Pub Date : 2026-01-09DOI: 10.1038/s41577-026-01264-8
Emery Hoos, Malcolm J. W. Sim
A preprint by McCarron et al. investigates immunodominance hierarchies in response to cancer vaccines targeting neoantigens.
McCarron等人的预印本研究了针对新抗原的癌症疫苗的免疫优势等级反应。
{"title":"T cell competition in multi-neoantigen cancer vaccines","authors":"Emery Hoos, Malcolm J. W. Sim","doi":"10.1038/s41577-026-01264-8","DOIUrl":"10.1038/s41577-026-01264-8","url":null,"abstract":"A preprint by McCarron et al. investigates immunodominance hierarchies in response to cancer vaccines targeting neoantigens.","PeriodicalId":19049,"journal":{"name":"Nature Reviews Immunology","volume":"26 2","pages":"88-88"},"PeriodicalIF":60.9,"publicationDate":"2026-01-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145937783","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2026-01-09DOI: 10.1038/s41577-025-01255-1
Lukas Rindlisbacher,Maria N Navarro,Burkhard Becher
Within the IL-12 superfamily of heterodimeric cytokines, IL-12 and IL-23, which share a subunit, are among the most pro-inflammatory members. Both are primarily produced by phagocytes and have key roles in activating and regulating T lymphocytes, natural killer cells and innate lymphoid cells. IL-12 predominantly promotes type 1 immune responses, whereas IL-23 is closely associated with type 3 immunity. Their receptors are also heterodimeric and, upon engagement, they trigger 'cytokine polarization' (the imprinting of functional identities on immune cells by activating lineage-defining transcription factors), which contributes to inflammation and immunopathology. IL-12 has a key role in various inflammatory conditions and is a potent driver of antitumour immunity, and IL-12 delivery is being explored in several clinical trials in cancer. By contrast, IL-23 is essential for maintaining barrier tissue integrity, yet its dysregulation is a central driver of autoimmune diseases such as psoriasis. Beyond their well-established pro-inflammatory roles, studies of both cytokines have also yielded paradoxical findings. Emerging evidence suggests that both IL-12 and IL-23 can also attenuate immune responses. In this Review, we explore the discovery of IL-12 and IL-23, their canonical pro-inflammatory functions, and recent insights into their immunoregulatory roles in inflammation, cancer and autoimmunity.
{"title":"Inflame and restrain - the paradoxical roles of IL-12 and IL-23 in immunity.","authors":"Lukas Rindlisbacher,Maria N Navarro,Burkhard Becher","doi":"10.1038/s41577-025-01255-1","DOIUrl":"https://doi.org/10.1038/s41577-025-01255-1","url":null,"abstract":"Within the IL-12 superfamily of heterodimeric cytokines, IL-12 and IL-23, which share a subunit, are among the most pro-inflammatory members. Both are primarily produced by phagocytes and have key roles in activating and regulating T lymphocytes, natural killer cells and innate lymphoid cells. IL-12 predominantly promotes type 1 immune responses, whereas IL-23 is closely associated with type 3 immunity. Their receptors are also heterodimeric and, upon engagement, they trigger 'cytokine polarization' (the imprinting of functional identities on immune cells by activating lineage-defining transcription factors), which contributes to inflammation and immunopathology. IL-12 has a key role in various inflammatory conditions and is a potent driver of antitumour immunity, and IL-12 delivery is being explored in several clinical trials in cancer. By contrast, IL-23 is essential for maintaining barrier tissue integrity, yet its dysregulation is a central driver of autoimmune diseases such as psoriasis. Beyond their well-established pro-inflammatory roles, studies of both cytokines have also yielded paradoxical findings. Emerging evidence suggests that both IL-12 and IL-23 can also attenuate immune responses. In this Review, we explore the discovery of IL-12 and IL-23, their canonical pro-inflammatory functions, and recent insights into their immunoregulatory roles in inflammation, cancer and autoimmunity.","PeriodicalId":19049,"journal":{"name":"Nature Reviews Immunology","volume":"20 1","pages":""},"PeriodicalIF":100.3,"publicationDate":"2026-01-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145937782","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2026-01-07DOI: 10.1038/s41577-025-01248-0
Lydia Sorokin
{"title":"Biochemical signals from the extracellular matrix in inflammation and tumour immunology","authors":"Lydia Sorokin","doi":"10.1038/s41577-025-01248-0","DOIUrl":"https://doi.org/10.1038/s41577-025-01248-0","url":null,"abstract":"","PeriodicalId":19049,"journal":{"name":"Nature Reviews Immunology","volume":"53 1","pages":""},"PeriodicalIF":100.3,"publicationDate":"2026-01-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145907944","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2026-01-05DOI: 10.1038/s41577-025-01239-1
João Mello-Vieira, Ivan Dikic
{"title":"Ubiquitination and autophagy in host–pathogen interactions: from immune surveillance to therapeutic targeting","authors":"João Mello-Vieira, Ivan Dikic","doi":"10.1038/s41577-025-01239-1","DOIUrl":"https://doi.org/10.1038/s41577-025-01239-1","url":null,"abstract":"","PeriodicalId":19049,"journal":{"name":"Nature Reviews Immunology","volume":"29 1","pages":""},"PeriodicalIF":100.3,"publicationDate":"2026-01-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145902346","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2026-01-02DOI: 10.1038/s41577-025-01249-z
Mary Jo Turk, Yina H Huang
Vitiligo is an autoimmune disease of melanocyte destruction, which manifests as progressive, patchy loss of pigmentation in the skin. As one of most common autoimmune diseases, vitiligo inflicts a significant psychosocial burden. Research over the past two decades has revealed the underlying immune mechanisms of vitiligo, with key studies combining detailed analyses of patient tissue samples with mechanistic experiments in mouse models. Vitiligo has emerged as a prototypical CD8+ T cell-mediated autoimmune disease, with cooperation between innate immune cells, dendritic cells, T cells, keratinocytes and fibroblasts driving autoimmune pathology against the uniquely susceptible melanocyte target. The study of vitiligo has also revealed aspects of CD8+ T cell memory and resident memory against self-antigens. This work has drawn from, and contributed to, the study of melanoma immunology. Whereas drugs used for other autoimmune conditions have been largely ineffective in treating vitiligo, a growing base of knowledge recently led to the first successful FDA-approved immune-modulating drugs for vitiligo. This review focuses on the immunology of vitiligo: the mechanisms that drive melanocyte destruction, the biology of aberrant T cell responses against melanocytes and therapeutic means for counteracting this autoimmune condition.
{"title":"The immunology of vitiligo.","authors":"Mary Jo Turk, Yina H Huang","doi":"10.1038/s41577-025-01249-z","DOIUrl":"https://doi.org/10.1038/s41577-025-01249-z","url":null,"abstract":"<p><p>Vitiligo is an autoimmune disease of melanocyte destruction, which manifests as progressive, patchy loss of pigmentation in the skin. As one of most common autoimmune diseases, vitiligo inflicts a significant psychosocial burden. Research over the past two decades has revealed the underlying immune mechanisms of vitiligo, with key studies combining detailed analyses of patient tissue samples with mechanistic experiments in mouse models. Vitiligo has emerged as a prototypical CD8<sup>+</sup> T cell-mediated autoimmune disease, with cooperation between innate immune cells, dendritic cells, T cells, keratinocytes and fibroblasts driving autoimmune pathology against the uniquely susceptible melanocyte target. The study of vitiligo has also revealed aspects of CD8<sup>+</sup> T cell memory and resident memory against self-antigens. This work has drawn from, and contributed to, the study of melanoma immunology. Whereas drugs used for other autoimmune conditions have been largely ineffective in treating vitiligo, a growing base of knowledge recently led to the first successful FDA-approved immune-modulating drugs for vitiligo. This review focuses on the immunology of vitiligo: the mechanisms that drive melanocyte destruction, the biology of aberrant T cell responses against melanocytes and therapeutic means for counteracting this autoimmune condition.</p>","PeriodicalId":19049,"journal":{"name":"Nature Reviews Immunology","volume":" ","pages":""},"PeriodicalIF":60.9,"publicationDate":"2026-01-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145892779","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2026-01-02DOI: 10.1038/s41577-025-01263-1
Sara Lamorte, Tracy L. McGaha
A preprint by Boulat et al. reports that tumour-derived lactate blocks B cell migration from cancer-associated lymph nodes, preventing the formation of tertiary lymphoid structures in the tumour.
{"title":"Tumour lactate bars B cell entry","authors":"Sara Lamorte, Tracy L. McGaha","doi":"10.1038/s41577-025-01263-1","DOIUrl":"10.1038/s41577-025-01263-1","url":null,"abstract":"A preprint by Boulat et al. reports that tumour-derived lactate blocks B cell migration from cancer-associated lymph nodes, preventing the formation of tertiary lymphoid structures in the tumour.","PeriodicalId":19049,"journal":{"name":"Nature Reviews Immunology","volume":"26 2","pages":"87-87"},"PeriodicalIF":60.9,"publicationDate":"2026-01-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145892734","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2025-12-15DOI: 10.1038/s41577-025-01261-3
Andrew C Chan,Greg D Martyn,Paul J Carter
{"title":"Publisher Correction: Fifty years of monoclonals: the past, present and future of antibody therapeutics.","authors":"Andrew C Chan,Greg D Martyn,Paul J Carter","doi":"10.1038/s41577-025-01261-3","DOIUrl":"https://doi.org/10.1038/s41577-025-01261-3","url":null,"abstract":"","PeriodicalId":19049,"journal":{"name":"Nature Reviews Immunology","volume":"20 1","pages":""},"PeriodicalIF":100.3,"publicationDate":"2025-12-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145760092","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2025-12-09DOI: 10.1038/s41577-025-01260-4
Lucy Bird
Besides killing infected or transformed cells, interferon-activated natural killer cells can kill T follicular helper cells and may contribute to poor antibody responses in some individuals infected with SARS-CoV-2.
{"title":"NK cells limit antibody breadth","authors":"Lucy Bird","doi":"10.1038/s41577-025-01260-4","DOIUrl":"10.1038/s41577-025-01260-4","url":null,"abstract":"Besides killing infected or transformed cells, interferon-activated natural killer cells can kill T follicular helper cells and may contribute to poor antibody responses in some individuals infected with SARS-CoV-2.","PeriodicalId":19049,"journal":{"name":"Nature Reviews Immunology","volume":"26 1","pages":"3-3"},"PeriodicalIF":60.9,"publicationDate":"2025-12-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145715059","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2025-12-09DOI: 10.1038/s41577-025-01257-z
Yvonne Bordon
Respiratory infections in early life combine with genetic and maternal factors to drive asthma development in childhood.
生命早期的呼吸道感染与遗传和母亲因素相结合，推动儿童哮喘的发展。
{"title":"Parental allergy and early life infection combine to promote asthma in childhood","authors":"Yvonne Bordon","doi":"10.1038/s41577-025-01257-z","DOIUrl":"10.1038/s41577-025-01257-z","url":null,"abstract":"Respiratory infections in early life combine with genetic and maternal factors to drive asthma development in childhood.","PeriodicalId":19049,"journal":{"name":"Nature Reviews Immunology","volume":"26 1","pages":"2-2"},"PeriodicalIF":60.9,"publicationDate":"2025-12-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145710785","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
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