Journal Browser

► Journal Browser

Special Issue Editors

Dr. Sachin Mulik

E-Mail Website
Guest Editor

Department of Pulmonary Immunology, Center for Biomedical Research, The University of Texas Health Science Center at Tyler, Tyler, TX, USA
Interests: natural killer cells; memory NK cells

Dr. Pranay Dogra

E-Mail Website
Guest Editor

Genentech, 1 DNA Way, South San Francisco, CA 94080, USA
Interests: microbiology; immunology; epigenetics; CMV; NK cells

Dr. Nabila Jabrane-Ferrat

E-Mail Website
Guest Editor

Center for Pathophysiology of Toulouse Purpan, CNRS - Inserm - University of Toulouse, 31024 Toulouse, France
Interests: immunology; pregnancy; viral transmission

Special Issue Information

Dear Colleagues,

We invite submissions of original articles, review articles and commentaries for this Special Issue on “NK cell subsets in health and disease: new developments” in International Journal of Molecular Sciences.

This Special Issue will focus on NK cell subpopulations found in viral infections as well as other microbial contexts and tumors. The newer approaches such as single cell analysis and mass cytometry to identify NK subpopulations will be prefered. NK cell immunotherapy is an emerging cellular therapy for cancer. We also welcome research articles on novel functions of NK cells in tumors and cytokine induced memory NK and CAR NK cell-based therapies for cancer.

Dr. Sachin Mulik
Dr. Pranay Dogra
Dr. Nabila Jabrane-Ferrat
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

NK cell subsets
single cell analysis
tumor NK
virus infections
cancer
NK biology

Published Papers (2 papers)

Download All Papers

Research

Jump to: Other

20 pages, 6035 KiB

Open AccessArticle

NKG2C+ NK Cells for Immunotherapy of Glioblastoma Multiforme

by Shafiq Murad, Susanne Michen, Alexander Becker, Monika Füssel, Gabriele Schackert, Torsten Tonn, Frank Momburg and Achim Temme

Int. J. Mol. Sci. 2022, 23(10), 5857; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms23105857 - 23 May 2022

Cited by 9 | Viewed by 3485

Abstract

In glioblastoma, non-classical human leucocyte antigen E (HLA-E) and HLA-G are frequently overexpressed. HLA-E loaded with peptides derived from HLA class I and from HLA-G contributes to inhibition of natural killer (NK) cells with expression of the inhibitory receptor CD94/NKG2A. We investigated whether NK cells expressing the activating CD94/NKG2C receptor counterpart were able to exert anti-glioma effects. NKG2C+ subsets were preferentially expanded by a feeder cell line engineered to express an artificial disulfide-stabilized trimeric HLA-E ligand (HLA-E*spG). NK cells expanded by a feeder cell line, which facilitates outgrowth of conventional NKG2A+, and fresh NK cells, were included for comparison. Expansion via the HLA-E*spG feeder cells selectively increased the fraction of NKG2C+ NK cells, which displayed a higher frequency of KIR2DL2/L3/S2 and CD16 when compared to expanded NKG2A+ NK cells. NKG2C+ NK cells exhibited increased cytotoxicity against K562 and KIR:HLA-matched and -mismatched primary glioblastoma multiforme (GBM) cells when compared to NKG2A+ NK cells and corresponding fresh NK cells. Cytotoxic responses of NKG2C+ NK cells were even more pronounced when utilizing target cells engineered with HLA-E*spG. These findings support the notion that NKG2C+ NK cells have potential therapeutic value for treating gliomas. Full article

(This article belongs to the Special Issue NK Cell Subsets in Health and Disease: New Developments)

► Show Figures

Figure 1

Other

Jump to: Research

13 pages, 1007 KiB

Open AccessBrief Report

Costimulatory CD226 Signaling Regulates Proliferation of Memory-like NK Cells in Healthy Individuals with Latent Mycobacterium tuberculosis Infection

by Oscar Murillo, Josimar Dornelas Moreira, Weshely Kujur, Karen Velasco-Alzate, Sumit Sen Santara, Nagarjun V. Konduru and Sachin Mulik

Int. J. Mol. Sci. 2022, 23(21), 12838; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms232112838 - 25 Oct 2022

Viewed by 1672

Abstract

It is now widely accepted that NK cells can acquire memory, and this makes them more effective to protect against some pathogens. Prior reports indicate memory-like NK cells (mlNKs) in murine model of Mycobacterium tuberculosis (Mtb) as well as in healthy individuals with latent TB infection (LTBI). The increased expression of CD226 was evident in mlNKs from LTBI+ people after stimulation with γ-irradiated Mtb (γ-Mtb). We thus evaluated the contribution of costimulatory CD226 signaling in the functionality of mlNKs in LTBI+ people. We found that blockade of CD226 signaling using the antibody- or CRISPR/Cas9-mediated deletion of the CD226 gene in NK cells diminished the proliferation of mlNKs from LTBI+ people. Blocking CD226 signaling also reduced the phosphorylation of FOXO1 and cMyc expression. Additionally, cMyc inhibition using a chemical inhibitor reduced proliferation by mlNKs from LTBI+ people. Moreover, blocking CD226 signaling reduced glycolysis in NK cells, and the inhibition of glycolysis led to reduced effector function of mlNKs from LTBI+ people. Overall, our results provide a role for CD226 signaling in mlNK responses to Mtb. Full article

(This article belongs to the Special Issue NK Cell Subsets in Health and Disease: New Developments)

► Show Figures