The intricate interplay of these pathways is pivotal for establishing innate immune memory in distinct cellular compartments. We explore in particular the case of resident lung alveolar macrophages. We propose that leveraging the memory of the innate immune system may present therapeutic potential. Specifically, targeting the metabolic programs of innate immune cells is an emerging strategy for clinical interventions, either to boost immune responses in immunosuppressed conditions or to mitigate maladaptive activation in hyperinflammatory diseases.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 39060761 · DOI · PMC11282170
Trained immunity: induction of an inflammatory memory in disease [3]
Abstract reading summary — source excerpts
- Opening excerpt
- The innate immune system adapts its behavior based on previous insults, mounting an enhanced response upon re-exposure.
- Closing excerpt
- By understanding how trained immunity is involved in processes leading to health and disease, novel therapeutic strategies can be developed.
- Interpretation limits
- Verbatim excerpts from the authors’ abstract; the closing excerpt may describe a finding, limitation or recommendation. Design, population, effect size and uncertainty have not been independently extracted or appraised. Read the complete abstract and linked paper before interpreting the findings.
Read complete abstract (142 words)
The innate immune system adapts its behavior based on previous insults, mounting an enhanced response upon re-exposure. Hematopoietic progenitors in the bone marrow and peripheral innate immune cells can undergo epigenetic and metabolic reprogramming, establishing an innate immune memory known as trained immunity. The concept of trained immunity recently gained relevance in our understanding of how innate immunity is regulated in various diseases. This review explores the role of trained immunity in infections, autoimmune disease, cardiovascular disease, cancer, and neurodegenerative disease. We discuss how trained immunity can provide heterologous protection against infections, as it has been induced for decades by the Bacillus Calmette Guérin vaccine, how it can help counteract immunosuppression, and how it can be inappropriately induced leading to chronic inflammation. By understanding how trained immunity is involved in processes leading to health and disease, novel therapeutic strategies can be developed.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 41083592 · DOI · PMC12589594
Antigen reactivity defines tissue-resident memory and exhausted T cells in tumors [4]
Abstract reading summary — source excerpts
- Opening excerpt
- CD8+ T cells are an important weapon in the therapeutic armamentarium against cancer.
- Closing excerpt
- These results highlight unique functions for TRM and TEX cells in tumor control, underscoring the need for distinct strategies to harness these populations for cancer therapies.
- Interpretation limits
- Verbatim excerpts from the authors’ abstract; the closing excerpt may describe a finding, limitation or recommendation. Design, population, effect size and uncertainty have not been independently extracted or appraised. Read the complete abstract and linked paper before interpreting the findings.
Read complete abstract (180 words)
CD8+ T cells are an important weapon in the therapeutic armamentarium against cancer. While CD8+CD103+ T cells with a tissue-resident memory T (TRM) cell phenotype are associated with favorable prognoses, the tumor microenvironment also contains dysfunctional exhausted T (TEX) cells that exhibit a variety of TRM-like features. Here we deconvolute TRM and TEX cells across human cancers, ascribing markers and gene signatures that distinguish these populations and enable their functional distinction. Although TRM cells have superior functionality and are associated with long-term survival post-tumor resection, they are not associated with responsiveness to immune checkpoint blockade. Tumor-associated TEX and TRM cells are clonally distinct, with the latter comprising tumor-independent bystanders and tumor-specific cells segregated from cognate antigen. Intratumoral TRM cells can be forced toward an exhausted fate when chronic antigen stimulation occurs, indicating that the presence or absence of continuous antigen exposure within the microenvironment is the key distinction between tumor-associated TEX and TRM populations. These results highlight unique functions for TRM and TEX cells in tumor control, underscoring the need for distinct strategies to harness these populations for cancer therapies.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 41461987 · DOI · PMC12764432
Key reviews and meta-analyses
The most cited review-type papers among PubMed’s best-match results for this heading, listed with bibliographic details only. Follow the links for the full text and access terms.
- Research article Defining trained immunity and its role in health and disease [5]
- Research article Location, location, location: Tissue resident memory T cells in mice and humans [6]
- Research article B cell memory: building two walls of protection against pathogens [7]
- Research article Challenges and Opportunities for Consistent Classification of Human B Cell and Plasma Cell Populations [8]
- Research article Innate and Adaptive Immune Memory: an Evolutionary Continuum in the Host's Response to Pathogens [9]
- Research article Therapeutic targeting of trained immunity [10]
References
- Reina-Campos M, Monell A, Ferry A, Luna V, Cheung KP, Galletti G, et al.. Tissue-resident memory CD8 T cell diversity is spatiotemporally imprinted. . 2025. PMID 39843748 · DOI · PMC11903307
- Ferreira AV, Domínguez-Andrés J, Merlo Pich LM, Joosten LAB, Netea MG. Metabolic Regulation in the Induction of Trained Immunity. . 2024. PMID 39060761 · DOI · PMC11282170
- Schlüter T, van Elsas Y, Priem B, Ziogas A, Netea MG. Trained immunity: induction of an inflammatory memory in disease. . 2025. PMID 41083592 · DOI · PMC12589594
- Burn TN, Schröder J, Gandolfo LC, Osman M, Wainwright EN, Lam EYN, et al.. Antigen reactivity defines tissue-resident memory and exhausted T cells in tumors. . 2026. PMID 41461987 · DOI · PMC12764432
- Netea MG, Domínguez-Andrés J, Barreiro LB, Chavakis T, Divangahi M, Fuchs E, et al.. Defining trained immunity and its role in health and disease. Nat Rev Immunol. 2020. PMID 32132681 · DOI · PMC7186935
- Szabo PA, Miron M, Farber DL. Location, location, location: Tissue resident memory T cells in mice and humans. Sci Immunol. 2019. PMID 30952804 · DOI · PMC6778482
- Akkaya M, Kwak K, Pierce SK. B cell memory: building two walls of protection against pathogens. Nat Rev Immunol. 2020. PMID 31836872 · DOI · PMC7223087
- Sanz I, Wei C, Jenks SA, Cashman KS, Tipton C, Woodruff MC, et al.. Challenges and Opportunities for Consistent Classification of Human B Cell and Plasma Cell Populations. Front Immunol. 2019. PMID 31681331 · DOI · PMC6813733
- Netea MG, Schlitzer A, Placek K, Joosten LAB, Schultze JL. Innate and Adaptive Immune Memory: an Evolutionary Continuum in the Host's Response to Pathogens. Cell Host Microbe. 2019. PMID 30629914 · DOI
- Mulder WJM, Ochando J, Joosten LAB, Fayad ZA, Netea MG. Therapeutic targeting of trained immunity. Nat Rev Drug Discov. 2019. PMID 30967658 · DOI · PMC7069501
About this article
- Sources
- NLM Medical Subject Headings (definition, synonyms); NCBI PubMed (counts, identifiers); Europe PMC (open-access abstracts and citation counts).
- Verification
- Every reference was resolved against PubMed on 2026-10-31; title, year and DOI matched.
- Review state
- automated source verified; no human expert review has been recorded yet.
- Version
- 1, last updated 2026-10-29.
See how EvidenceLib is built. Spotted an error? Email support@evidencehelix.com.
Evidence strength
EvidenceHelix's computed view of the study designs behind this topic: how common meta-analyses, randomized trials and reviews are, how recent the literature is, and a plain-language reading. It describes the design mix of the literature. It is not a quality appraisal of any study, and it is not medical advice.