Search for Articles:
Title / Keyword
Author / Affiliation / Email
Journal
Article Type
 
 
Advanced Search
 
Section
Special Issue
Volume
Issue
Number
Page
 
8.1
4.9
Journals
IJMS
Special Issues
Autophagy in Immune-Mediated Disease
ijms-logo
Submit to IJMS Review for IJMS Propose a Special Issue

Journal Menu

► Journal Menu

Journal Browser

► Journal Browser
share announcement

Autophagy in Immune-Mediated Disease

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Immunology".

Deadline for manuscript submissions: closed (30 June 2023) | Viewed by 7858

Special Issue Editor

Prof. Dr. Renate Kain

E-Mail Website
Guest Editor
Department of Pathology, Medical University Vienna, 1090 Vienna, Austria
Interests: autoimmune and inflammatory diseases

Special Issue Information

Dear Colleagues,

Autophagy summarizes evolutionarily conserved and ordered cellular machineries designed to degrade cytoplasmic proteins and organelles. Three distinct types of autophagy have been described, namely macroautophagy, chaperone-mediated autophagy, and microautophagy. Initially described as means for cells to dispose of or recycle cytoplasmic contents or defective organelles, the essential and diverse roles of autophagy in cellular functions, including immunity and inflammation, are now firmly established. Autophagic pathways critically modulate immune cell function and responses that are dysregulated in auto-immune disorders. Moreover, polymorphisms of autophagy genes have been linked to the susceptibility of various auto-immune disorders, including systemic lupus erythematosus and inflammatory bowel disease. These observations strongly support the role of autophagy in auto-immune diseases and potentially open venues for new therapeutic approaches, such as autophagy modulators.  

In this Special Issue on “Autophagy in Immune-Related disease”, we will welcome a selection of original articles and reviews covering basic and translational research on autophagy and its contribution to auto-immune disorders. The distinct forms of autophagy will be embraced, and their contribution, protective or pathogenic, will be investigated. Furthermore, we will focus on the role of autophagy in immunomodulation and the contribution of its dysregulation to the development of auto-immune-related diseases. Finally, the potential of autophagy modulators as new therapeutic agents will also be explored.  

Dr. Virginie Hubert ([email protected]), whose central research interest is CMA and who is a Member of the Advice in Science of the “Women in Autophagy” Network, is serving as co-Guest Editor and will assist Prof. Renate Kain on managing this Issue.

Prof. Dr. Renate Kain
Guest Editor

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All submissions that pass pre-check are peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.

Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. International Journal of Molecular Sciences is an international peer-reviewed open access semimonthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. There is an Article Processing Charge (APC) for publication in this open access journal. For details about the APC please see here. Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Benefits of Publishing in a Special Issue

  • Ease of navigation: Grouping papers by topic helps scholars navigate broad scope journals more efficiently.
  • Greater discoverability: Special Issues support the reach and impact of scientific research. Articles in Special Issues are more discoverable and cited more frequently.
  • Expansion of research network: Special Issues facilitate connections among authors, fostering scientific collaborations.
  • External promotion: Articles in Special Issues are often promoted through the journal's social media, increasing their visibility.
  • e-Book format: Special Issues with more than 10 articles can be published as dedicated e-books, ensuring wide and rapid dissemination.

Further information on MDPI's Special Issue polices can be found here.

Published Papers (3 papers)

Download All Papers
Order results
Result details
Show export options expand_more Show export options expand_less
Select all
Export citation of selected articles as:

Research

Jump to: Review

14 pages, 6918 KiB  
Article
Effect of Lacking ZKSCAN3 on Autophagy, Lysosomal Biogenesis and Senescence
by Xiao-Min Li, Jun-Hao Wen, Ze-Sen Feng, Yun-Shan Wu, Dong-Yi Li, Shan Liang, Dan Wu, Hong-Luan Wu, Shang-Mei Li, Zhen-Nan Ye, Chen Yang, Lin Sun, Ji-Xin Tang and Hua-Feng Liu
Int. J. Mol. Sci. 2023, 24(9), 7786; https://doi.org/10.3390/ijms24097786 - 24 Apr 2023
Cited by 2 | Viewed by 2078
Abstract
Transcription factors can affect autophagy activity by promoting or inhibiting the expression of autophagic and lysosomal genes. As a member of the zinc finger family DNA-binding proteins, ZKSCAN3 has been reported to function as a transcriptional repressor of autophagy, silencing of which can [...] Read more.
Transcription factors can affect autophagy activity by promoting or inhibiting the expression of autophagic and lysosomal genes. As a member of the zinc finger family DNA-binding proteins, ZKSCAN3 has been reported to function as a transcriptional repressor of autophagy, silencing of which can induce autophagy and promote lysosomal biogenesis in cancer cells. However, studies in Zkscan3 knockout mice showed that the deficiency of ZKSCAN3 did not induce autophagy or increase lysosomal biogenesis. In order to further explore the role of ZKSCAN3 in the transcriptional regulation of autophagic genes in human cancer and non-cancer cells, we generated ZKSCAN3 knockout HK-2 (non-cancer) and Hela (cancer) cells via the CRISPR/Cas9 system and analyzed the differences in gene expression between ZKSCAN3 deleted cells and non-deleted cells through fluorescence quantitative PCR, western blot and transcriptome sequencing, with special attention to the differences in expression of autophagic and lysosomal genes. We found that ZKSCAN3 may be a cancer-related gene involved in cancer progression, but not an essential transcriptional repressor of autophagic or lysosomal genes, as the lacking of ZKSCAN3 cannot significantly promote the expression of autophagic and lysosomal genes. Full article
(This article belongs to the Special Issue Autophagy in Immune-Mediated Disease)
►▼ Show Figures

Figure 1

19 pages, 3871 KiB  
Article
SIRT1 Promotes Host Protective Immunity against Toxoplasma gondii by Controlling the FoxO-Autophagy Axis via the AMPK and PI3K/AKT Signalling Pathways
by Jina Lee, Jinju Kim, Jae-Hyung Lee, Yong Min Choi, Hyeonil Choi, Hwan-Doo Cho, Guang-Ho Cha, Young-Ha Lee, Eun-Kyeong Jo, Byung-Hyun Park and Jae-Min Yuk
Int. J. Mol. Sci. 2022, 23(21), 13578; https://doi.org/10.3390/ijms232113578 - 5 Nov 2022
Cited by 9 | Viewed by 3044
Abstract
Sirtuin 1 (SIRT1) regulates cellular processes by deacetylating non-histone targets, including transcription factors and intracellular signalling mediators; thus, its abnormal activation is closely linked to the pathophysiology of several diseases. However, its function in Toxoplasma gondii infection is unclear. We found that SIRT1 [...] Read more.
Sirtuin 1 (SIRT1) regulates cellular processes by deacetylating non-histone targets, including transcription factors and intracellular signalling mediators; thus, its abnormal activation is closely linked to the pathophysiology of several diseases. However, its function in Toxoplasma gondii infection is unclear. We found that SIRT1 contributes to autophagy activation via the AMP-activated protein kinase (AMPK) and PI3K/AKT signalling pathways, promoting anti-Toxoplasma responses. Myeloid-specific Sirt1−/− mice exhibited an increased cyst burden in brain tissue compared to wild-type mice following infection with the avirulent ME49 strain. Consistently, the intracellular survival of T. gondii was markedly increased in Sirt1-deficient bone-marrow-derived macrophages (BMDMs). In contrast, the activation of SIRT1 by resveratrol resulted in not only the induction of autophagy but also a significantly increased anti-Toxoplasma effect. Notably, SIRT1 regulates the FoxO-autophagy axis in several human diseases. Importantly, the T. gondii-induced phosphorylation, acetylation, and cytosolic translocation of FoxO1 was enhanced in Sirt1-deficient BMDMs and the pharmacological inhibition of PI3K/AKT signalling reduced the cytosolic translocation of FoxO1 in BMDMs infected with T. gondii. Further, the CaMKK2-dependent AMPK signalling pathway is responsible for the effect of SIRT1 on the FoxO3a-autophagy axis and for its anti-Toxoplasma activity. Collectively, our findings reveal a previously unappreciated role for SIRT1 in Toxoplasma infection. Full article
(This article belongs to the Special Issue Autophagy in Immune-Mediated Disease)
►▼ Show Figures

Figure 1

Review

Jump to: Research

16 pages, 1506 KiB  
Review
Harnessing Autophagy to Overcome Antigen-Specific T-Cell Dysfunction: Implication for People Living with HIV-1
by Nazanin Ghahari, Roman Telittchenko, Hamza Loucif, Stephane Isnard, Jean-Pierre Routy, David Olagnier and Julien van Grevenynghe
Int. J. Mol. Sci. 2023, 24(13), 11018; https://doi.org/10.3390/ijms241311018 - 3 Jul 2023
Cited by 1 | Viewed by 1889
Abstract
Like other chronic viral infections, HIV-1 persistence inhibits the development of antigen-specific memory T-cells, resulting in the exhaustion of the immune response and chronic inflammation. Autophagy is a major lysosome-dependent mechanism of intracellular large-target degradation such as lipid and protein aggregates, damaged organelles, [...] Read more.
Like other chronic viral infections, HIV-1 persistence inhibits the development of antigen-specific memory T-cells, resulting in the exhaustion of the immune response and chronic inflammation. Autophagy is a major lysosome-dependent mechanism of intracellular large-target degradation such as lipid and protein aggregates, damaged organelles, and intracellular pathogens. Although it is known that autophagy may target HIV-1 for elimination, knowledge of its function as a metabolic contributor in such viral infection is only in its infancy. Recent data show that elite controllers (EC), who are HIV-1-infected subjects with natural and long-term antigen (Ag)-specific T-cell protection against the virus, are characterized by distinct metabolic autophagy-dependent features in their T-cells compared to other people living with HIV-1 (PLWH). Despite durable viral control with antiretroviral therapy (ART), HIV-1-specific immune dysfunction does not normalize in non-controller PLWH. Therefore, the hypothesis of inducing autophagy to strengthen their Ag-specific T-cell immunity against HIV-1 starts to be an enticing concept. The aim of this review is to critically analyze promises and potential limitations of pharmacological and dietary interventions to activate autophagy in an attempt to rescue Ag-specific T-cell protection among PLWH. Full article
(This article belongs to the Special Issue Autophagy in Immune-Mediated Disease)
►▼ Show Figures

Figure 1

Show export options expand_more Show export options expand_less
Select all
Export citation of selected articles as:
 
Displaying articles 1-3
Back to TopTop