دورية أكاديمية
أعرض في EDS

RACK1 enhances STAT3 stability and promotes T follicular helper cell development and function during blood-stage Plasmodium infection in mice.

التفاصيل البيبلوغرافية
العنوان: RACK1 enhances STAT3 stability and promotes T follicular helper cell development and function during blood-stage Plasmodium infection in mice.
المؤلفون: Cheng Q; Beijing Institute of Basic Medical Sciences, Beijing, China., Yang X; Beijing Institute of Basic Medical Sciences, Beijing, China., Zou T; Beijing Institute of Basic Medical Sciences, Beijing, China., Sun L; Shanghai Immune Therapy Institute, Shanghai Jiao Tong University School of Medicine-Affiliated Renji Hospital, Shanghai, China., Zhang X; Beijing Institute of Basic Medical Sciences, Beijing, China., Deng L; Beijing Institute of Basic Medical Sciences, Beijing, China., Wu M; Beijing Institute of Basic Medical Sciences, Beijing, China., Gai W; Beijing Institute of Basic Medical Sciences, Beijing, China., Jiang H; Beijing Institute of Basic Medical Sciences, Beijing, China., Guo T; Beijing Institute of Basic Medical Sciences, Beijing, China., Lu Y; Beijing Institute of Basic Medical Sciences, Beijing, China., Dong J; Beijing Institute of Basic Medical Sciences, Beijing, China., Niu C; Beijing Institute of Basic Medical Sciences, Beijing, China., Pan W; Department of Tropical Diseases, Navy Medical University, Shanghai, China., Zhang J; Beijing Institute of Basic Medical Sciences, Beijing, China.; Chinese Institute for Brain Research, Beijing, China.
المصدر: PLoS pathogens [PLoS Pathog] 2024 Jul 18; Vol. 20 (7), pp. e1012352. Date of Electronic Publication: 2024 Jul 18 (Print Publication: 2024).
نوع المنشور: Journal Article
اللغة: English
بيانات الدورية: Publisher: Public Library of Science Country of Publication: United States NLM ID: 101238921 Publication Model: eCollection Cited Medium: Internet ISSN: 1553-7374 (Electronic) Linking ISSN: 15537366 NLM ISO Abbreviation: PLoS Pathog Subsets: MEDLINE
أسماء مطبوعة: Original Publication: San Francisco, CA : Public Library of Science, c2005-
مواضيع طبية MeSH: Receptors for Activated C Kinase*/metabolism , STAT3 Transcription Factor*/metabolism , Malaria*/immunology , Malaria*/parasitology , Plasmodium yoelii*/immunology , Cell Differentiation* , T Follicular Helper Cells*/immunology , T Follicular Helper Cells*/metabolism, Animals ; Mice ; Mice, Inbred C57BL ; T-Lymphocytes, Helper-Inducer/immunology ; T-Lymphocytes, Helper-Inducer/metabolism ; Mice, Knockout ; Germinal Center/immunology
مستخلص: CD4+ T cells are central mediators of protective immunity to blood-stage malaria, particularly for their capacity in orchestrating germinal center reaction and generating parasite-specific high-affinity antibodies. T follicular helper (Tfh) cells are predominant CD4+ effector T cell subset implicated in these processes, yet the factors and detailed mechanisms that assist Tfh cell development and function during Plasmodium infection are largely undefined. Here we provide evidence that receptor for activated C kinase 1 (RACK1), an adaptor protein of various intracellular signals, is not only important for CD4+ T cell expansion as previously implied but also plays a prominent role in Tfh cell differentiation and function during blood-stage Plasmodium yoelii 17XNL infection. Consequently, RACK1 in CD4+ T cells contributes significantly to germinal center formation, parasite-specific IgG production, and host resistance to the infection. Mechanistic exploration detects specific interaction of RACK1 with STAT3 in P. yoelii 17XNL-responsive CD4+ T cells, ablation of RACK1 leads to defective STAT3 phosphorylation, accompanied by substantially lower amount of STAT3 protein in CD4+ T cells, whereas retroviral overexpression of RACK1 or STAT3 in RACK1-deficient CD4+ T cells greatly restores STAT3 activity and Bcl-6 expression under the Tfh polarization condition. Further analyses suggest RACK1 positively regulates STAT3 stability by inhibiting the ubiquitin-proteasomal degradation process, thus promoting optimal STAT3 activity and Bcl-6 induction during Tfh cell differentiation. These findings uncover a novel mechanism by which RACK1 participates in posttranslational regulation of STAT3, Tfh cell differentiation, and subsequent development of anti-Plasmodium humoral immunity.
Competing Interests: The authors have declared that no competing interests exist.
(Copyright: © 2024 Cheng et al. This is an open access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.)
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المشرفين على المادة: 0 (Receptors for Activated C Kinase)
0 (STAT3 Transcription Factor)
0 (Stat3 protein, mouse)
0 (RACK1 protein, mouse)
تواريخ الأحداث: Date Created: 20240718 Date Completed: 20240730 Latest Revision: 20240801
رمز التحديث: 20240801
مُعرف محوري في PubMed: PMC11288429
DOI: 10.1371/journal.ppat.1012352
PMID: 39024388
قاعدة البيانات: MEDLINE
الوصف
تدمد:1553-7374
DOI:10.1371/journal.ppat.1012352