Parasite-Mediated Immune Responses
A special issue of Vaccines (ISSN 2076-393X). This special issue belongs to the section "Vaccines against Tropical and other Infectious Diseases".
Deadline for manuscript submissions: closed (30 September 2023) | Viewed by 2665
Special Issue Editor
Special Issue Information
Dear Colleagues,
Malaria infection induces complex and diverse immune responses. The emergence of multi-drug resistance (MDR) highlights the importance of discovering novel targets/drugs to combat malaria. One target drug which is currently most explored is the “host and parasite’s ubiquitin system”. Ubiquitination, similar to phosphorylation, is an elaborated post-translational modification process that regulates a wide spectrum of cellular functions, including protein degradation through proteasomal degradation machinery, endocytosis, cell cycle progression, DNA repair, sorting and trafficking of transmembrane proteins, transcriptional regulation, and immune signaling, and is associated with various diseases. E3 ubiquitin ligase regulates parasite growth and host virulence by generating different immune responses. One of the hosts, E3 ubiquitin ligase (March1), clustered with interferon (IFN)-stimulated genes, inhibits MAVS/STING/TRIF-induced type I IFN (IFN-I) signaling in vitro and in vivo and reduces IFN-I production by activating inhibitors such as SOCS1, USP18, and TRIM24. It alters immune cell populations in malaria-infected (Plasmodium yoelii) hosts in March1 deficiency. Its deficiency increases CD86+ DC (dendritic cell) populations and levels of IFN-γ and interleukin 10 (IL-10) post-infection, leading to improved host survival. Another ubiquitin ligase (March8) suppressed the binding of cGAS to DNA, resulting in the inhibition of the production of cGAMP and type I IFN and enhancing the interaction of March8 with cGAS which may be a strategy to treat some autoimmune diseases. Thus, E3 ligase functions in innate immune responses and provides potential avenues for activating antiparasitic immunity and enhancing vaccine efficacy.
This Special Issue welcomes the submission of original articles, systematic reviews, communications, and other types of articles on related topics. The research areas may include, but are not limited to, the following: Immunity, IFN signaling, T cell, ubiquitination, E3 ligase, drug target, and vaccine efficacy. We look forward to receiving your contributions.
Dr. Brajesh Kumar Singh
Guest Editor
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Keywords
- immunity
- IFN signaling
- T cell
- ubiquitination
- E3 ligase
- drug target
- vaccine efficacy
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