دورية أكاديمية

Soluble CD72, is a T-cell activator probably via binding to CD6 in homeostasis and autoimmunity.

التفاصيل البيبلوغرافية
العنوان: Soluble CD72, is a T-cell activator probably via binding to CD6 in homeostasis and autoimmunity.
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
الوصف
تدمد:1664-3224
DOI:10.3389/fimmu.2024.1367120