Modulation of Human Immune Parameters by Anticancer Therapies

Editorial

02 December 2020

Editorial: Modulation of Human Immune Parameters by Anticancer Therapies

Ulrich Sack

Attila Tarnok

Frank Preijers

Ulrike Köhl

and

Il-Kang Na

1,892 views

1 citations

Editors

Ulrich Sack

Leipzig University

Attila Tarnok

Fraunhofer Institute for Cell Therapy and Immunology (IZI)

Il-Kang Na

Charité University Medicine Berlin

Frank Preijers

Radboud University Medical Centre

Impact

Kinetic of tumor development in pre-, early-, and late-therapeutic period upon application of chemo- and/or radiation therapy: current situation in the clinic. (A) In the pre-therapeutic situation, heterogeneous tumors are composed of several cell types, including CSC, tumor cells, TAMs, and CAFs; all characterized by biomarkers. (B) In the early post-therapeutic period, upon application of the first-line treatment (that currently uses mostly chemo- or radiotherapeutic regimens) several important changes occur in the tumor, in particular: tumor cells or CAFs die due to the therapy or become senescent, whereas CSCs mostly survive the treatment. Senescent cells (tumor cells and CAFs) attract immune cells toward the senescent site via SASP. The SASP therefore plays a positive role and attracts immune cells in this early post-therapeutic situation. Attracted immune cells promote the clearance of dead, of necrotic, and senescent tumor cells and CAFs. (C) In the late post-therapeutic situation uncleared senescent tumor cells and senescent CAFs and SASP thereof play a negative (pro-tumorigenic) role and support tumor development. SASP molecules provide stimulating factors for CSCs for further uncontrolled proliferation as well as their maintenance. Also, remaining senescent tumor cells acquire additional mutations that promote activation of a stemness phenotype and finally a tumor relapse.

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CXCL10 expression is positively correlated with survival and expression of T lymphocyte markers in patients with GC. (A) Kaplan-Meier analysis of overall survival in GC patients with high CXCL10 expression and low CXCL10 expression (P = 0.0078, n = 438). (B) Kaplan-Meier analysis of relapse free survival in GC patients with high CXCL10 expression and low CXCL10 expression (P = 0.029, n = 320 and 321, respectively). (C–G) Scatter plots showing the correlation of CXCL10 with CD3D (C), CD3E (D), CD3G (E), CD4 (F), and CD8 (G) (Spearman's correlation test).

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TNF-α induces MACC1 via c-Jun/AP1. (A) HCT116 cells were transiently transfected with the MACC1 promoter reporter plasmids with either mutated AP-1 or Sp1 transcription factor binding sites along with a renilla luciferase control plasmid for 24 h. Cells were then treated with increasing concentrations of TNF-α. After 24 h of TNF-α treatment luciferase activity was measured and normalized to renilla luciferase activity. (B,C) HCT116 cells were transfected with the target-specific predesigned c-Jun siRNA or scrambled control siRNA for 24 h. Cells were then stimulated with increasing concentrations of TNF-α for another 24 h. Cells without TNF-α treatment served as controls. Cells were analyzed to assess the c-Jun and MACC1 mRNA and protein expression levels using qRT-PCR and Western blotting, respectively. The data is presented as mean ± SEM with the statistical significance levels: **p ≤ 0.01, ***p ≤ 0.001, and ****p ≤ 0.0001.

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Representative image of different dimensionality reduction techniques that are widely used in single cell studies. As shown by analyzing freely available scRNA-seq dataset (3k PBMC, from 10X Genomics), UMAP preserves much of the local and more of the global data structure, highlighting its ability to resolve even subtly differing cell population. From left to right PCA, t-SNE, UMAP.

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