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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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.

At Cell Communication and Signaling, we are passionate about the dissemination of research.

We are pleased to announce that as of the 12th August 2019, all authors whose papers are accepted will receive a Video Byte.

Created by our partners, Research Square, a Video Byte is a 1-2 minute video summary of a paper that will be incorporated into the abstract of the paper and published on the journal website. Authors will also receive a shareable version of their Video Byte.

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.