دورية أكاديمية
Soluble CD72, is a T-cell activator probably via binding to CD6 in homeostasis and autoimmunity.
العنوان: | Soluble CD72, is a T-cell activator probably via binding to CD6 in homeostasis and autoimmunity. |
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المؤلفون: | Eiza N; The Proteomic Unit, Bnai Zion Medical Center, Haifa, Israel.; The Rappaport Faculty of Medicine, Technion, Israel Institute of Technology, Haifa, Israel., Sabag A; The Proteomic Unit, Bnai Zion Medical Center, Haifa, Israel., Kessler O; The Rappaport Faculty of Medicine, Technion, Israel Institute of Technology, Haifa, Israel., Toubi E; The Proteomic Unit, Bnai Zion Medical Center, Haifa, Israel., Vadasz Z; The Proteomic Unit, Bnai Zion Medical Center, Haifa, Israel.; The Rappaport Faculty of Medicine, Technion, Israel Institute of Technology, Haifa, Israel. |
المصدر: | Frontiers in immunology [Front Immunol] 2024 Jul 04; Vol. 15, pp. 1367120. Date of Electronic Publication: 2024 Jul 04 (Print Publication: 2024). |
نوع المنشور: | Journal Article |
اللغة: | English |
بيانات الدورية: | Publisher: Frontiers Research Foundation] Country of Publication: Switzerland NLM ID: 101560960 Publication Model: eCollection Cited Medium: Internet ISSN: 1664-3224 (Electronic) Linking ISSN: 16643224 NLM ISO Abbreviation: Front Immunol Subsets: MEDLINE |
أسماء مطبوعة: | Original Publication: [Lausanne : Frontiers Research Foundation] |
مواضيع طبية MeSH: | Lymphocyte Activation*/immunology , Autoimmunity* , CD4-Positive T-Lymphocytes*/immunology , CD4-Positive T-Lymphocytes*/metabolism , Antigens, CD*/metabolism , Antigens, CD*/immunology , Homeostasis*/immunology, Humans ; Antigens, Differentiation, T-Lymphocyte/metabolism ; Antigens, Differentiation, T-Lymphocyte/immunology ; Signal Transduction ; Cell Proliferation ; Protein Binding ; Cytokines/metabolism ; Antigens, Differentiation, B-Lymphocyte |
مستخلص: | Background: CD72 is a highly required regulatory molecule in B cells. Its sufficient expression is crucial for maintaining self-tolerance. In contrast, soluble CD72 (sCD72) is reported to be increased in the serum of autoimmune diseases such as systemic lupus erythematosus and primary Sjogren's syndrome (pSS). Objective: We wanted to assess the biological effect of sCD72 on CD4 + T cells. Methods: We performed mass spectrometry and co-immunoprecipitation experiments to look for a sCD72 receptor on activated CD4 + T cells. Afterward, to explore the biological functions of sCD72, we used flow cytometry for the cytokine secretion profile, a phosphorylation assay for the signaling pathway, and a CFSE dye-based assay for cell proliferation. Results: We found and validated the sCD72 and CD6 interaction as a possible ligand-receptor interaction. We also demonstrated that sCD72 significantly increases the expression of pro-inflammatory cytokines, namely IL-17A and IFN-γ, in activated CD4 + T cells and increases the proliferation of CD4 + T cells, possibly through its activation of the SLP-76-AKT-mTOR pathway. Conclusion: The sCD72-CD6 axis on activated CD4 + T cells is probably a new signaling pathway in the induction of immune-mediated diseases. Therefore, targeting sCD72 may become a valuable therapeutic tool in some autoimmune disorders. Competing Interests: The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest. (Copyright © 2024 Eiza, Sabag, Kessler, Toubi and Vadasz.) |
References: | Immunity. 2000 Nov;13(5):621-31. (PMID: 11114375) Sci Rep. 2022 Dec 9;12(1):21319. (PMID: 36494415) J Exp Med. 2016 Jul 25;213(8):1387-97. (PMID: 27377588) J Autoimmun. 2022 Oct;132:102870. (PMID: 35872102) Trends Immunol. 2004 Oct;25(10):543-50. (PMID: 15364057) Immune Netw. 2019 Feb 13;19(1):e1. (PMID: 30838156) Curr Drug Targets. 2016;17(6):619-29. (PMID: 26302795) BMC Immunol. 2020 Apr 19;21(1):21. (PMID: 32306893) Proc Natl Acad Sci U S A. 2017 Mar 7;114(10):2687-2692. (PMID: 28209777) Int Immunol. 2005 Oct;17(10):1277-82. (PMID: 16113236) J Exp Med. 2016 Nov 14;213(12):2691-2706. (PMID: 27810925) J Autoimmun. 2010 Dec;35(4):336-41. (PMID: 20810246) Tissue Antigens. 2004 Mar;63(3):255-9. (PMID: 14989715) Clin Immunol. 2016 Mar;164:114-8. (PMID: 26883681) J Immunol. 2000 Feb 1;164(3):1223-9. (PMID: 10640734) Semin Arthritis Rheum. 2014 Jun;43(6):767-71. (PMID: 24461079) Ann Indian Acad Neurol. 2016 Oct-Dec;19(4):491-494. (PMID: 27994359) Inflamm Res. 2023 Feb;72(2):313-328. (PMID: 36538077) J Immunol. 1989 Oct 15;143(8):2439-47. (PMID: 2794503) J Immunol. 1998 May 15;160(10):4662-5. (PMID: 9590210) Cells. 2020 Dec 03;9(12):. (PMID: 33287301) Iran J Immunol. 2020 Dec;17(4):324-332. (PMID: 33382389) Expert Rev Clin Immunol. 2019 Jun;15(6):629-637. (PMID: 30874446) Autoimmunity. 2007 Feb;40(1):9-15. (PMID: 17364492) Neurology. 1986 Jun;36(6):777-84. (PMID: 3486383) Arthritis Rheumatol. 2020 Sep;72(9):1505-1513. (PMID: 32307907) Autoimmun Rev. 2018 May;17(5):493-503. (PMID: 29526637) Trends Mol Med. 2017 Jul;23(7):615-635. (PMID: 28623084) J Neuroimmunol. 2014 Nov 15;276(1-2):98-103. (PMID: 25216742) J Clin Invest. 2022 Jan 4;132(1):. (PMID: 34981775) BioDrugs. 2013 Jun;27(3):191-202. (PMID: 23568178) |
فهرسة مساهمة: | Keywords: CD6; T cells; autoimmunity; cytokines; signaling; soluble CD72 |
المشرفين على المادة: | 0 (Antigens, CD) 0 (CD72 protein, human) 0 (Antigens, Differentiation, T-Lymphocyte) 0 (CD6 antigen) 0 (Cytokines) 0 (Antigens, Differentiation, B-Lymphocyte) |
تواريخ الأحداث: | Date Created: 20240719 Date Completed: 20240719 Latest Revision: 20240720 |
رمز التحديث: | 20240720 |
مُعرف محوري في PubMed: | PMC11254670 |
DOI: | 10.3389/fimmu.2024.1367120 |
PMID: | 39026665 |
قاعدة البيانات: | MEDLINE |
تدمد: | 1664-3224 |
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DOI: | 10.3389/fimmu.2024.1367120 |