دورية أكاديمية
أعرض في EDS

γδ T cells are effectors of immunotherapy in cancers with HLA class I defects.

التفاصيل البيبلوغرافية
العنوان: γδ T cells are effectors of immunotherapy in cancers with HLA class I defects.
المؤلفون: de Vries NL; Department of Pathology, Leiden University Medical Center, Leiden, The Netherlands.; Department of Immunology, Leiden University Medical Center, Leiden, The Netherlands., van de Haar J; Department of Molecular Oncology and Immunology, Netherlands Cancer Institute, Amsterdam, The Netherlands.; Oncode Institute, Utrecht, The Netherlands.; Division of Molecular Carcinogenesis, Netherlands Cancer Institute, Amsterdam, The Netherlands., Veninga V; Department of Molecular Oncology and Immunology, Netherlands Cancer Institute, Amsterdam, The Netherlands.; Oncode Institute, Utrecht, The Netherlands., Chalabi M; Department of Molecular Oncology and Immunology, Netherlands Cancer Institute, Amsterdam, The Netherlands.; Gastrointestinal Oncology, Netherlands Cancer Institute, Amsterdam, The Netherlands.; Medical Oncology, Netherlands Cancer Institute, Amsterdam, The Netherlands., Ijsselsteijn ME; Department of Pathology, Leiden University Medical Center, Leiden, The Netherlands., van der Ploeg M; Department of Pathology, Leiden University Medical Center, Leiden, The Netherlands., van den Bulk J; Department of Pathology, Leiden University Medical Center, Leiden, The Netherlands., Ruano D; Department of Pathology, Leiden University Medical Center, Leiden, The Netherlands., van den Berg JG; Department of Pathology, Netherlands Cancer Institute, Amsterdam, The Netherlands., Haanen JB; Department of Molecular Oncology and Immunology, Netherlands Cancer Institute, Amsterdam, The Netherlands.; Medical Oncology, Netherlands Cancer Institute, Amsterdam, The Netherlands., Zeverijn LJ; Department of Molecular Oncology and Immunology, Netherlands Cancer Institute, Amsterdam, The Netherlands.; Oncode Institute, Utrecht, The Netherlands., Geurts BS; Department of Molecular Oncology and Immunology, Netherlands Cancer Institute, Amsterdam, The Netherlands.; Oncode Institute, Utrecht, The Netherlands., de Wit GF; Department of Molecular Oncology and Immunology, Netherlands Cancer Institute, Amsterdam, The Netherlands.; Oncode Institute, Utrecht, The Netherlands., Battaglia TW; Department of Molecular Oncology and Immunology, Netherlands Cancer Institute, Amsterdam, The Netherlands.; Oncode Institute, Utrecht, The Netherlands., Gelderblom H; Department of Medical Oncology, Leiden University Medical Center, Leiden, The Netherlands., Verheul HMW; Department of Medical Oncology, Erasmus MC, Rotterdam, The Netherlands., Schumacher TN; Department of Molecular Oncology and Immunology, Netherlands Cancer Institute, Amsterdam, The Netherlands.; Oncode Institute, Utrecht, The Netherlands.; Department of Hematology, Leiden University Medical Center, Leiden, The Netherlands., Wessels LFA; Oncode Institute, Utrecht, The Netherlands.; Division of Molecular Carcinogenesis, Netherlands Cancer Institute, Amsterdam, The Netherlands.; Faculty of EEMCS, Delft University of Technology, Delft, The Netherlands., Koning F; Department of Immunology, Leiden University Medical Center, Leiden, The Netherlands., de Miranda NFCC; Department of Pathology, Leiden University Medical Center, Leiden, The Netherlands. n.f.de_miranda@lumc.nl., Voest EE; Department of Molecular Oncology and Immunology, Netherlands Cancer Institute, Amsterdam, The Netherlands. e.voest@nki.nl.; Oncode Institute, Utrecht, The Netherlands. e.voest@nki.nl.
المصدر: Nature [Nature] 2023 Jan; Vol. 613 (7945), pp. 743-750. Date of Electronic Publication: 2023 Jan 11.
نوع المنشور: Journal Article; Research Support, Non-U.S. Gov't
اللغة: English
بيانات الدورية: Publisher: Nature Publishing Group Country of Publication: England NLM ID: 0410462 Publication Model: Print-Electronic Cited Medium: Internet ISSN: 1476-4687 (Electronic) Linking ISSN: 00280836 NLM ISO Abbreviation: Nature Subsets: MEDLINE
أسماء مطبوعة: Publication: Basingstoke : Nature Publishing Group
Original Publication: London, Macmillan Journals ltd.
مواضيع طبية MeSH: Colonic Neoplasms*/drug therapy , Colonic Neoplasms*/genetics , Colonic Neoplasms*/immunology , Colonic Neoplasms*/therapy , Histocompatibility Antigens Class I*/genetics , Histocompatibility Antigens Class I*/immunology , Immune Checkpoint Inhibitors*/pharmacology , Immune Checkpoint Inhibitors*/therapeutic use , Immunotherapy* , Receptors, Antigen, T-Cell, gamma-delta*/immunology , T-Lymphocytes*/immunology , Genes, MHC Class I*/genetics, Humans ; beta 2-Microglobulin/deficiency ; beta 2-Microglobulin/genetics ; DNA Mismatch Repair/genetics ; Receptors, KIR ; Cell Line, Tumor ; Organoids ; Antigen Presentation
مستخلص: DNA mismatch repair-deficient (MMR-d) cancers present an abundance of neoantigens that is thought to explain their exceptional responsiveness to immune checkpoint blockade (ICB) 1,2 . Here, in contrast to other cancer types 3-5 , we observed that 20 out of 21 (95%) MMR-d cancers with genomic inactivation of β2-microglobulin (encoded by B2M) retained responsiveness to ICB, suggesting the involvement of immune effector cells other than CD8 + T cells in this context. We next identified a strong association between B2M inactivation and increased infiltration by γδ T cells in MMR-d cancers. These γδ T cells mainly comprised the Vδ1 and Vδ3 subsets, and expressed high levels of PD-1, other activation markers, including cytotoxic molecules, and a broad repertoire of killer-cell immunoglobulin-like receptors. In vitro, PD-1 + γδ T cells that were isolated from MMR-d colon cancers exhibited enhanced reactivity to human leukocyte antigen (HLA)-class-I-negative MMR-d colon cancer cell lines and B2M-knockout patient-derived tumour organoids compared with antigen-presentation-proficient cells. By comparing paired tumour samples from patients with MMR-d colon cancer that were obtained before and after dual PD-1 and CTLA-4 blockade, we found that immune checkpoint blockade substantially increased the frequency of γδ T cells in B2M-deficient cancers. Taken together, these data indicate that γδ T cells contribute to the response to immune checkpoint blockade in patients with HLA-class-I-negative MMR-d colon cancers, and underline the potential of γδ T cells in cancer immunotherapy.
(© 2023. The Author(s).)
التعليقات: Comment in: Nat Rev Immunol. 2023 Mar;23(3):137. doi: 10.1038/s41577-023-00842-4. (PMID: 36726035)
Comment in: Nat Immunol. 2023 Mar;24(3):387-388. doi: 10.1038/s41590-023-01429-w. (PMID: 36781987)
Comment in: Med. 2023 Mar 10;4(3):141-142. doi: 10.1016/j.medj.2023.02.007. (PMID: 36905925)
References: Sci Rep. 2015 Aug 26;5:13321. (PMID: 26306458)
Oncoimmunology. 2015 Jan 22;4(3):e992749. (PMID: 25949914)
Curr Biol. 1996 Dec 1;6(12):1695-7. (PMID: 8994836)
Bioinformatics. 2013 Jan 1;29(1):15-21. (PMID: 23104886)
Nat Rev Cancer. 2020 Apr;20(4):218-232. (PMID: 32024970)
Nat Biotechnol. 2011 Jan;29(1):24-6. (PMID: 21221095)
Nat Cancer. 2022 Jun;3(6):696-709. (PMID: 35637401)
Am J Pathol. 1999 Jun;154(6):1805-13. (PMID: 10362805)
Immunity. 2019 Aug 20;51(2):411-412. (PMID: 31433971)
Nature. 1993 Jun 10;363(6429):558-61. (PMID: 8505985)
J Exp Med. 1996 Apr 1;183(4):1681-96. (PMID: 8666926)
Gut. 2020 Apr;69(4):691-703. (PMID: 31270164)
Eur J Immunol. 1997 Nov;27(11):2812-21. (PMID: 9394804)
Cancer Discov. 2017 Dec;7(12):1420-1435. (PMID: 29025772)
Cell Genom. 2022 Mar 22;2(4):100112. (PMID: 36776527)
Nat Commun. 2017 Oct 26;8(1):1136. (PMID: 29070816)
Cancer Discov. 2021 Jul;11(7):1844-1859. (PMID: 33653693)
IEEE Trans Vis Comput Graph. 2021 Jan;27(1):98-110. (PMID: 31369380)
Nat Biotechnol. 2012 May;30(5):413-21. (PMID: 22544022)
Cancer Cell. 2018 Apr 9;33(4):676-689.e3. (PMID: 29622463)
Cytometry A. 2021 Dec;99(12):1187-1197. (PMID: 34196108)
JCI Insight. 2019 Dec 19;4(24):. (PMID: 31689241)
Science. 1998 Mar 13;279(5357):1737-40. (PMID: 9497295)
BMC Cancer. 2007 Feb 22;7:33. (PMID: 17316446)
Nat Protoc. 2020 Jan;15(1):15-39. (PMID: 31853056)
Nature. 2017 Dec 7;552(7683):116-120. (PMID: 29186113)
Nat Methods. 2017 Sep;14(9):865-868. (PMID: 28759029)
Clin Cancer Res. 2014 Oct 1;20(19):5064-74. (PMID: 24714771)
Cancer Res. 2005 Jul 15;65(14):6418-24. (PMID: 16024646)
JCO Precis Oncol. 2019;3:. (PMID: 31008436)
Nat Rev Cancer. 2019 Jul;19(7):392-404. (PMID: 31209264)
J Immunother Cancer. 2017 Feb 21;5:18. (PMID: 28239471)
Cancer Discov. 2021 Sep;11(9):2168-2185. (PMID: 33846173)
Nat Methods. 2019 Dec;16(12):1226-1232. (PMID: 31570887)
Nucleic Acids Res. 2015 Apr 20;43(7):e47. (PMID: 25605792)
Nat Commun. 2018 Jul 13;9(1):2724. (PMID: 30006565)
J Exp Med. 1989 Apr 1;169(4):1277-94. (PMID: 2564416)
Nat Med. 2020 Sep;26(9):1468-1479. (PMID: 32778827)
Cancer Immunol Immunother. 2013 Mar;62(3):571-83. (PMID: 23100099)
Nat Methods. 2020 Mar;17(3):261-272. (PMID: 32015543)
Nature. 2014 Nov 27;515(7528):568-71. (PMID: 25428505)
Clin Cancer Res. 2016 Dec 1;22(23):5795-5804. (PMID: 27307596)
J Clin Oncol. 2018 Mar 10;36(8):773-779. (PMID: 29355075)
Pathology. 2010;42(5):409-13. (PMID: 20632815)
Nat Med. 2020 Apr;26(4):566-576. (PMID: 32251400)
Cell. 2018 Sep 6;174(6):1586-1598.e12. (PMID: 30100188)
Nature. 2019 Nov;575(7781):210-216. (PMID: 31645765)
Bioinformatics. 2010 Jan 1;26(1):139-40. (PMID: 19910308)
Nat Methods. 2019 Jul;16(7):619-626. (PMID: 31209384)
Nat Biotechnol. 2018 Jun;36(5):421-427. (PMID: 29608177)
Sci Transl Med. 2019 Oct 9;11(513):. (PMID: 31597756)
Genome Biol. 2014 Feb 03;15(2):R29. (PMID: 24485249)
Front Immunol. 2017 Jun 30;8:776. (PMID: 28713391)
Cell. 2019 Jun 13;177(7):1888-1902.e21. (PMID: 31178118)
Lancet Oncol. 2017 Sep;18(9):1182-1191. (PMID: 28734759)
Front Immunol. 2019 Oct 29;10:2534. (PMID: 31736961)
Proc Natl Acad Sci U S A. 1999 Jun 8;96(12):6879-84. (PMID: 10359807)
Br J Cancer. 2019 Apr;120(8):815-818. (PMID: 30862951)
Proc Natl Acad Sci U S A. 1997 Mar 4;94(5):1896-901. (PMID: 9050876)
Nat Med. 2016 Nov;22(11):1342-1350. (PMID: 27694933)
Cancer Res. 2004 Dec 15;64(24):9172-9. (PMID: 15604289)
N Engl J Med. 2016 Sep 1;375(9):819-29. (PMID: 27433843)
Science. 2017 Jul 28;357(6349):409-413. (PMID: 28596308)
Nature. 2019 Oct;574(7776):127-131. (PMID: 31570881)
Genome Biol. 2006;7(10):R100. (PMID: 17076895)
المشرفين على المادة: 0 (Histocompatibility Antigens Class I)
0 (Immune Checkpoint Inhibitors)
0 (Receptors, Antigen, T-Cell, gamma-delta)
0 (beta 2-Microglobulin)
0 (PDCD1 protein, human)
0 (Receptors, KIR)
0 (CTLA4 protein, human)
SCR Disease Name: Turcot syndrome
تواريخ الأحداث: Date Created: 20230111 Date Completed: 20230201 Latest Revision: 20240912
رمز التحديث: 20240912
مُعرف محوري في PubMed: PMC9876799
DOI: 10.1038/s41586-022-05593-1
PMID: 36631610
قاعدة البيانات: MEDLINE
الوصف
تدمد:1476-4687
DOI:10.1038/s41586-022-05593-1