Table of contents

Volume 3, Issue 5, pp. 139 - 164, May 2019

Issue cover
Cover: This month in Cell Stress: Autophagy in neurological disorders. Composite image from a motor neuron (Fayette A Reynolds, Berkshire Community College Bioscience Image Library) and a photo by Johannes Plenio from Images modified by Cell Stress. The cover is published under the CC BY 4.0 license. Enlarge issue cover


The targeting of tumor-associated macrophages by vaccination

Mads Hald Andersen

page 139-140 | 10.15698/cst2019.05.185 | Full text | PDF | Abstract

Many different therapeutic strategies focus on targeting tumor-associated macrophages (TAMs), due to their vital role in creating an immune suppressive tumor microenvironment (TME) with the aim to deplete, reprogram or target the functional mediators secreted by these cells. Immune modulatory vaccination is an emerging strategy to target immune suppressive myeloid populations in the TME.  In contrast to the other clinical strategies that target TAMs, this combines both TAM depletion (through direct killing by cytotoxic T cells) and TAM reprogramming (by introducing pro-inflammatory cytokines into the immune suppressive microenvironment).


Recent progress in the role of autophagy in neurological diseases

Tian Meng, Shiyin Lin, Haixia Zhuang, Haofeng Huang, Zhengjie He, Yongquan Hu, Qing Gong and Du Feng

page 141-161 | 10.15698/cst2019.05.186 | Full text | PDF | Abstract

Autophagy (here refers to macroautophagy) is a catabolic pathway by which large protein aggregates and damaged organelles are first sequestered into a double-membraned structure called autophagosome and then delivered to lysosome for destruction. Recently, tremendous progress has been made to elucidate the molecular mechanism and functions of this essential cellular metabolic process. In addition to being either a rubbish clearing system or a cellular surviving program in response to different stresses, autophagy plays important roles in a large number of pathophysiological conditions, such as cancer, diabetes, and especially neurodegenerative disorders. Here we review recent progress in the role of autophagy in neurological diseases and discuss how dysregulation of autophagy initiation, autophagosome formation, maturation, and/or autophagosome-lysosomal fusion step contributes to the pathogenesis of these disorders in the nervous system.


Tissue-resident memory T cells orchestrate tumour-immune equilibrium

Simone L. Park, Laura K. Mackay, Jason Waithman and Thomas Gebhardt

page 162-164 | 10.15698/cst2019.05.187 | Full text | PDF | Abstract

The immune system can prevent tumour development by engaging in a process termed cancer immunosurveillance, during which immune cells such as T cells restrict tumour growth either by completely eradicating cancer cells in a process of ‘elimination’ or by suppressing cancer cell outgrowth by establishing a state of tumour-immune ‘equilibrium’. Most cancers develop within epithelial layers of tissues but circulating T cells are largely excluded from these epithelial tissue compartments in the absence of infection or overt inflammation. In contrast, CD8+ tissue-resident memory T (TRM) cells reside permanently within epithelial layers of peripheral tissues without recirculating in blood. Accumulating evidence suggests that TRM cells are found in diverse human solid cancers where they correlate with improved prognosis and can protect against tumour challenge in mice. However, the mechanisms through which these cells mediate cancer protection are poorly understood. In our recent study (Park SL et al, Nature 565(7739), 2019) we developed a melanoma model that allowed us to identify a critical role for TRM cells in the establishment and maintenance of tumour-immune equilibrium in skin. Our findings provide insight into the immune cell populations important for maintaining long-term tumour dormancy in peripheral tissues and imply that targeting TRM cells may serve as a novel cancer treatment strategy.

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