Analyse de Données Omiques

@article{Laubreton2026,

title = {Transient tumor exposure induces persistent functional defects in memory CD8+ T cells},

author = {Daphné Laubreton and Margaux Prieux and Sophia Djebali and Maxence Dubois and Simon De Bernard and Olivier Gandrillon and Christophe Arpin and Jacqueline Marvel},

doi = {10.1016/j.isci.2026.115556},

issn = {2589-0042},

year  = {2026},

date = {2026-04-01},

urldate = {2026-04-00},

journal = {iScience},

publisher = {Elsevier BV},

abstract = {Memory CD8+ T cells generated during acute infections exhibit enhanced effector functions upon reactivation. However, persistent antigen exposure, such as in cancer, can impair their functionality. In this study, we compared memory CD8+ T cells generated following tumor rejection (Tum-CD8+) with those arising from an acute viral infection (Vir-CD8+). Using vaccinia virus and EL4 tumor models expressing the same antigen, we found that Tum-CD8+ cells displayed a distinct phenotype, including sustained expression of inhibitory receptors (PD-1, TIM-3), altered integrins expression and reduced production of IFNγ and TNF. Despite retaining cytotoxic activity, their protective capacity was compromised, even after viral recall. Transcriptomic and functional analyses revealed that transient tumor exposure imprints a stable, exhaustion-like program on memory CD8+ T cells. These findings highlight how suboptimal priming conditions during tumor challenge durably shape memory T cell responses.},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{Elliott2026,

title = {Systems vaccinology analysis of saRNA immunization identifies an acute innate immune signature correlated with adaptive immunity},

author = {Tamara Elliott and Ziyin Wang and Olivia Bonduelle and Abbey Evans and Suzanne Day and Leon R. McFarlane and Simon de Bernard and Karine Alves and Julien Nourikyan and Michele Wokam and Katrina Pollock and Hannah M. Cheeseman and Behazine Combadiere and Robin J. Shattock and John S. Tregoning},

doi = {10.1016/j.omta.2026.201706},

issn = {3117-387X},

year  = {2026},

date = {2026-03-12},

urldate = {2026-03-12},

journal = {Molecular Therapy Advances},

volume = {34},

number = {1},

publisher = {Elsevier BV},

abstract = {Self-amplifying ribonucleic acid (saRNA) vaccines are a next-generation RNA vaccine platform with great potential. Systems vaccinology provides a potent tool to interrogate vaccine-induced responses in volunteers and to dissect the mechanisms by which vaccines elicit a protective immune response or cause reactogenicity. In the current study, we performed transcriptomic analysis on blood samples collected from volunteers vaccinated as part of a phase I study of an saRNA vaccine expressing the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) spike antigen. We observed significant gene over-expression following both the prime and boost vaccinations. Over-expressed genes were predominantly associated with type I interferon signaling pathways and innate immune cell recruitment. This transcriptomic signature was reflected by an increase in cytokines in the plasma at the same time points and a significant increase in monocytes in the blood, both of which correlated with the antibody response to the vaccine. When individuals were segregated by the degree of reactogenicity, we also detected differences in gene expression related to immune responses. Overall, results show that saRNA induces a potent, acute inflammatory response with similarities to other RNA vaccines, and it will be important to further dissect the role of the over-expressed genes in immunogenicity and reactogenicity.},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{Klann2026,

title = {Cell-cell communication as underlying principle governing color pattern formation in teleost fishes},

author = {Marleen Klann and Saori Miura and Shu-Hua Lee and Stefano Davide Vianello and Robert Ross and Masakatsu Watanabe and Emma Gairin and Yipeng Liang and Harrison W. Hutto and Braedan M. McCluskey and Marcela Herrera and Lila Solnica-Krezel and Laurence Besseau and Simone Pigolotti and David M. Parichy and Masato Kinoshita and Vincent Laudet},

doi = {10.1038/s41467-026-69524-8},

issn = {2041-1723},

year  = {2026},

date = {2026-02-18},

urldate = {2026-02-18},

journal = {Nat Commun},

publisher = {Springer Science and Business Media LLC},

abstract = {The diverse pigmentation patterns of animals are crucial for predation avoidance and behavioral display. This diversity arises from interactions among distinct pigment cell types, yet mechanisms generating pattern variation across teleost fishes remain incompletely understood. In zebrafish, Turing models have been proposed to explain stripe patterns, but it is unclear if they apply to other fishes. Here, we investigate the Snowflake mutant of the anemonefish Amphiprion ocellaris, which displays enlarged white bars with irregular boundaries. Using genome-wide association mapping and targeted sequencing, we identify a missense mutation (E42K) in gja5b, encoding the gap junction protein Connexin 41.8. CRISPR/Cas9-mediated genome editing recapitulates the Snowflake phenotype, while pharmacological inhibition of gap junctions phenocopies the boundary defects, supporting a causal role for impaired intercellular communication. Expression analyses reveal that, unlike zebrafish, anemonefish gja5b is predominantly expressed in iridophores. With functional in vitro assays we demonstrate that the E42K mutation acts as a dominant negative, strongly reducing gap junctional coupling. Introducing the same mutation in zebrafish reveals context-dependent effects on pigment patterning. Taken together our findings highlighting gap junction-mediated communication as a conserved but flexible mechanism controlling pigment boundary positioning and pattern diversification.},

keywords = {},

pubstate = {published},

tppubtype = {article}

}