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Cells
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Autophagy in Innate Immune Response and Inflammation
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Autophagy in Innate Immune Response and Inflammation

A special issue of Cells (ISSN 2073-4409). This special issue belongs to the section "Autophagy".

Deadline for manuscript submissions: closed (1 June 2023) | Viewed by 1407

Special Issue Editor

Dr. Nataša Kopitar Jerala

E-Mail Website
Guest Editor
Department of Biochemistry and Molecular and Structural Biology, Jožef Stefan Institute, 1000 Ljubljana, Slovenia
Interests: innate immune response; inflammasome; mitochondria; oxidative stress; proteinases and inhibitors
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Autophagy is a homeostatic process of sequestration of cytoplasmic components by double-membraned autophagosomes for degradation upon fusion with lysosomes.   Autophagy affects different cell types, including myeloid cells and limits inflammasome activation. Inflammation is an essential immune response of the host against pathogens , however when it is over-activated results in pathological The autophagy dysfunction can lead to diseases with inflammatory components, including metabolic disorders, infections, autoimmunity, neurodegeneration and cancer.

This Special issue aims to cover new progress in studying the roles of autophagy in the regulation of innate immune functions, inflammasome activation,  as well as diseases. Understanding how defective autophagy disrupts immune regulation to cause autoimmune, inflammatory diseases and cancer will be valuable for identifying molecular targets in the autophagy pathways for therapeutic intervention.

Dr. Nataša Kopitar Jerala
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. Cells is an international peer-reviewed open access semimonthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 2700 CHF (Swiss Francs). 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.

Keywords

  • autophagy
  • inflammation
  • inflammasome activation
  • interferon
  • mitochondria
  • lysosome

Published Papers (1 paper)

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Research

16 pages, 2693 KiB  
Article
Stefin B Inhibits NLRP3 Inflammasome Activation via AMPK/mTOR Signalling
by Mojca Trstenjak-Prebanda, Monika Biasizzo, Klemen Dolinar, Sergej Pirkmajer, Boris Turk, Veronique Brault, Yann Herault and Nataša Kopitar-Jerala
Cells 2023, 12(23), 2731; https://doi.org/10.3390/cells12232731 - 29 Nov 2023
Viewed by 1050
Abstract
Stefin B (cystatin B) is an inhibitor of lysosomal and nuclear cysteine cathepsins. The gene for stefin B is located on human chromosome 21 and its expression is upregulated in the brains of individuals with Down syndrome. Biallelic loss-of-function mutations in the stefin [...] Read more.
Stefin B (cystatin B) is an inhibitor of lysosomal and nuclear cysteine cathepsins. The gene for stefin B is located on human chromosome 21 and its expression is upregulated in the brains of individuals with Down syndrome. Biallelic loss-of-function mutations in the stefin B gene lead to Unverricht–Lundborg disease-progressive myoclonus epilepsy type 1 (EPM1) in humans. In our past study, we demonstrated that mice lacking stefin B were significantly more sensitive to sepsis induced by lipopolysaccharide (LPS) and secreted higher levels of interleukin 1-β (IL-1β) due to increased inflammasome activation in bone marrow-derived macrophages. Here, we report lower interleukin 1-β processing and caspase-11 expression in bone marrow-derived macrophages prepared from mice that have an additional copy of the stefin B gene. Increased expression of stefin B downregulated mitochondrial reactive oxygen species (ROS) generation and lowered the NLR family pyrin domain containing 3 (NLRP3) inflammasome activation in macrophages. We determined higher AMP-activated kinase phosphorylation and downregulation of mTOR activity in stefin B trisomic macrophages—macrophages with increased stefin B expression. Our study showed that increased stefin B expression downregulated mitochondrial ROS generation and increased autophagy. The present work contributes to a better understanding of the role of stefin B in regulation of autophagy and inflammasome activation in macrophages and could help to develop new treatments. Full article
(This article belongs to the Special Issue Autophagy in Innate Immune Response and Inflammation)
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