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 (685 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 ordered rearrangement of gene regions by DNA recombination such as that which occurs normally during development.
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: Gene Rearrangements; Rearrangement, Gene; Rearrangements, Gene; DNA Rearrangement; DNA Rearrangements; Rearrangement, DNA; Rearrangements, DNA.
Where it fits in the MeSH classification
- Broader topics
- Genetic Phenomena
- Narrower topics
- Gene Rearrangement, B-Lymphocyte; Gene Rearrangement, T-Lymphocyte; V(D)J Recombination
- See also
- Antibody Diversity; Genes, Immunoglobulin; Immunoglobulin Variable Region; Translocation, Genetic; VDJ Recombinases
Research landscape
PubMed indexes 24,322 records tagged with the MeSH heading “Gene Rearrangement” (counts retrieved 2026-10-29). 3,059 of them (12.6%) were published from 2020 onward, and the busiest period so far is through 1999 with 8,320 records.
Reviews account for 3,249 records (13.4%) and meta-analyses for 33. Randomized controlled trials number 51 (0.2%) 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 | 8,320 |
| 2000-2009 | 6,571 |
| 2010-2019 | 6,372 |
| 2020 onward | 3,059 |
Publication-type chart data
| Type | Records | Share |
|---|---|---|
| Reviews | 3,249 | 13.4% |
| Meta-analyses | 33 | 0.1% |
| Randomized controlled trials | 51 | 0.2% |
Method: PubMed query "Gene Rearrangement"[MeSH Terms] with publication-type and date filters, retrieved 2026-10-29.
Reading the evidence in genetics and genomics
Genetic findings vary widely in strength. A variant linked to a condition in one study may not replicate in other ancestries, and most common variants have small effects that are meaningful only in aggregate. Studies of rare, high-impact variants can support strong causal claims about a gene, while association studies describe statistical links that need functional and independent replication. Check the sample size, the ancestry of participants, whether results were replicated, and whether a laboratory or clinical outcome was actually measured.
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 |
|---|---|---|---|---|
| Phylogenetic analysis of migration, differentiation, and class switching in B cells | 2022 | Research article Design not recorded in structured metadata | 112 | cc by PMID 35468128 · DOI · PMC9037912 |
| A humanized mouse that mounts mature class-switched, hypermutated and neutralizing antibody responses | 2024 | Research article Design not recorded in structured metadata | 66 | cc by PMID 38918608 · DOI · PMC11291283 |
| Nociceptor neurons promote IgE class switch in B cells | 2021 | Research article Design not recorded in structured metadata | 43 | cc by PMID 34727095 · DOI · PMC8783686 |
| Intranasal booster drives class switching and homing of memory B cells for mucosal IgA response | 2026 | Research article Design not recorded in structured metadata | 8 | cc by PMID 41433108 · DOI · PMC12892890 |
Phylogenetic analysis of migration, differentiation, and class switching in B cells [1]
Abstract reading summary — source excerpts
- Opening excerpt
- B cells undergo rapid mutation and selection for antibody binding affinity when producing antibodies capable of neutralizing pathogens.
- Closing excerpt
- io.
- 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 (147 words)
B cells undergo rapid mutation and selection for antibody binding affinity when producing antibodies capable of neutralizing pathogens. This evolutionary process can be intermixed with migration between tissues, differentiation between cellular subsets, and switching between functional isotypes. B cell receptor (BCR) sequence data has the potential to elucidate important information about these processes. However, there is currently no robust, generalizable framework for making such inferences from BCR sequence data. To address this, we develop three parsimony-based summary statistics to characterize migration, differentiation, and isotype switching along B cell phylogenetic trees. We use simulations to demonstrate the effectiveness of this approach. We then use this framework to infer patterns of cellular differentiation and isotype switching from high throughput BCR sequence datasets obtained from patients in a study of HIV infection and a study of food allergy. These methods are implemented in the R package dowser, available at https://dowser.readthedocs.io.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 35468128 · DOI · PMC9037912
A humanized mouse that mounts mature class-switched, hypermutated and neutralizing antibody responses [2]
Abstract reading summary — source excerpts
- Opening excerpt
- Humanized mice are limited in terms of modeling human immunity, particularly with regards to antibody responses.
- Closing excerpt
- By leveraging estrogen activity to support human immune cell differentiation and maturation of antibody responses, THX mice provide a platform to study the human immune system and to develop human vaccines and therapeutics.
- 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 (216 words)
Humanized mice are limited in terms of modeling human immunity, particularly with regards to antibody responses. Here we constructed a humanized (THX) mouse by grafting non-γ-irradiated, genetically myeloablated KitW-41J mutant immunodeficient pups with human cord blood CD34+ cells, followed by 17β-estradiol conditioning to promote immune cell differentiation. THX mice reconstitute a human lymphoid and myeloid immune system, including marginal zone B cells, germinal center B cells, follicular helper T cells and neutrophils, and develop well-formed lymph nodes and intestinal lymphoid tissue, including Peyer's patches, and human thymic epithelial cells. These mice have diverse human B cell and T cell antigen receptor repertoires and can mount mature T cell-dependent and T cell-independent antibody responses, entailing somatic hypermutation, class-switch recombination, and plasma cell and memory B cell differentiation. Upon flagellin or a Pfizer-BioNTech coronavirus disease 2019 (COVID-19) mRNA vaccination, THX mice mount neutralizing antibody responses to Salmonella or severe acute respiratory syndrome coronavirus 2 Spike S1 receptor-binding domain, with blood incretion of human cytokines, including APRIL, BAFF, TGF-β, IL-4 and IFN-γ, all at physiological levels. These mice can also develop lupus autoimmunity after pristane injection. By leveraging estrogen activity to support human immune cell differentiation and maturation of antibody responses, THX mice provide a platform to study the human immune system and to develop human vaccines and therapeutics.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 38918608 · DOI · PMC11291283
Nociceptor neurons promote IgE class switch in B cells [3]
Abstract reading summary — source excerpts
- Opening excerpt
- Nociceptors, the high-threshold primary sensory neurons that trigger pain, interact with immune cells in the periphery to modulate innate immune responses.
- Closing excerpt
- Our findings suggest that nociceptors, in addition to their contributions to innate immunity, play a key role in modulating the adaptive immune response, particularly B cell antibody class switching to IgE.
- 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 (143 words)
Nociceptors, the high-threshold primary sensory neurons that trigger pain, interact with immune cells in the periphery to modulate innate immune responses. Whether they also participate in adaptive and humoral immunity is, however, not known. In this study, we probed if nociceptors have a role in distinct airway and skin models of allergic inflammation. In both models, the genetic ablation and pharmacological silencing of nociceptors substantially reduced inflammatory cell infiltration to the affected tissue. Moreover, we also found a profound and specific deficit in IgE production in these models of allergic inflammation. Mechanistically, we discovered that the nociceptor-released neuropeptide substance P helped trigger the formation of antibody-secreting cells and their release of IgE. Our findings suggest that nociceptors, in addition to their contributions to innate immunity, play a key role in modulating the adaptive immune response, particularly B cell antibody class switching to IgE.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 34727095 · DOI · PMC8783686
Intranasal booster drives class switching and homing of memory B cells for mucosal IgA response [4]
Abstract reading summary — source excerpts
- Opening excerpt
- Mucosal secretory IgA (sIgA) plays a central role in protecting against the invasion of respiratory pathogen via the upper respiratory tract.
- Closing excerpt
- Our findings demonstrate that intranasal booster can be an effective strategy for inducing upper respiratory mucosal sIgA and establishing mucosal immune protection.
- 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 (179 words)
Mucosal secretory IgA (sIgA) plays a central role in protecting against the invasion of respiratory pathogen via the upper respiratory tract. To understand how intranasal booster induces mucosal sIgA response in humans, we first used liquid chromatography-tandem mass spectrometry for peptide identification of immunoglobulin (MS Ig-seq) and single-cell B cell receptor sequencing (scBCR-seq) to identify 42 mucosal spike-specific sIgA monoclonal antibodies (mAbs) after intranasal booster. These mucosal sIgA mAbs exhibited enhanced neutralization up to 100-fold against SARS-CoV-2 variants compared with their monomeric IgG and IgA isotypes. Deep sequencing and longitudinal analysis of B cell receptor repertoires revealed that intranasal booster restimulates memory B cells primed by intramuscular vaccination to undergo IgA class switching, somatic hypermutation, and clonal expansion. Single-cell RNA-seq (scRNA-seq) revealed that intranasal booster upregulated the expression of mucosal homing receptors in spike-specific IgA-expressing B cells. This increase coincided with a transient increase of cytokines and chemokines that facilitate B cell recruitment in the nasal mucosa. Our findings demonstrate that intranasal booster can be an effective strategy for inducing upper respiratory mucosal sIgA and establishing mucosal immune protection.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 41433108 · DOI · PMC12892890
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 Mechanism and regulation of class switch recombination [5]
- Research article V(D)J recombination: mechanisms of initiation [6]
- Research article Mechanisms of programmed DNA lesions and genomic instability in the immune system [7]
- Research article Immunoglobulin class-switch DNA recombination: induction, targeting and beyond [8]
- Research article Genomic rearrangements and sporadic disease [9]
- Research article The molecular basis for public T-cell responses? [10]
References
- Hoehn KB, Pybus OG, Kleinstein SH. Phylogenetic analysis of migration, differentiation, and class switching in B cells. . 2022. PMID 35468128 · DOI · PMC9037912
- Chupp DP, Rivera CE, Zhou Y, Xu Y, Ramsey PS, Xu Z, et al.. A humanized mouse that mounts mature class-switched, hypermutated and neutralizing antibody responses. . 2024. PMID 38918608 · DOI · PMC11291283
- Mathur S, Wang JC, Seehus CR, Poirier F, Crosson T, Hsieh YC, et al.. Nociceptor neurons promote IgE class switch in B cells. . 2021. PMID 34727095 · DOI · PMC8783686
- Chen S, Zhang Z, Lin Z, Yin L, Ning L, Liu W, et al.. Intranasal booster drives class switching and homing of memory B cells for mucosal IgA response. . 2026. PMID 41433108 · DOI · PMC12892890
- Stavnezer J, Guikema JE, Schrader CE. Mechanism and regulation of class switch recombination. Annu Rev Immunol. 2008. PMID 18370922 · DOI · PMC2707252
- Schatz DG, Swanson PC. V(D)J recombination: mechanisms of initiation. Annu Rev Genet. 2011. PMID 21854230 · DOI
- Alt FW, Zhang Y, Meng FL, Guo C, Schwer B. Mechanisms of programmed DNA lesions and genomic instability in the immune system. Cell. 2013. PMID 23374339 · DOI · PMC4382911
- Xu Z, Zan H, Pone EJ, Mai T, Casali P. Immunoglobulin class-switch DNA recombination: induction, targeting and beyond. Nat Rev Immunol. 2012. PMID 22728528 · DOI · PMC3545482
- Lupski JR. Genomic rearrangements and sporadic disease. Nat Genet. 2007. PMID 17597781 · DOI
- Venturi V, Price DA, Douek DC, Davenport MP. The molecular basis for public T-cell responses?. Nat Rev Immunol. 2008. PMID 18301425 · DOI
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.