Journal of immunology最新文献

{"title":"A gavage-fomite based method to generate mouse models with natural microbiota.","authors":"Geongoo Han, Mohammad H Hasan, Olumide Adesioye, Jessica Pacia, Julian C Ramprashad, Gregorio Valdez, Shipra Vaishnava, Lalit K Beura","doi":"10.1093/jimmun/vkag242","DOIUrl":"10.1093/jimmun/vkag242","url":null,"abstract":"<p><p>Laboratory-raised specific pathogen-free (SPF) mice have been indispensable for fundamental immunology research, yet their reliability in predicting human clinical outcomes has been questionable. A major factor contributing to this disconnect is the sanitized housing environment, which deprives laboratory mice of physiological microbial exposure critical for immune maturation. Various approaches have been developed to introduce microbes to SPF mice, aiming to mimic human-like microbial experiences and engender adult human-like immune traits. However, some of these methods, specifically the pet store mice cohousing approach suffer from significant variability in pathogen exposure driven by the uncontrolled nature of microbial exchange and is associated with heightened mortality. Here we present an alternative gavage-fomite (GaF) method that exposes mice to a similarly diverse array of pathogens and commensal as the pet store cohousing method while limiting mortality. GaF-treated mice exhibited consistent gut microbial composition, robust immune maturation characterized by mucosal T cell distribution, elevated serum inflammatory cytokines, and a splenic immune transcriptional signature closely aligned with that of adult humans. Furthermore, these mice demonstrated enhanced protection against a virulent bacterial challenge. The simplicity and effectiveness of the GaF method for generating \"mice with natural microbiota,\" may support broader use of these models in basic and translational immunological research across institutions.</p>","PeriodicalId":16045,"journal":{"name":"Journal of immunology","volume":"215 9","pages":""},"PeriodicalIF":4.0,"publicationDate":"2026-08-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13588700/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149001928","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Virus-specific memory CD4 T cells sustain long-term numerical and functional impairment following whole-body irradiation.","authors":"Shravan Kumar Kannan, Mohammad Heidarian, Elizabeth A Escue, John T Harty, Vladimir P Badovinac","doi":"10.1093/jimmun/vkag244","DOIUrl":"10.1093/jimmun/vkag244","url":null,"abstract":"<p><p>The increasing demand for nuclear power and radiotherapy has expanded potential avenues for human exposure to whole-body irradiation (WBI), underscoring the need to understand its impact on immune cells. While prior studies have explored radiation-induced disruptions in immune homeostasis, the direct effect of WBI on pre-existing memory CD4 T cells remains elusive. Using T cell receptor transgenic CD4 T cell chimeric mice infected with lymphocytic choriomeningitis virus-Armstrong, we demonstrate that a sublethal WBI dose (5 Gy) causes a significant and persistent reduction in the numbers of memory CD4 T cells for at least 30 d post-WBI. At 8 d post-WBI, memory CD4 T cells exhibited an increased frequency of Ly6C+ T helper 1 cells and a decreased frequency of PSGL1+Ly6C- central memory cells in the spleen compared with mock-irradiated (0 Gy) control mice. These subset imbalances were no longer detectable by 30 d post-WBI. However, surviving memory CD4 T cells exhibited intrinsic functional impairments, including reduced production of the proinflammatory cytokines IFNγ, TNFα, and IL-2 upon ex vivo stimulation with the gp61-80 peptide. Furthermore, irradiated T cell receptor transgenic memory CD4 T cells exhibited defective secondary expansion upon pathogen re-encounter in unmanipulated hosts. Finally, the irradiated primary memory CD4 T cells exhibited poor protection potential, as they were unable to clear the pathogen upon re-exposure as effectively as their 0 Gy counterpart. In summary, sublethal WBI impairs the kinetics, subset composition, and function of memory CD4 T cells, ultimately compromising their ability to mount effective recall responses to clear the infection.</p>","PeriodicalId":16045,"journal":{"name":"Journal of immunology","volume":"215 9","pages":""},"PeriodicalIF":4.0,"publicationDate":"2026-08-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13561510/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148929975","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"ZFP335-MYBL2 transcriptional axis orchestrates Th17 cell differentiation and psoriatic inflammation.","authors":"Wenhua Li, Biao Yang, Ning Yuan, Xin Wang, Xiaoxuan Jia, Yanhong Su, Xiaoran Zhang, Tianzhe Zhang, Yang Gao, Jun Liu, Yuying Ren, Jiapeng Song, Xiaofeng Yang, Lei Lei, Baojun Zhang","doi":"10.1093/jimmun/vkag260","DOIUrl":"https://doi.org/10.1093/jimmun/vkag260","url":null,"abstract":"<p><p>T helper 17 (Th17) cell differentiation is governed by a complex transcriptional network centered on the lineage-specifying factor RORγt, accompanied by STAT3, IRF4, and SMAD2/3. However, the complete repertoire of transcriptional regulators controlling Il17a gene transcription and Th17 commitment remains incompletely defined. Here, we identify zinc finger protein 335 (ZFP335) as a critical regulator of Th17 differentiation. Mechanistically, ZFP335 directly binds and activates the Mybl2 promoter, and the resulting MYBL2 protein cooperates with RORγt to drive Il17a transcription. Genetic ablation of Zfp335 attenuated imiquimod-induced psoriasis-like skin inflammation and diminished Th17 cell responses in vivo. Notably, Mybl2 deficiency phenocopied these protective effects. Collectively, these findings establish a ZFP335-MYBL2-IL17A transcriptional axis that governs Th17 differentiation and identify this pathway as a potential therapeutic target for Th17-mediated inflammatory diseases.</p>","PeriodicalId":16045,"journal":{"name":"Journal of immunology","volume":"215 9","pages":""},"PeriodicalIF":4.0,"publicationDate":"2026-08-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149074878","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Improving peptide vaccine manufacturability without sacrificing immunogenicity: substitution of methionine and cysteine with oxidation-resistant isosteres.","authors":"Andrew S Ishizuka, Christopher M Garliss, Robert N Goddu, Maria Merolle, Alec Schrager, Andrei Ramirez-Valdez, Qiuyin Ren, Faezzah Baharom, Matthew Essandoh, Nicholas G Palacorolla, John P Finnigan, Daniel C Douek, Nina Bhardwaj, Robert A Seder, Geoffrey M Lynn, David R Wilson","doi":"10.1093/jimmun/vkag232","DOIUrl":"10.1093/jimmun/vkag232","url":null,"abstract":"<p><p>Vaccines comprising peptide antigens for inducing T cell immunity are being developed for a broad range of therapeutic applications including prevention and treatment of cancer, autoimmunity, and infectious diseases. However, many peptide antigens contain cysteine and/or methionine, which are prone to form oxidation products that can present challenges to manufacturing and reduce biological activity. To address this challenge, we introduced oxidation resistant (OXR) antigens wherein the cysteine and methionine residues of naturally occurring, wild type (WT) peptide antigens are substituted with isosteric residues that are structurally related but omit the oxidation-prone sulfur atom. Using multiple murine epitope models in C57BL/6 mice, we showed that vaccination with OXR antigens substituting cysteine and methionine with isosteres alpha-aminobutyric acid and norleucine, respectively, induced immune responses to the WT antigen that were equivalent or higher than those induced by vaccination with WT antigens. T cell responses were not affected by the position of the amino acid substitutions indicating that the isosteres do not negatively impact major histocompatibility complex (MHC) binding or T cell recognition. The T cells induced were high quality and associated with anti-tumor efficacy in vivo. Interestingly, substitution of cysteine with serine, which replaces the sulfur for an oxygen, did not yield cross-reactive T cell responses, highlighting the high degree of molecular discernment of peptide-MHC processing and presentation. In sum, OXR antigens provide a generalizable strategy for eliminating sulfur oxidation products and improving the manufacturability and shelf-life of peptide-based vaccines without affecting desired biologic activity.</p>","PeriodicalId":16045,"journal":{"name":"Journal of immunology","volume":"215 9","pages":""},"PeriodicalIF":4.0,"publicationDate":"2026-08-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13622990/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149080935","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"A circular RNA modulates IL-6 transcription via HuR-dependent stabilization of C/EBPβ mRNA.","authors":"Shuya Hiroki, Daisuke Ori, Kisaragi Agari, Norisuke Kano, Taro Kawai","doi":"10.1093/jimmun/vkag251","DOIUrl":"https://doi.org/10.1093/jimmun/vkag251","url":null,"abstract":"<p><p>Inflammatory responses require precise posttranscriptional control of gene expression, yet the contribution of circular RNAs (circRNAs) to this process remains poorly understood. Here, we performed circRNA sequencing in murine macrophages stimulated with lipopolysaccharide (LPS) and identified dynamic and stimulus-dependent changes in circRNA expression. Among 1,298 high-confidence circRNAs, 54 showed significant expression changes upon LPS stimulation. We focused on circNav1, which was downregulated upon LPS stimulation. Functional analyses revealed that circNav1 enhances LPS-induced Il6 expression in macrophages. Transcriptomic and mechanistic studies identified C/EBPβ as a key downstream effector of circNav1. CircNav1 interacts with the RNA-binding protein HuR (ELAVL1) and promotes HuR-dependent stabilization of Cebpb mRNA, thereby reinforcing Il6 transcription. Consistent with these findings, circNav1 expression was markedly reduced in murine models of colitis and septic shock. Together, these results uncover a circNav1-HuR-C/EBPβ regulatory axis that fine-tunes Il6 expression during inflammatory responses and highlight circRNAs as dynamic posttranscriptional regulators in innate immunity.</p>","PeriodicalId":16045,"journal":{"name":"Journal of immunology","volume":"215 9","pages":""},"PeriodicalIF":4.0,"publicationDate":"2026-08-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149061745","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Nanobodies specific for Vβ11 enable detection and noninvasive imaging of antigen-specific T cells in vivo.","authors":"Stephanie D Scharmann, Francisca Faber, Lauren Hoorens van Heyningen, Mirna Reljić, Brooke D Huisman, Priscilla P M Faas, Himadri Medhi, Manpreet Meyer, Camille Le Gall, Ishani Sahay, Pavana Suresh, Floris J van Dalen, Nanette Becht, Leif S Ludwig, Michael E Birnbaum, Hidde L Ploegh, Novalia Pishesha","doi":"10.1093/jimmun/vkag237","DOIUrl":"10.1093/jimmun/vkag237","url":null,"abstract":"<p><p>Through screening of a VHH phage display library constructed from an alpaca immunized with the recombinantly expressed murine myelin oligodendrocyte (MOG)-specific 2D2 T cell receptor (TCR), we identified nanobodies that reduced antigen-driven 2D2 T cell activation in vitro. Immunoblotting and staining confirmed TCRβ chain reactivity and Vβ11-associated recognition in polyclonal T cell populations. Site-specific sortase-mediated conjugation with desferrioxamine and 89Zr enabled nanobody-based immuno-PET/CT. In vivo imaging showed tracer accumulation in secondary lymphoid organs in settings enriched for Vβ11-expressing 2D2 T cells. In mice symptomatic for experimental autoimmune encephalomyelitis that had received MOG-specific 2D2 T cells, we observed a spinal cord-associated signal. This corresponded to accumulation of transferred Vβ11-expressing 2D2 T cells within inflamed spinal cord tissue. Compared with full-length immunoglobulins and multimeric peptide-MHC reagents that primarily support ex vivo detection of antigen-specific T cells, TCR-specific nanobodies show rapid clearance and improved tissue penetration that favor high-contrast immuno-PET/CT imaging of defined T cell populations in vivo.</p>","PeriodicalId":16045,"journal":{"name":"Journal of immunology","volume":"215 9","pages":""},"PeriodicalIF":4.0,"publicationDate":"2026-08-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13525469/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148850903","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Distinct effects of two different human interferon-alpha subtypes on indicators of T-cell proliferation, activation and inhibition.","authors":"Madeline T H Stewart, Yunyun Di, Noah D Lim, Saurav S Rout, Ulf Dittmer, Kathrin Sutter, Kerry J Lavender","doi":"10.1093/jimmun/vkag259","DOIUrl":"https://doi.org/10.1093/jimmun/vkag259","url":null,"abstract":"<p><p>Humans produce 12 distinct interferon alpha (IFN-α) subtypes that were previously thought to be functionally redundant. Recent studies have revealed that IFN-α subtypes differ in their ability to control different viral infections. However, little is known about how IFN-α subtypes differentially modulate immune cells to mediate these effects. This study compared the effects of IFN-α2 and IFN-α14, subtypes identified to differentially control viral infection, on T cells both in vivo in humanized TKO-BLT mice and in vitro using human peripheral blood mononuclear cells (PBMC). Treatment of humanized mice with the 2 IFN-α subtypes resulted in the differential modulation of genes associated with T-cell immunity, such as proliferation, activation and inhibition. Therefore, we assessed whether stimulation of PBMC in the presence of IFN-α2 or IFN-α14 resulted in subtype-specific effects on T cells in vitro. IFN-α14 decreased the proliferation of human CD4+ and CD8+ T cells significantly more than IFN-α2. Additionally, IFN-α14 increased expression of T-cell activation markers and the frequency of IL-2 producing T cells to a significantly greater extent compared to IFN-α2. However, the co-culture of CD8+ T cells with IFN-α-treated, autologous CD4+ T cells or IFN-α-matured monocyte-derived dendritic cells (mo-DC) only increased the expression of CD38 compared to no IFN-α treatment in a non-subtype specific manner. Overall, we identified IFN-α subtype-specific effects on the proliferation and activation of T cells. However, there were no significant differences detected directly between the IFN-α subtypes when the effects on CD8+ T cells arose through IFN-α pre-treatment of CD4+ T cells or mo-DC.</p>","PeriodicalId":16045,"journal":{"name":"Journal of immunology","volume":"215 9","pages":""},"PeriodicalIF":4.0,"publicationDate":"2026-08-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149061673","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The Qβ bacteriophage nanoparticle contributes to the adjuvanticity of antiglycan vaccines through a unique inflammatory pathway.","authors":"Kenna Nagy, Jeffery Noble, Shenglou Deng, Robert Hincapie, Anne Costanzo, Lisa Kain, Paul B Savage, M G Finn, Luc Teyton","doi":"10.1093/jimmun/vkag252","DOIUrl":"https://doi.org/10.1093/jimmun/vkag252","url":null,"abstract":"<p><p>Current glycoconjugate vaccines often fail to induce durable B cell memory or to provide sufficiently high-affinity antibodies limiting their utility for prophylactic protection against most bacterial and fungal pathogens. We address this limitation by engineering a chemically functionalized protein nanoparticle vaccine capable of eliciting protective nanomolar affinity antiglycan antibodies and long-term humoral memory. This platform incorporates a combination of two B cell-focused adjuvants, a TLR7 agonist and a natural killer T cell agonist, in order to enhance the antiglycan antibody maturation and memory formation. To define the contributions of each pathway, the antiglycan responses were evaluated at early and late time points following immunization. Although mice deficient in both TLR7 and natural killer T cell signaling revealed diminished primary immunization responses, an unexpectedly robust antiglycan antibody titer still developed and persisted for at least 1 yr after a two-dose immunization. These results indicate that durable antiglycan humoral immunity can develop independent of the chosen adjuvant pathways and may be driven by intrinsic adjuvanticity of the recombinant bacteriophage nanoparticle. Mechanistically, this effect was associated with an inflammatory response in which IFNγ and IL-1α appeared to play important roles. Together, these findings identify a previously unappreciated component contributing to long-term antiglycan immunity and support the use of bacteriophage-derived nanoparticles as platforms for vaccines against emerging antibiotic-resistant microorganisms.</p>","PeriodicalId":16045,"journal":{"name":"Journal of immunology","volume":"215 9","pages":""},"PeriodicalIF":4.0,"publicationDate":"2026-08-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149061707","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Exacerbation of inflammatory bone loss in TET2-driven clonal hematopoiesis.","authors":"Hui Wang, Nan Hu, Marko Barovic, Bohu Pan, Guoping Cheng, Xiaofei Li, Yue Li, Jong-Hyung Lim, Ying Zhou, Peter J Murray, Lydia Kalafati, Julia Chronopoulos, Triantafyllos Chavakis, George Hajishengallis","doi":"10.1093/jimmun/vkag248","DOIUrl":"10.1093/jimmun/vkag248","url":null,"abstract":"<p><p>Clonal hematopoiesis of indeterminate potential (CHIP) arises from age-related somatic mutations in hematopoietic stem cells in the bone marrow (BM), driving clonal expansion and altered phenotypes. Loss-of-function mutations in the epigenetic regulator TET2 are among the most frequent in CHIP and increase the risk of hematologic malignancies and chronic inflammatory disorders. Here, we investigated the impact of TET2-driven CHIP on inflammatory bone loss. Partial BM reconstitution with TET2-deficient (Tet2-/-) cells promoted clonal expansion and spontaneous periodontitis, characterized by gingival inflammation and alveolar bone loss. Furthermore, mice with TET2-driven CHIP exhibited heightened susceptibility to experimentally induced bone loss, including ligature-induced periodontitis and collagen antibody-induced arthritis. This inflammatory bone loss phenotype was associated with increased tissue infiltration of hyperinflammatory Tet2-/- neutrophils and monocytes, elevated IL-17-producing CD4⁺ T cells (Th17), and enhanced osteoclastogenesis driven by paracrine signals from Tet2-/- myeloid cells acting on wild-type osteoclast precursors. Although T cell-intrinsic TET2 deficiency minimally affected Th17 differentiation in vitro, Tet2-/- dendritic cells exhibited enhanced capacity to drive Th17 differentiation from wild-type CD4⁺ T cells. These findings reveal mechanistic links between TET2-driven CHIP and the pathogenesis of inflammatory bone loss disorders.</p>","PeriodicalId":16045,"journal":{"name":"Journal of immunology","volume":"215 9","pages":""},"PeriodicalIF":4.0,"publicationDate":"2026-08-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13602485/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148990179","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Immunopeptidomics-driven MHC class II peptide-binding motif discovery for 2 common canine DR alleles.","authors":"Haeree P Lang, Aysha Rana, Farah F Almeer, Thamotharampillai Dileepan, Marc Jenkins, Steven G Friedenberg","doi":"10.1093/jimmun/vkag243","DOIUrl":"https://doi.org/10.1093/jimmun/vkag243","url":null,"abstract":"<p><p>Despite the central role of major histocompatibility complex (MHC) class II in adaptive immunity, peptide-binding motifs have yet to be characterized for any canine MHC class II allele. Here, we report the first immunopeptidomics-derived binding motifs for DLA-DRB1*015:01 (DLA-DR15) and DLA-DRB1*012:01 (DLA-DR12), 2 alleles overrepresented in breeds predisposed to immune-mediated diseases. Because dogs co-express DLA-DR and DLA-DQ, the MHC class II Ab clone YKIX334.2 was validated to be DLA-DR-specific, enabling allele-selective immunoaffinity purification of DLA-DR molecules from homozygous DLA-DR15 and DLA-DR12 donor spleens. Mass spectrometry and GibbsCluster motif deconvolution of 838 DLA-DR15-associated and 644 DLA-DR12-associated peptides eluted from their respective peptide-binding grooves revealed distinct allele-specific binding motifs, with characterization of anchor residue preferences, peptide-length distributions, cross-species comparisons with human and murine MHC class II motifs, and source protein composition of the eluted self-peptidome. To evaluate the translational utility of these motifs, recombinant DLA-DR15 and DLA-DR12 molecules were used to screen rabies virus glycoprotein and nucleoprotein peptide libraries via fluorescence-based peptide competition assays, identifying high-affinity candidate binders for both alleles. Spearman rank correlation between immunopeptidomics-derived position-specific scoring matrix scores and peptide competition assay rankings demonstrated modest associations, consistent with these approaches capturing complementary dimensions of peptide-MHC class II interaction. Ultimately, these findings establish what we believe is the first allele-specific peptide-binding motif framework for canine MHC class II, providing a foundation for DLA-allele-informed CD4+ T-cell epitope discovery studies and Ag-specific immune response characterization in the dog.</p>","PeriodicalId":16045,"journal":{"name":"Journal of immunology","volume":"215 9","pages":""},"PeriodicalIF":4.0,"publicationDate":"2026-08-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148990248","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}