Table of contents

Volume 3, Issue 10, pp. 310 - 327, October 2019

Issue cover
Cover: This month in Cell Stress: Inflammation induced PD-L1-specific T cells. Scanning electron microscope image of circulating human blood cells (red blood cells, white blood cells including lymphocytes and small disc-shaped platelets). Public domain image by Bruce Wetzel and Harry Schaefer. Modified by Cell Stress. The cover is published under the CC BY 4.0 license. Enlarge issue cover

News and Thoughts

Anti-regulatory T cells are natural regulatory effector T cells

Niels Ødum

page 310-311 | 10.15698/cst2019.10.199 | Full text | PDF |


Acyl-CoA-binding protein (ACBP): the elusive ‘hunger factor’ linking autophagy to food intake

José Manuel Bravo-San Pedro, Valentina Sica, Frank Madeo and Guido Kroemer

page 312-318 | 10.15698/cst2019.10.200 | Full text | PDF | Abstract

The best-known appetite-regulating factors identified in rodents are leptin, an appetite inhibitor, and ghrelin, an appetite stimulator. Rare cases of loss-of-functions mutations affecting leptin and its receptor, as well as polymorphisms concerning ghrelin and its receptor, have been documented in human obesity, apparently validating the relevance of leptin and ghrelin for human physiology. Paradoxically, however, the overwhelming majority of obese individuals manifest high leptin and low ghrelin plasma levels, suggesting that both factors are not directly disease-relevant. We recently discovered that acyl-CoA-binding protein (ACBP), also known as diazepam-binding inhibitor (DBI), acts as an efficient lipogenic and appetite stimulator in mice. Indeed, in response to starvation, ACBP/DBI is released from tissues in an autophagy-dependent fashion and increases in the plasma. Intravenous injection of ACBP/DBI stimulates feeding behavior through a reduction of circulating glucose levels, and consequent activation of orexigenic neurons in the hypothalamus. In contrast, neutralization of ACBP/DBI abolishes the hyperphagia observed after starvation of mice. Of note, ACBP/DBI is increased in the plasma of obese persons and mice, pointing to a convergence (rather than divergence) between its role in appetite stimulation and human obesity. Based on our results, we postulate a novel ‘hunger reflex’ in which starvation induces a surge in extracellular ACBP/DBI, which in turn stimulates feeding behavior. Thus, ACBP/DBI might be the elusive ‘hunger factor’ that explains increased food uptake in obesity.

Research Reports

Inflammation induced PD-L1-specific T cells

Shamaila Munir, Mia Thorup Lundsager, Mia Aabroe Jørgensen, Morten Hansen, Trine Hilkjær Petersen, Charlotte Menne Bonefeld, Christina Friese, Özcan Met, Per thor Straten and Mads Hald Andersen

page 319-327 | 10.15698/cst2019.10.201 | Full text | PDF | Abstract

PD-L1-specific T cells are a natural part of the T-cell repertoire in humans. Hence, we have previously described spontaneous CD8+ and CD4+ T-cell reactivity against PD-L1 in the peripheral blood of patients with various cancers as well as in healthy donors. It is well described that the expression of the PD-L1 protein is introduced in cells by pro-inflammatory cytokines, e.g. IFN-γ. In the current study, we were able to directly link inflammation with PD-L1-specific T cells by showing that inflammatory mediators such as IFN-γ generate measurable numbers of PD-L1-specific T cells in human PBMCs as well as in in vivo models. These PD-L1-specific T cells can vigorously modulate the cell compartments of the local environment. PD-L1-specific T cells may be important for immune homeostasis by sustaining the ongoing inflammatory response by the suppression of regulatory cell function both directly and indirectly.

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