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 (545 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
The inherent or induced capacity of plants to withstand or ward off biological attack by pathogens.
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: Immunities, Plant; Immunity, Plant; Plant Immunities; Plant Immune Response; Immune Response, Plant; Immune Responses, Plant; Plant Immune Responses; Response, Plant Immune.
Where it fits in the MeSH classification
- Broader topics
- Immunity; Plant Physiological Phenomena
- Narrower topics
- Disease Resistance; Plant Systemic Acquired Resistance
Research landscape
PubMed indexes 19,646 records tagged with the MeSH heading “Plant Immunity” (counts retrieved 2026-10-29). 10,045 of them (51.1%) were published from 2020 onward, and the busiest period so far is 2020 onward with 10,045 records.
Reviews account for 2,284 records (11.6%) and meta-analyses for 44. Randomized controlled trials number 18 (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 | 0 |
| 2000-2009 | 4 |
| 2010-2019 | 9,784 |
| 2020 onward | 10,045 |
Publication-type chart data
| Type | Records | Share |
|---|---|---|
| Reviews | 2,284 | 11.6% |
| Meta-analyses | 44 | 0.2% |
| Randomized controlled trials | 18 | 0.1% |
Method: PubMed query "Plant 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 |
|---|---|---|---|---|
| Changes in gene regulation are associated with the evolution of resistance to a novel parasite | 2026 | Research article Design not recorded in structured metadata | 4 | cc by PMID 41836432 · DOI · PMC12979160 |
| Reprogramming of host energy metabolism mediated by the TNF-iNOS-HIF-1α axis plays a key role in host resistance to Plasmodium infection | 2026 | Research article Design not recorded in structured metadata | 3 | cc by PMID 42506979 · DOI · PMC13405620 |
| Engineering an Exo70 integrated domain of a barley NLR for improved blast resistance | 2026 | Research article Design not recorded in structured metadata | 3 | cc by PMID 42263189 · DOI · PMC13291817 |
Changes in gene regulation are associated with the evolution of resistance to a novel parasite [1]
Abstract reading summary — source excerpts
- Opening excerpt
- IntroductionHost-parasite interactions are ubiquitous and are important drivers of host diversification and evolution.
- Closing excerpt
- ConclusionOur results provide strong evidence that changes in gene regulation and increased negative feedback to mitigate immunopathology are essential steps in the evolutionary co-option of an existing pathway to defend against a new parasite infection.
- 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 (264 words)
IntroductionHost-parasite interactions are ubiquitous and are important drivers of host diversification and evolution. In particular, host immune systems are frequent targets of parasite-driven selection. The resulting rapid evolution of immune genes is usually framed as an ongoing 'arms race' between a co-evolving pair of host and parasite species. However, immune evolution may often be driven by the acquisition of a new and unfamiliar parasite. For instance, when marine populations of threespine stickleback (Gasterosteus aculeatus) colonized freshwater lakes approximately 12,000 years ago, they encountered the freshwater-restricted cestode Schistocephalus solidus and evolved resistance.MethodsWe compared the transcriptomic responses of lab-reared sticklebacks from three populations of stickleback with varying cestode susceptibilities when exposed to several immune stimuli (alum, cestode protein, or a control injection).ResultsThe resulting changes in expression reveal strong evidence of shared and population-specific responses during the evolution of defense against a new parasite. Our investigation highlights the roles of several key immunological processes in underlying a general physiological response to tissue damage (fibrosis) and the importance of regulating fibrosis as a necessary step for its co-option into defense against S. solidus tapeworms. Furthermore, we highlighted changes in the expression of fibrosis-associated genes, which facilitate faster and more targeted deployment of this defense mechanism against parasites. Fish from the most fibrosis-prone population exhibited constitutively higher expression of fibrosis-associated genes and stronger downregulation of these genes after an initial stimulus from injected cestode proteins.ConclusionOur results provide strong evidence that changes in gene regulation and increased negative feedback to mitigate immunopathology are essential steps in the evolutionary co-option of an existing pathway to defend against a new parasite infection.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 41836432 · DOI · PMC12979160
Reprogramming of host energy metabolism mediated by the TNF-iNOS-HIF-1α axis plays a key role in host resistance to Plasmodium infection [2]
Abstract reading summary — source excerpts
- Opening excerpt
- TNF has a dual effect in Plasmodium infection, bolstering the host's immune defense while also inducing sickness behavior.
- Closing excerpt
- Altogether, our results indicate that TNF-iNOS-HIF-1α-induced glycolysis in monocytes plays a critical role in host defense and sickness behavior in Pc-infected mice.
- 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 (133 words)
TNF has a dual effect in Plasmodium infection, bolstering the host's immune defense while also inducing sickness behavior. Here, we confirm that TNF signaling hampers physical activity, food intake, and energy expenditure while enhancing glucose uptake by the liver and spleen, as well as controlling parasitemia in Plasmodium chabaudi (Pc)-infected mice. We also report that TNF is required for expression of inducible nitric oxide synthase (iNOS), stabilization of hypoxia-inducible factor 1α (HIF-1α), expression of glucose transporter GLUT1, and enhanced glycolysis in monocytic cells from Pc-infected mice. Importantly, Pc-infected Nos2-/-, TNFR1 cKO, and HIF-1a cKO mice show impaired release of TNF and glycolysis in monocytes, along with increased parasitemia and disease tolerance. Altogether, our results indicate that TNF-iNOS-HIF-1α-induced glycolysis in monocytes plays a critical role in host defense and sickness behavior in Pc-infected mice.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 42506979 · DOI · PMC13405620
Engineering an Exo70 integrated domain of a barley NLR for improved blast resistance [3]
Abstract reading summary — source excerpts
- Opening excerpt
- Intracellular immune receptors protect plants from microbial invasion by detecting and responding to pathogen-derived effector molecules, often triggering cell death responses.
- Closing excerpt
- These results demonstrate the potential of engineering NLR receptors as an effective strategy for improving resistance toward one of the most destructive diseases affecting cereal production.
- 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 (148 words)
Intracellular immune receptors protect plants from microbial invasion by detecting and responding to pathogen-derived effector molecules, often triggering cell death responses. However, pathogen effectors can evolve to avoid immune recognition, resulting in devastating diseases that threaten global agriculture. Here, we show that an integrated Exo70 domain from the barley intracellular nucleotide-binding leucine-rich repeat (NLR) RGH2 can interact with both the rice blast pathogen effector AVR-Pii and a closely related wheat blast causing variant. We used structure-led engineering to develop RGH2+ that shows increased binding affinity toward AVR-Pii variants and increased cell death responses on heterologous expression in Nicotiana benthamiana. Infection assays in transgenic barley lines carrying RGH2+ with the paired NLR RGH3 indicate a reduced susceptibility to blast strains expressing AVR-Pii variants. These results demonstrate the potential of engineering NLR receptors as an effective strategy for improving resistance toward one of the most destructive diseases affecting cereal production.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 42263189 · DOI · PMC13291817
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 Thirty years of resistance: Zig-zag through the plant immune system [4]
- Research article The plant immune system: From discovery to deployment [5]
- Research article Molecular mechanisms of early plant pattern-triggered immune signaling [6]
- Research article Plant immune networks [7]
- Research article Ca2+ signals in plant immunity [8]
- Research article Salicylic acid in plant immunity and beyond [9]
References
- Fuess LE, Hund AK, Kenney ML, Maciejewski MF, Marini JM, Bolnick DI. Changes in gene regulation are associated with the evolution of resistance to a novel parasite. . 2026. PMID 41836432 · DOI · PMC12979160
- Matteucci KC, Leite NPS, Assis PA, Hirako IC, Pioto F, Ojelabi O, et al.. Reprogramming of host energy metabolism mediated by the TNF-iNOS-HIF-1α axis plays a key role in host resistance to Plasmodium infection. . 2026. PMID 42506979 · DOI · PMC13405620
- Saado I, Brabham HJ, Bennett JW, Lam AHC, Hernández-Pinzón I, Moscou MJ, et al.. Engineering an Exo70 integrated domain of a barley NLR for improved blast resistance. . 2026. PMID 42263189 · DOI · PMC13291817
- Ngou BPM, Ding P, Jones JDG. Thirty years of resistance: Zig-zag through the plant immune system. Plant Cell. 2022. PMID 35167697 · DOI · PMC9048904
- Jones JDG, Staskawicz BJ, Dangl JL. The plant immune system: From discovery to deployment. Cell. 2024. PMID 38670067 · DOI
- DeFalco TA, Zipfel C. Molecular mechanisms of early plant pattern-triggered immune signaling. Mol Cell. 2021. PMID 34403694 · DOI
- Ngou BPM, Jones JDG, Ding P. Plant immune networks. Trends Plant Sci. 2022. PMID 34548213 · DOI
- Köster P, DeFalco TA, Zipfel C. Ca2+ signals in plant immunity. EMBO J. 2022. PMID 35560235 · DOI · PMC9194748
- Spoel SH, Dong X. Salicylic acid in plant immunity and beyond. Plant Cell. 2024. PMID 38163634 · DOI · PMC11062473
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.