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Autophagy and Immunoregulation in Human Diseases

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Pathology, Diagnostics, and Therapeutics".

Deadline for manuscript submissions: closed (29 April 2024) | Viewed by 1592

Special Issue Editors


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Guest Editor
1. Departamento de Química Biológica, Facultad de Ciencias Exactas y Naturales, Universidad de Buenos Aires, Intendente Güiraldes 2160, Pabellón II, 4°piso, Ciudad Universitaria, Buenos Aires C1428EGA, Argentina
2. Instituto de Química Biológica de la Facultad de Ciencias Exactas y Naturales (IQUIBICEN), Facultad de Ciencias Exactas y Naturales, Universidad de Buenos Aires, Consejo Nacional de Investigaciones Científicas y Técnicas, Intendente Güiraldes 2160, Pabellón II, 4°piso, Ciudad Universitaria, Buenos Aires C1428EGA, Argentina
Interests: autophagy; immunoregulation; host immune response; immune evasion; signaling

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Guest Editor
Consejo Nacional de Investigaciones Científicas y Técnicas, Buenos Aires U9120ACD, Argentina
Interests: autophagy; kinase; host immune response

Special Issue Information

Dear Colleagues, 

Autophagy is an evolutionarily conserved catabolic pathway that mediates the lysosomal degradation of unwanted cytoplasmic structures and organelles, allowing eukaryotic cells to generate nutrients under starvation circumstances and maintain cellular homeostasis. Three types of autophagy have been described: chaperone-mediated autophagy, microautophagy, and macroautophagy, herein collectively referred to as autophagy. Importantly, autophagy participates in the immune response of the host against intracellular pathogens dealing with viruses or bacteria that gain access to the cytoplasm of the cell. Nevertheless, throughout evolution, the constant interaction between the autophagy pathway and pathogens allowed many pathogens to develop strategies to avoid autophagy, promoting their intracellular multiplication. Notably, autophagy constitutes an anti-inflammatory mechanism that protects against endomembrane damage triggered by several endogenous components or infectious agents, and precludes excessive inflammation. Moreover, selective autophagy modulates host immunity by turning over specific immunoregulators. In fact, the autophagy process can be modulated by diverse immunological mediators such as cytokines, lipid mediators or non-coding RNAs, among others. It has also been proposed that vaccines which may induce an autophagic response could be more successful in the prevention of several infections. Furthermore, it has been suggested that autophagy may be also considered an as adjuvant therapy in the treatment of some bacterial diseases. Therefore, improving our understanding of the connections between autophagy and host immunoregulation may have wide applications, given that the pathology accompanying several diseases involves some form of inflammation. This Special Issue welcomes the submission of original research articles and reviews on the topic “Autophagy and Immunoregulation in Human Diseases”, focused on understanding the immunoregulation of the autophagy process by the host immune system. We are interested in all aspects of in vitro and in vivo research. This Research Topic intends to provide an overview of the autophagy process and immunoregulators, focusing on the molecular strategies developed by pathogens to manipulate selective autophagy for their own benefit.

Dr. Veronica Edith Garcia
Dr. María Isabel Colombo
Guest Editors

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.

Keywords

  • autophagy
  • immunoregulation
  • pathogens
  • host immune response
  • immune evasion
  • signaling
  • non-coding RNAs
  • lipid mediators
  • cytokines
  • host defense

Published Papers (1 paper)

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Review

15 pages, 659 KiB  
Review
Cytoprotective, Cytotoxic and Cytostatic Roles of Autophagy in Response to BET Inhibitors
by Ahmed M. Elshazly and David A. Gewirtz
Int. J. Mol. Sci. 2023, 24(16), 12669; https://doi.org/10.3390/ijms241612669 - 11 Aug 2023
Cited by 4 | Viewed by 1229
Abstract
The bromodomain and extra-terminal domain (BET) family inhibitors are small molecules that target the dysregulated epigenetic readers, BRD2, BRD3, BRD4 and BRDT, at various transcription-related sites, including super-enhancers. BET inhibitors are currently under investigation both in pre-clinical cell culture and tumor-bearing animal models, [...] Read more.
The bromodomain and extra-terminal domain (BET) family inhibitors are small molecules that target the dysregulated epigenetic readers, BRD2, BRD3, BRD4 and BRDT, at various transcription-related sites, including super-enhancers. BET inhibitors are currently under investigation both in pre-clinical cell culture and tumor-bearing animal models, as well as in clinical trials. However, as is the case with other chemotherapeutic modalities, the development of resistance is likely to constrain the therapeutic benefits of this strategy. One tumor cell survival mechanism that has been studied for decades is autophagy. Although four different functions of autophagy have been identified in the literature (cytoprotective, cytotoxic, cytostatic and non-protective), primarily the cytoprotective and cytotoxic forms appear to function in different experimental models exposed to BET inhibitors (with some evidence for the cytostatic form). This review provides an overview of the cytoprotective, cytotoxic and cytostatic functions of autophagy in response to BET inhibitors in various tumor models. Our aim is to determine whether autophagy targeting or modulation could represent an effective therapeutic strategy to enhance the response to these modalities and also potentially overcome resistance to BET inhibition. Full article
(This article belongs to the Special Issue Autophagy and Immunoregulation in Human Diseases)
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