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 (547 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
Alteration of the immune system or of an immune response by agents that activate or suppress its function. This can include immunization or administration of immunomodulatory drugs. Immunomodulation can also encompass non-therapeutic alteration of the immune system effected by endogenous or exogenous substances.
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: Immunomodulations; Immunomodulatory Therapy; Immunomodulatory Therapies; Therapies, Immunomodulatory; Therapy, Immunomodulatory.
Where it fits in the MeSH classification
- Broader topics
- Biological Therapy; Immune System Phenomena
- Narrower topics
- Immunotherapy; Immune Tolerance; Neuroimmunomodulation
Related concepts
- Immunization
Research landscape
PubMed indexes 438,837 records tagged with the MeSH heading “Immunomodulation” (counts retrieved 2026-10-29). 117,757 of them (26.8%) were published from 2020 onward, and the busiest period so far is through 1999 with 142,279 records.
Reviews account for 91,505 records (20.9%) and meta-analyses for 2,645. Randomized controlled trials number 9,517 (2.2%) as a share of all records on the topic.
Show the data
| Period | Records |
|---|---|
| through 1999 | 142,279 |
| 2000-2009 | 71,567 |
| 2010-2019 | 107,234 |
| 2020 onward | 117,757 |
Publication-type chart data
| Type | Records | Share |
|---|---|---|
| Reviews | 91,505 | 20.9% |
| Meta-analyses | 2,645 | 0.6% |
| Randomized controlled trials | 9,517 | 2.2% |
Method: PubMed query "Immunomodulation"[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 |
|---|---|---|---|---|
| MicroRNAs and polymorphisms influencing MICA immune modulation | 2026 | Review article Design not recorded in structured metadata | 0 | cc by PMID 42900444 · DOI · PMC13683511 |
| Tumor cell-intrinsic stress states drive sensitivity to CAR T cell therapy in pancreatic cancer | 2026 | Research article Design not recorded in structured metadata | 0 | cc by PMID 42826199 · DOI · PMC13641470 |
| Breast cancer immunogenicity as a spectrum: evolving concepts and therapeutic implications | 2026 | Review article Design not recorded in structured metadata | 0 | cc by PMID 42820285 · DOI · PMC13626844 |
MicroRNAs and polymorphisms influencing MICA immune modulation [1]
Abstract reading summary — source excerpts
- Opening excerpt
- MicroRNAs (miRNAs) are small non-coding RNAs that play a central role in post-transcriptional gene regulation.
- Closing excerpt
- Furthermore, it highlights current knowledge gaps and future perspectives regarding allele-specific regulation.
- 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 (228 words)
MicroRNAs (miRNAs) are small non-coding RNAs that play a central role in post-transcriptional gene regulation. They act mainly by interacting with sequences located in the 3' untranslated regions (3'UTRs) of messenger RNAs (mRNAs), thereby influencing mRNA stability and translation. Through these mechanisms, miRNAs contribute to the fine-tuning of multiple biological pathways, including immune activation, inflammatory signaling, and cellular stress responses. Among the genes involved in immune surveillance, the major histocompatibility complex class I polypeptide-related sequence A (MICA) has emerged as an important target for post-transcriptional regulation due to its role as a ligand for the activating receptor NKG2D (natural killer cell group 2-D), which is expressed in natural killer (NK) cells and cytotoxic T lymphocytes. MICA is highly polymorphic, and several allelic variants differ in sequence composition, structural organization, and expression patterns, potentially influencing miRNA-mRNA interactions. Growing evidence suggests that miRNA-mediated regulation of MICA contributes to immune modulation in cancer, viral infections, and autoimmune disorders, particularly through mechanisms associated with immune evasion and altered NKG2D signaling. In addition, genetic polymorphisms and structural variations within regulatory regions, especially within the 3'UTR, can alter miRNA binding affinity by creating, disrupting, or modifying target sites. This mini review discusses the current understanding of miRNA-mediated regulation of MICA, emphasizing the impact of allelic diversity and regulatory polymorphisms on post-transcriptional control. Furthermore, it highlights current knowledge gaps and future perspectives regarding allele-specific regulation.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 42900444 · DOI · PMC13683511
Tumor cell-intrinsic stress states drive sensitivity to CAR T cell therapy in pancreatic cancer [2]
Abstract reading summary — source excerpts
- Opening excerpt
- Chimeric antigen receptor (CAR) T cell therapy has transformed the treatment of hematologic cancers but has shown limited efficacy in solid tumors, including pancreatic ductal adenocarcinoma (PDAC).
- Closing excerpt
- These findings provide a foundation to improve efficacy of CAR T cell therapy in solid malignancies and to better stratify patients with cancer by tumor genotype.
- 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 (162 words)
Chimeric antigen receptor (CAR) T cell therapy has transformed the treatment of hematologic cancers but has shown limited efficacy in solid tumors, including pancreatic ductal adenocarcinoma (PDAC). The cellular and molecular factors that influence CAR T cell therapy response remain largely unknown. By integrating modular in vivo CRISPR screens with single-cell genomics and immunocompetent orthotopic models of PDAC, we uncover oxidative and proteotoxic stress pathways as previously unknown modulators of CAR T cell therapy response. Disruption of stress regulatory genes, particularly Keap1 and Slc33a1, sensitizes PDAC tumors to CAR T cell killing in vivo. Hyperactivation of the Nrf2 pathway by genetic ablation of Keap1 or endogenous engineering of clinically observed Keap1 or Nfe2l2 mutations enhances tumor susceptibility to CAR T cell therapy. Thus, tumor-intrinsic molecular stress phenotypes can induce unexpected cell state-specific vulnerabilities to cell-based immunotherapies. These findings provide a foundation to improve efficacy of CAR T cell therapy in solid malignancies and to better stratify patients with cancer by tumor genotype.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 42826199 · DOI · PMC13641470
Breast cancer immunogenicity as a spectrum: evolving concepts and therapeutic implications [3]
Abstract reading summary — source excerpts
- Opening excerpt
- Immunotherapy has revolutionized the therapeutic landscape for many cancers, but its application in solid tumors has lagged.
- Closing excerpt
- Improved identification of immunologically active subsets and deeper mechanistic insight will be essential to expand the therapeutic benefit of immunotherapy to broader patient cohorts and to refine care of patients with breast cancer.
- 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)
Immunotherapy has revolutionized the therapeutic landscape for many cancers, but its application in solid tumors has lagged. There is now evidence that immunotherapy can improve outcomes in triple-negative breast cancer, but hormone receptor-positive (HR+) breast cancer has traditionally been considered immunologically cold. However, emerging evidence challenges this binary paradigm, suggesting that a biologically relevant subset of HR+/human epidermal growth factor receptor 2-negative (HER2-) tumors exhibit meaningful immunogenic features and clinically relevant sensitivity to immune-based treatment. In this Review we summarize the current understanding of immunogenicity and clinical use of immune-based treatments across breast cancer subtypes. We argue for a broader view of a spectrum of breast cancer immunogenicity and highlight the importance of host factors, including parity and lactation history, in shaping antitumor immunity. Improved identification of immunologically active subsets and deeper mechanistic insight will be essential to expand the therapeutic benefit of immunotherapy to broader patient cohorts and to refine care of patients with breast cancer.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 42820285 · DOI · PMC13626844
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 Second Primary Malignancies after CAR T-Cell Therapy: A Systematic Review and Meta-analysis of 5,517 Lymphoma and Myeloma Patients [4]
- Research article Improved Event-Free Survival After Complete or Major Pathologic Response in Patients With Resectable NSCLC Treated With Neoadjuvant Chemoimmunotherapy Regardless of Adjuvant Treatment: A Systematic Review and Individual Patient Data Meta-Analysis [5]
- Research article Efficacy and safety of passive immunotherapies targeting amyloid beta in Alzheimer's disease: A systematic review and meta-analysis [6]
- Research article Efficacy and safety of natural killer cell therapy in patients with solid tumors: a systematic review and meta-analysis [7]
- Research article Impact of vein-to-vein time in patients with R/R LBCL treated with axicabtagene ciloleucel [8]
- Research article Healthcare worker practices for HPV vaccine recommendation: A systematic review and meta-analysis [9]
References
- Nicoletti MB, Ferraz IM, Moço AC, da Cruz Castelli E, Castro CFB. MicroRNAs and polymorphisms influencing MICA immune modulation. . 2026. PMID 42900444 · DOI · PMC13683511
- Fröse J, Chen E, Whittaker CA, Leclerc P, Doherty S, Langenbucher A, et al.. Tumor cell-intrinsic stress states drive sensitivity to CAR T cell therapy in pancreatic cancer. . 2026. PMID 42826199 · DOI · PMC13641470
- Kay J, Dixon-Douglas JR, Harris MA, van Geelen CT, Loi S. Breast cancer immunogenicity as a spectrum: evolving concepts and therapeutic implications. . 2026. PMID 42820285 · DOI · PMC13626844
- Tix T, Alhomoud M, Shouval R, Cliff ERS, Perales MA, Cordas Dos Santos DM, et al.. Second Primary Malignancies after CAR T-Cell Therapy: A Systematic Review and Meta-analysis of 5,517 Lymphoma and Myeloma Patients. Clin Cancer Res. 2024. PMID 39256908 · DOI · PMC11546643
- Marinelli D, Nuccio A, Di Federico A, Ambrosi F, Bertoglio P, Faccioli E, et al.. Improved Event-Free Survival After Complete or Major Pathologic Response in Patients With Resectable NSCLC Treated With Neoadjuvant Chemoimmunotherapy Regardless of Adjuvant Treatment: A Systematic Review and Individual Patient Data Meta-Analysis. J Thorac Oncol. 2025. PMID 39389220 · DOI
- Tonegawa-Kuji R, Hou Y, Hu B, Lorincz-Comi N, Pieper AA, Tousi B, et al.. Efficacy and safety of passive immunotherapies targeting amyloid beta in Alzheimer's disease: A systematic review and meta-analysis. PLoS Med. 2025. PMID 40163534 · DOI · PMC12002640
- Park H, Kim G, Kim N, Ha S, Yim H. Efficacy and safety of natural killer cell therapy in patients with solid tumors: a systematic review and meta-analysis. Front Immunol. 2024. PMID 39478866 · DOI · PMC11522797
- Locke FL, Siddiqi T, Jacobson CA, Nikiforow S, Ahmed S, Miklos DB, et al.. Impact of vein-to-vein time in patients with R/R LBCL treated with axicabtagene ciloleucel. Blood Adv. 2025. PMID 39883946 · DOI · PMC12155625
- Bakare D, Gobbo E, Akinsola KO, Bakare AA, Salako J, Hanson C, et al.. Healthcare worker practices for HPV vaccine recommendation: A systematic review and meta-analysis. Hum Vaccin Immunother. 2024. PMID 39400296 · DOI · PMC11486212
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.