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 (646 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 process by which antigen is presented to lymphocytes in a form they can recognize. This is performed by antigen presenting cells (APCs). Some antigens require processing before they can be recognized. Antigen processing consists of ingestion and partial digestion of the antigen by the APC, followed by presentation of fragments on the cell surface. (From Rosen et al., Dictionary of Immunology, 1989)
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: Antigen Presentations; Antigen Processing; Antigen Processings.
Where it fits in the MeSH classification
- Broader topics
- Immune System Phenomena; Immunity, Cellular
- See also
- Immunological Synapses
Research landscape
PubMed indexes 16,502 records tagged with the MeSH heading “Antigen Presentation” (counts retrieved 2026-10-29). 2,185 of them (13.2%) were published from 2020 onward, and the busiest period so far is 2000-2009 with 6,669 records.
Reviews account for 3,998 records (24.2%) and meta-analyses for 5. Randomized controlled trials number 20 (0.1%) 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 | 2,954 |
| 2000-2009 | 6,669 |
| 2010-2019 | 4,694 |
| 2020 onward | 2,185 |
Publication-type chart data
| Type | Records | Share |
|---|---|---|
| Reviews | 3,998 | 24.2% |
| Meta-analyses | 5 | 0.0% |
| Randomized controlled trials | 20 | 0.1% |
Method: PubMed query "Antigen Presentation"[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 |
|---|---|---|---|---|
| Cancer Immune Evasion Through Loss of MHC Class I Antigen Presentation | 2021 | Review article Design not recorded in structured metadata | 896 | cc by PMID 33767702 · DOI · PMC7986854 |
| Identification of a Kupffer cell subset capable of reverting the T cell dysfunction induced by hepatocellular priming | 2021 | Research article Design not recorded in structured metadata | 142 | cc by PMID 34469774 · DOI · PMC8459394 |
| Antigen presentation by lung epithelial cells directs CD4+ TRM cell function and regulates barrier immunity | 2021 | Research article Design not recorded in structured metadata | 132 | cc by PMID 34611166 · DOI · PMC8492657 |
| The antigen-presenting molecule MR1 binds host-generated riboflavin catabolites | 2026 | Research article Design not recorded in structured metadata | 6 | cc by PMID 41295949 · DOI · PMC12650265 |
Cancer Immune Evasion Through Loss of MHC Class I Antigen Presentation [1]
Abstract reading summary — source excerpts
- Opening excerpt
- Major histocompatibility class I (MHC I) molecules bind peptides derived from a cell's expressed genes and then transport and display this antigenic information on the cell surface.
- Closing excerpt
- We discuss new insights into some common underlying mechanisms through which some cancers inactivate the MHC I pathway and consider some possible strategies to overcome this limitation in ways that could restore immune control of tumors and improve immunotherapy.
- 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 (187 words)
Major histocompatibility class I (MHC I) molecules bind peptides derived from a cell's expressed genes and then transport and display this antigenic information on the cell surface. This allows CD8 T cells to identify pathological cells that are synthesizing abnormal proteins, such as cancers that are expressing mutated proteins. In order for many cancers to arise and progress, they need to evolve mechanisms to avoid elimination by CD8 T cells. MHC I molecules are not essential for cell survival and therefore one mechanism by which cancers can evade immune control is by losing MHC I antigen presentation machinery (APM). Not only will this impair the ability of natural immune responses to control cancers, but also frustrate immunotherapies that work by re-invigorating anti-tumor CD8 T cells, such as checkpoint blockade. Here we review the evidence that loss of MHC I antigen presentation is a frequent occurrence in many cancers. We discuss new insights into some common underlying mechanisms through which some cancers inactivate the MHC I pathway and consider some possible strategies to overcome this limitation in ways that could restore immune control of tumors and improve immunotherapy.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 33767702 · DOI · PMC7986854
Identification of a Kupffer cell subset capable of reverting the T cell dysfunction induced by hepatocellular priming [2]
Abstract reading summary — source excerpts
- Opening excerpt
- Kupffer cells (KCs) are highly abundant, intravascular, liver-resident macrophages known for their scavenger and phagocytic functions.
- Closing excerpt
- In summary, by sensing IL-2 and cross-presenting hepatocellular antigens, KC2 overcome the tolerogenic potential of the hepatic microenvironment, suggesting new strategies for boosting hepatic T cell immunity.
- 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 (151 words)
Kupffer cells (KCs) are highly abundant, intravascular, liver-resident macrophages known for their scavenger and phagocytic functions. KCs can also present antigens to CD8+ T cells and promote either tolerance or effector differentiation, but the mechanisms underlying these discrepant outcomes are poorly understood. Here, we used a mouse model of hepatitis B virus (HBV) infection, in which HBV-specific naive CD8+ T cells recognizing hepatocellular antigens are driven into a state of immune dysfunction, to identify a subset of KCs (referred to as KC2) that cross-presents hepatocellular antigens upon interleukin-2 (IL-2) administration, thus improving the antiviral function of T cells. Removing MHC-I from all KCs, including KC2, or selectively depleting KC2 impaired the capacity of IL-2 to revert the T cell dysfunction induced by intrahepatic priming. In summary, by sensing IL-2 and cross-presenting hepatocellular antigens, KC2 overcome the tolerogenic potential of the hepatic microenvironment, suggesting new strategies for boosting hepatic T cell immunity.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 34469774 · DOI · PMC8459394
Antigen presentation by lung epithelial cells directs CD4+ TRM cell function and regulates barrier immunity [3]
Abstract reading summary — source excerpts
- Opening excerpt
- Barrier tissues are populated by functionally plastic CD4+ resident memory T (TRM) cells.
- Closing excerpt
- Thus, we establish epithelial antigen presentation as a critical regulator of CD4+ TRM cell function and identify epithelial-CD4+ TRM cell immune interactions as core elements of barrier immunity.
- 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 (150 words)
Barrier tissues are populated by functionally plastic CD4+ resident memory T (TRM) cells. Whether the barrier epithelium regulates CD4+ TRM cell locations, plasticity and activities remains unclear. Here we report that lung epithelial cells, including distinct surfactant protein C (SPC)lowMHChigh epithelial cells, function as anatomically-segregated and temporally-dynamic antigen presenting cells. In vivo ablation of lung epithelial MHC-II results in altered localization of CD4+ TRM cells. Recurrent encounters with cognate antigen in the absence of epithelial MHC-II leads CD4+ TRM cells to co-express several classically antagonistic lineage-defining transcription factors, changes their cytokine profiles, and results in dysregulated barrier immunity. In addition, lung epithelial MHC-II is needed for surface expression of PD-L1, which engages its ligand PD-1 to constrain lung CD4+ TRM cell phenotypes. Thus, we establish epithelial antigen presentation as a critical regulator of CD4+ TRM cell function and identify epithelial-CD4+ TRM cell immune interactions as core elements of barrier immunity.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 34611166 · DOI · PMC8492657
The antigen-presenting molecule MR1 binds host-generated riboflavin catabolites [4]
Abstract reading summary — source excerpts
- Opening excerpt
- MHC class I-related protein (MR1) presents vitamin B-based antigens (Ags) to mucosal-associated invariant T (MAIT) cells.
- Closing excerpt
- Collectively, we identified three-ringed isoalloxazines that bind MR1 and reduce surface levels, suggesting a potential role in dampening MAIT cell immunity.
- 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 (158 words)
MHC class I-related protein (MR1) presents vitamin B-based antigens (Ags) to mucosal-associated invariant T (MAIT) cells. While microbial riboflavin (RF) precursors are well-documented MR1 ligands, it is unclear whether host-generated RF catabolites influence MR1 immunity. Here, we report that RF catabolites, including 10-formylmethylflavin (FMF), lumichrome, lumiflavin, and alloxazine, bind to MR1 with moderate affinity, while RF itself binds weakly. In contrast to the MR1-upregulating microbial RF precursors, RF catabolites reduced the surface level of MR1 by inducing its retention in the endoplasmic reticulum and inhibiting exit. These RF catabolites weakly competed with vitamin B-based Ags for MR1 binding, thereby selectively inhibiting MAIT activation. The crystal structures of MR1 with RF, FMF, lumiflavin, and lumichrome show binding in the A'-pocket of MR1. Here, lumichrome formed a "flavin bond" covalent interaction with MR1-Lys43 differing from the typical Schiff base. Collectively, we identified three-ringed isoalloxazines that bind MR1 and reduce surface levels, suggesting a potential role in dampening MAIT cell immunity.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 41295949 · DOI · PMC12650265
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 Antigen presentation in cancer: insights into tumour immunogenicity and immune evasion [5]
- Research article Pathways of antigen processing [6]
- Research article The ins and outs of MHC class II-mediated antigen processing and presentation [7]
- Research article Monocyte differentiation and antigen-presenting functions [8]
- Research article A guide to antigen processing and presentation [9]
- Research article Present Yourself! By MHC Class I and MHC Class II Molecules [10]
References
- Dhatchinamoorthy K, Colbert JD, Rock KL. Cancer Immune Evasion Through Loss of MHC Class I Antigen Presentation. . 2021. PMID 33767702 · DOI · PMC7986854
- De Simone G, Andreata F, Bleriot C, Fumagalli V, Laura C, Garcia-Manteiga JM, et al.. Identification of a Kupffer cell subset capable of reverting the T cell dysfunction induced by hepatocellular priming. . 2021. PMID 34469774 · DOI · PMC8459394
- Shenoy AT, Lyon De Ana C, Arafa EI, Salwig I, Barker KA, Korkmaz FT, et al.. Antigen presentation by lung epithelial cells directs CD4+ TRM cell function and regulates barrier immunity. . 2021. PMID 34611166 · DOI · PMC8492657
- Abdelaal MR, Deng J, McInerney MP, Ito E, Purcell AW, Yamasaki S, et al.. The antigen-presenting molecule MR1 binds host-generated riboflavin catabolites. . 2026. PMID 41295949 · DOI · PMC12650265
- Jhunjhunwala S, Hammer C, Delamarre L. Antigen presentation in cancer: insights into tumour immunogenicity and immune evasion. Nat Rev Cancer. 2021. PMID 33750922 · DOI
- Blum JS, Wearsch PA, Cresswell P. Pathways of antigen processing. Annu Rev Immunol. 2013. PMID 23298205 · DOI · PMC4026165
- Roche PA, Furuta K. The ins and outs of MHC class II-mediated antigen processing and presentation. Nat Rev Immunol. 2015. PMID 25720354 · DOI · PMC6314495
- Jakubzick CV, Randolph GJ, Henson PM. Monocyte differentiation and antigen-presenting functions. Nat Rev Immunol. 2017. PMID 28436425 · DOI
- Pishesha N, Harmand TJ, Ploegh HL. A guide to antigen processing and presentation. Nat Rev Immunol. 2022. PMID 35418563 · DOI
- Rock KL, Reits E, Neefjes J. Present Yourself! By MHC Class I and MHC Class II Molecules. Trends Immunol. 2016. PMID 27614798 · DOI · PMC5159193
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.