ijms-logo

Journal Browser

Journal Browser

Antimicrobial Peptides, Cytokines, Chemokines and Danger Molecules in Immunity and Autoimmunity

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: 30 April 2024 | Viewed by 413

Special Issue Editor

Italian National Institute of Health, ISS, National Center for Global Health, 00161 Rome, Italy
Interests: autoimmunity; basic immunology; T-cell; B-cell and dendritic cell biology; transplantation; anti-infectious immune response
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Antimicrobial peptides and antimicrobial chemokines can act both as protein mediators of specific immunological and non-immunological pathways or as chemo-attractants for immune cells. It is the case of cathelicidin LL37, which has chemo-extractant roles for immune cells and also acts as a “danger signal” and stimulator of the immune response, when bound to nucleic acids, with important effects in immunity and autoimmunity. A similar role is played by CXCL4, also called platelet factor 4 (PF4), which is a chemokine with pleiotropic effector functions but also a trigger of TLR-mediated inflammation in complexes with DNA/RNA. Both LL37 and CXCL4 play a role in immunity and autoimmunity. Other cationic molecules, either produced endogenously in humans or of microbial origin, can have TLR triggering capacity if bound to nucleic acids. Interestingly, these kinds of mediators can also be post-translationally modified during inflammation. In this Research Topic, we invite original articles and reviews illustrating current research and opinions about molecules that have pleiotropic effects on immunity and the effect of their post-translational modifications on health and disease. The topic involves but is not limited to, DNA/RNA binding proteins that exert pro-inflammatory role in immunity and autoimmunity and the effect of post-translational modification on their functions during normal immune responses and in immune-mediated diseases.

Dr. Loredana Frasca
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.

Keywords

  • antimicrobial peptides
  • antimicrobial chemokines
  • immune cells
  • immune responses
  • autoimmunity

Published Papers (1 paper)

Order results
Result details
Select all
Export citation of selected articles as:

Research

23 pages, 5112 KiB  
Article
ERK1/2-CEBPB Axis-Regulated hBD1 Enhances Anti-Tuberculosis Capacity in Alveolar Type II Epithelial Cells
Int. J. Mol. Sci. 2024, 25(4), 2408; https://doi.org/10.3390/ijms25042408 - 18 Feb 2024
Viewed by 265
Abstract
Tuberculosis, caused by Mycobacterium tuberculosis (Mtb), remains a global health crisis with substantial morbidity and mortality rates. Type II alveolar epithelial cells (AEC-II) play a critical role in the pulmonary immune response against Mtb infection by secreting effector molecules such as antimicrobial peptides [...] Read more.
Tuberculosis, caused by Mycobacterium tuberculosis (Mtb), remains a global health crisis with substantial morbidity and mortality rates. Type II alveolar epithelial cells (AEC-II) play a critical role in the pulmonary immune response against Mtb infection by secreting effector molecules such as antimicrobial peptides (AMPs). Here, human β-defensin 1 (hBD1), an important AMP produced by AEC-II, has been demonstrated to exert potent anti-tuberculosis activity. HBD1 overexpression effectively inhibited Mtb proliferation in AEC-II, while mice lacking hBD1 exhibited susceptibility to Mtb and increased lung tissue inflammation. Mechanistically, in A549 cells infected with Mtb, STAT1 negatively regulated hBD1 transcription, while CEBPB was the primary transcription factor upregulating hBD1 expression. Furthermore, we revealed that the ERK1/2 signaling pathway activated by Mtb infection led to CEBPB phosphorylation and nuclear translocation, which subsequently promoted hBD1 expression. Our findings suggest that the ERK1/2-CEBPB-hBD1 regulatory axis can be a potential therapeutic target for anti-tuberculosis therapy aimed at enhancing the immune response of AEC-II cells. Full article
Show Figures

Figure 1

Back to TopTop