@article{Sanlaville2023.02.15.528594,

title = {CD4 T cells and neutrophils contribute to epithelial-mesenchymal transition in breast cancer},

author = {Amélien Sanlaville and Aurélien Voissière and Dominique Poujol and Margaux Hubert and Suzanne André and Clémence Perret and Jean-Philippe Foy and Nadège Goutagny and Marine Malfroy and Isabelle Durand and Marie Châlons-Cottavoz and Jenny Valladeau-Guilemond and Pierre Saintigny and Alain Puisieux and Christophe Caux and Marie-Cécile Michallet and Isabelle Puisieux and Nathalie Bendriss-Vermare},

url = {https://www.biorxiv.org/content/early/2023/02/15/2023.02.15.528594},

doi = {10.1101/2023.02.15.528594},

year  = {2023},

date = {2023-02-15},

urldate = {2023-01-01},

journal = {bioRxiv},

publisher = {Cold Spring Harbor Laboratory},

abstract = {Epithelial-mesenchymal transition (EMT) is a central oncogenic mechanism, contributing both to transformation and metastatic dissemination. Inflammation and innate immune cells are known to favor EMT induction, but the role of adaptive immunity still remains unclear. Using an original murine mammary tumor model in immune cell subpopulation depletion experiments, we demonstrated that tumor cells maintain their epithelial phenotype in mice deficient for adaptive immune response, but undergo EMT in the presence of T-cells. This phenotypic conversion involves the major contribution of CD4 T cells, but not CD8 T cells nor B cells, undoubtedly demonstrating the pro-EMT role of CD4 T cells specifically among adaptive immune cells. Moreover, combined intra-tumor immune infiltrate and transcriptomic analyses of murine mammary tumors with various EMT phenotype revealed an inverse correlation between mesenchymal tumor cell and intratumoral neutrophil proportions, due to the reduced ability of mesenchymal cells to recruit neutrophils. Last, selective in vivo depletion of neutrophils and transcriptomic analysis of human breast tumor cohorts demonstrated the pro-EMT role of neutrophils and suggest a cooperation with CD4 T cells in EMT promotion. Collectively, our data highlight a novel mechanism of EMT regulation by both innate and adaptive immune compartments.Competing Interest StatementThe authors have declared no competing interest.},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{pmid36007550,

title = {MXD4/MAD4 Regulates Human Keratinocyte Precursor Fate},

author = {Julien Coutier and Frédéric Auvré and Gilles Lemaître and Jean-Jacques Lataillade and Jean-François Deleuze and Paul-Henri Roméo and Michèle T Martin and Nicolas O Fortunel},

doi = {10.1016/j.jid.2022.07.020},

issn = {1523-1747},

year  = {2023},

date = {2023-01-01},

urldate = {2023-01-01},

journal = {J Invest Dermatol},

volume = {143},

number = {1},

pages = {105--114.e12},

abstract = {Deciphering the pathways that regulate human epidermal precursor cell fate is necessary for future developments in skin repair and graft bioengineering. Among them, characterization of pathways regulating the keratinocyte (KC) precursor immaturity versus differentiation balance is required for improving the efficiency of KC precursor ex vivo expansion. In this study, we show that the transcription factor MXD4/MAD4 is expressed at a higher level in quiescent KC stem/progenitor cells located in the basal layer of human epidermis than in cycling progenitors. In holoclone KCs, stable short hairpin-RNA‒mediated decreased expression of MXD4/MAD4 increases MYC expression, whose modulation increases the proliferation of KC precursors and maintenance of their clonogenic potential and preserves the functionality of these precursors in three-dimensional epidermis organoid generation. Altogether, these results characterize MXD4/MAD4 as a major piece of the stemness puzzle in the human epidermis KC lineage and pinpoint an original avenue for ex vivo expansion of human KC precursors.},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{pmid36482098,

title = {RNA-Seq comparative study reveals molecular effectors linked to the resistance of Pinna nobilis to Haplosporidium pinnae parasite},

author = {Pauline Salis and Claire Peyran and Titouan Morage and Simon de Bernard and Julien Nourikyan and Stéphane Coupé and Robert Bunet and Serge Planes},

doi = {10.1038/s41598-022-25555-x},

issn = {2045-2322},

year  = {2022},

date = {2022-12-01},

urldate = {2022-12-01},

journal = {Sci Rep},

volume = {12},

number = {1},

pages = {21229},

abstract = {With the intensification of maritime traffic, recently emerged infectious diseases have become major drivers in the decline and extinction of species. Since 2016, mass mortality events have decimated the endemic Mediterranean Sea bivalve Pinna nobilis, affecting ca. 100% of individuals. These events have largely been driven by Haplosporidium pinnae's infection, an invasive species which was likely introduced by shipping. While monitoring wild populations of P. nobilis, we observed individuals that survived such a mass mortality event during the summer of 2018 (France). We considered these individuals resistant, as they did not show any symptoms of the disease, while the rest of the population in the area was devastated. Furthermore, the parasite was not detected when we conducted a PCR amplification of a species-specific fragment of the small subunit ribosomal DNA. In parallel, the transcriptomic analysis showed evidence of some parasite RNA indicating that the resistant individuals had been exposed to the parasite without proliferating. To understand the underlying mechanisms of resistance in these individuals, we compared their gene expression with that of susceptible individuals. We performed de novo transcriptome assembly and annotated the expressed genes. A comparison of the transcriptomes in resistant and susceptible individuals highlighted a gene expression signature of the resistant phenotype. We found significant differential expressions of genes involved in immunity and cell architecture. This data provides the first insights into how individuals escape the pathogenicity associated with infection.},

keywords = {},

pubstate = {published},

tppubtype = {article}

}