Cell Communication and Signaling

Cell Communication and Signaling (CCS) is an open access journal that encompasses all basic and translational aspects of cellular communications and signaling pathways in normal and pathological conditions.

Beginning in January of 2019, CCS is pleased to announce their affiliation with the International Cell Death Society. 

The journal encourages submissions in all aspects of cell death, that include apoptotic and non-apoptotic mechanisms of cell death, cell death in model systems, autophagy, clearance of dying cells, as well as the immunological and pathological consequences of dying cells in the tissue microenvironment. 

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The 11th Annual Österreichische Gesellschaft für Molekulare Biowissenschaften und Biotechnologie (ÖGMBT) Meeting "Inside the World of Biomolecules" is taking place on 16th-18th September at the Wyndham Grand Salzburg Conference Centre in Salzburg.

The ÖGMBT Annual Meeting welcomes scientists from all research areas and all career levels and is an opportunity to connect with the brightest minds in life sciences.

Biology of phosphatidylserine (PS): basic physiology and implications in immunology, infectious disease, and cancer

This collection aims to address the biological functions of PS as well as its pathological role in various diseases. This issue will highlight recently published research as well as reviews that cover all facets of PS research.

25th Anniversary of the International Cell Death Society Collection

Curated by Editor-in-Chief Raymond Birge, we're celebrating the 25th anniversary of the ICDS with a collection highlighting the most important Cell Death papers published in Cell Communication and Signaling in the last decade.

Plasmodium infection inhibits the expansion and activation of MDSCs and Tregs in the tumor microenvironment in a murine Lewis lung cancer model

In this recent paper, Adah et al. sought to reveal the pathways by which the malaria causing parasite Plasmodium promotes lung cancer immunity in a murine model. They found that infection significantly reduced myeloid-derived suppressor cells and regulatory T cells owing to the downregulation of recruiting molecules and the blocking of cellular activation pathways. Notably, the infected cells contained high levels of perforin and granzyme B while inhibiting PD-1 expression.