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: 3 complete abstracts (486 words), 9 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
Protection from an infectious disease agent that is mediated by B- and T- lymphocytes following exposure to specific antigen, and characterized by immunologic memory. It can result from either previous infection with that agent or vaccination (immunity, active), or transfer of antibody or lymphocytes from an immune donor (immunization, passive).
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: Acquired Immunity; Immunity, Acquired; Adoptive Immunity; Immunity, Adoptive; Immunity, Adaptive; Adaptive Immune Response; Immune Response, Adaptive; Response, Adaptive Immune.
Where it fits in the MeSH classification
- Broader topics
- Immunity
- Narrower topics
- Clonal Selection, Antigen-Mediated; Immunity, Active; Immunity, Cellular; Immunity, Humoral; Immunologic Memory
- See also
- Immunity, Innate
Related concepts
- Lymphocytes
- Immunologic Memory
- Immunity
- Active
- Immunization
- Passive
Research landscape
PubMed indexes 263,912 records tagged with the MeSH heading “Adaptive Immunity” (counts retrieved 2026-10-29). 25,265 of them (9.6%) were published from 2020 onward, and the busiest period so far is through 1999 with 138,701 records.
Reviews account for 36,853 records (14.0%) and meta-analyses for 178. Randomized controlled trials number 2,602 (1.0%) 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 | 138,701 |
| 2000-2009 | 47,269 |
| 2010-2019 | 52,677 |
| 2020 onward | 25,265 |
Publication-type chart data
| Type | Records | Share |
|---|---|---|
| Reviews | 36,853 | 14.0% |
| Meta-analyses | 178 | 0.1% |
| Randomized controlled trials | 2,602 | 1.0% |
Method: PubMed query "Adaptive Immunity"[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 |
|---|---|---|---|---|
| Antibody-mediated diversification of primary and secondary humoral immune responses | 2026 | Research article Design not recorded in structured metadata | 4 | cc by PMID 42047685 · DOI · PMC13124041 |
| DNA methylation-mediated memory of obesity in CD4 T lymphocytes perpetuates immune dysregulation | 2026 | Research article Design not recorded in structured metadata | 3 | cc by PMID 42045443 · DOI · PMC13260840 |
| Regulation of immune signal integration and memory by inflammation-induced chromosome conformation | 2026 | Research article Design not recorded in structured metadata | 2 | cc by PMID 42743281 · DOI · PMC13598234 |
Antibody-mediated diversification of primary and secondary humoral immune responses [1]
Abstract reading summary — source excerpts
- Opening excerpt
- Humoral immune responses are characterized by increasing antibody affinity and diversity over time.
- Closing excerpt
- The data have significant implication for sequential vaccination approaches aimed at shepherding immunity to produce broadly neutralizing antibodies to highly diversified pathogens such as HIV-1 and influenza.
- 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 (153 words)
Humoral immune responses are characterized by increasing antibody affinity and diversity over time. Increased affinity is mediated by a combination of immunoglobulin gene somatic mutation and iterative cycles of selection in germinal centers. Less is understood about how diversity increases. Here, we examine the role of antibody feedback in diversifying immune responses in mice that produce B cells that are incapable of secreting antibodies. To this end, we produced two strains of mice, one that expresses only membrane and secreted forms of IgM, and a second that produces only the membrane-bound form of IgM. Analysis of primary and secondary immune responses shows that antibody feedback significantly diversifies both primary and secondary immune responses even when antibodies are present at levels that are 10-30-fold lower than physiologic. The data have significant implication for sequential vaccination approaches aimed at shepherding immunity to produce broadly neutralizing antibodies to highly diversified pathogens such as HIV-1 and influenza.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 42047685 · DOI · PMC13124041
DNA methylation-mediated memory of obesity in CD4 T lymphocytes perpetuates immune dysregulation [2]
Abstract reading summary — source excerpts
- Opening excerpt
- Obesity represents a major global healthcare crisis, with childhood obesity rising at an alarming rate.
- Closing excerpt
- These findings raise the possibility that targeting such pathways could support the restoration of immune homeostasis alongside weight loss 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 (176 words)
Obesity represents a major global healthcare crisis, with childhood obesity rising at an alarming rate. Children with obesity are highly likely to carry it into adulthood, bringing numerous associated health risks. Even more troubling is the emerging understanding of "obesity memory", which contributes to the frequent issue of weight regain. Here, we show that obesity imprints CD4 T cells through DNA methylation, leading to a long-time lag, spanning years, before adaptive immune homeostasis is restored after weight loss. Differential DNA methylation analysis highlights autophagy and immune senescence as potential key mechanisms underpinning this memory of obesity in CD4 T cells. In addition, particularly palmitate could be a key saturated fatty acid that can contribute to epigenetic alterations in CD4 T cells, potentially perpetuating this altered state. We identify molecular candidates (i.e., Stk26 and Cdkn1c) underpinning key cell functions (autophagy and immune senescence) that could be targeted to promote a return to immune homeostasis alongside weight loss. These findings raise the possibility that targeting such pathways could support the restoration of immune homeostasis alongside weight loss therapies.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 42045443 · DOI · PMC13260840
Regulation of immune signal integration and memory by inflammation-induced chromosome conformation [3]
Abstract reading summary — source excerpts
- Opening excerpt
- Three-dimensional (3D) genome conformation is central to gene expression regulation, yet our understanding of its contribution to rapid transcriptional responses, signal integration, and memory in immune cells is limited.
- Closing excerpt
- Collectively, these findings demonstrate that rapid and memory transcriptional responses to immunological stimuli are encoded in the 3D genome.
- 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)
Three-dimensional (3D) genome conformation is central to gene expression regulation, yet our understanding of its contribution to rapid transcriptional responses, signal integration, and memory in immune cells is limited. Here, we study the molecular regulation of the inflammatory response in primary macrophages using integrated transcriptomic, epigenomic, and chromosome conformation data, including base pair-resolution Micro Capture-C. We demonstrate that interleukin-4 (IL-4) primes the inflammatory response in macrophages by stably rewiring 3D genome conformation, juxtaposing endotoxin-, interferon-gamma-, and dexamethasone-responsive enhancers to their cognate gene promoters. CRISPR-based perturbations of enhancer-promoter contacts or CCCTC-binding factor (CTCF) boundary elements show that IL-4-driven conformation changes are required for enhanced and synergistic endotoxin-induced transcriptional responses, as well as transcriptional memory following stimulus removal. Moreover, transcriptional memory mediated by changes in chromosome conformation can occur in the absence of changes in chromatin accessibility or histone modifications. Collectively, these findings demonstrate that rapid and memory transcriptional responses to immunological stimuli are encoded in the 3D genome.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 42743281 · DOI · PMC13598234
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 Cross-priming in cancer immunology and immunotherapy [4]
- Research article Trained immunity in chronic inflammatory diseases and cancer [5]
- Research article Trained immunity: induction of an inflammatory memory in disease [6]
- Research article Neutrophil-to-lymphocyte ratio in age-related macular degeneration: a systematic review and meta-analysis [7]
- Research article The immune system in cardiovascular diseases: from basic mechanisms to therapeutic implications [8]
- Research article Resolving the mysteries of brain clearance and immune surveillance [9]
References
- Schaefer-Babajew D, Binet L, Silva Santos GS, Ruprecht C, Deimel LP, ElTanbouly MA, et al.. Antibody-mediated diversification of primary and secondary humoral immune responses. . 2026. PMID 42047685 · DOI · PMC13124041
- Niven J, Kucuk S, Gope A, Certo M, Cassidy FC, Arana Echarri A, et al.. DNA methylation-mediated memory of obesity in CD4 T lymphocytes perpetuates immune dysregulation. . 2026. PMID 42045443 · DOI · PMC13260840
- Daniel B, Chen AY, Sandor K, Zhang W, Miao Z, Yost KE, et al.. Regulation of immune signal integration and memory by inflammation-induced chromosome conformation. . 2026. PMID 42743281 · DOI · PMC13598234
- Luri-Rey C, Teijeira Á, Wculek SK, de Andrea C, Herrero C, Lopez-Janeiro A, et al.. Cross-priming in cancer immunology and immunotherapy. Nat Rev Cancer. 2025. PMID 39881005 · DOI
- Hajishengallis G, Netea MG, Chavakis T. Trained immunity in chronic inflammatory diseases and cancer. Nat Rev Immunol. 2025. PMID 39891000 · DOI · PMC12450111
- Schlüter T, van Elsas Y, Priem B, Ziogas A, Netea MG. Trained immunity: induction of an inflammatory memory in disease. Cell Res. 2025. PMID 41083592 · DOI · PMC12589594
- Niazi S, Krogh Nielsen M, Sørensen TL, Subhi Y. Neutrophil-to-lymphocyte ratio in age-related macular degeneration: a systematic review and meta-analysis. Acta Ophthalmol. 2019. PMID 30811869 · DOI
- Wang X, Chen L, Wei J, Zheng H, Zhou N, Xu X, et al.. The immune system in cardiovascular diseases: from basic mechanisms to therapeutic implications. Signal Transduct Target Ther. 2025. PMID 40404619 · DOI · PMC12098830
- Kipnis J, Benveniste H, Eichmann A, Thomas JL, Reich DS, Lewis LD, et al.. Resolving the mysteries of brain clearance and immune surveillance. Neuron. 2025. PMID 41289996 · DOI · PMC12757055
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.
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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.