RESUMEN
Highlights from the Science family of journals.
RESUMEN
Highlights from the Science family of journals.
RESUMEN
Highlights from the Science family of journals.
RESUMEN
Highlights from the Science family of journals.
RESUMEN
Highlights from the Science family of journals.
RESUMEN
Highlights from the Science family of journals.
RESUMEN
Highlights from the Science family of journals.
RESUMEN
Highlights from the Science family of journals.
RESUMEN
Highlights from the Science family of journals.
RESUMEN
Highlights from the Science family of journals.
RESUMEN
Highlights from the Science family of journals.
RESUMEN
Highlights from the Science family of journals.
RESUMEN
Highlights from the Science family of journals.
RESUMEN
Multicellular life requires altruistic cooperation between cells. The adaptive immune system is a notable exception, wherein germinal center B cells compete vigorously for limiting positive selection signals. Studying primary human lymphomas and developing new mouse models, we found that mutations affecting BTG1 disrupt a critical immune gatekeeper mechanism that strictly limits B cell fitness during antibody affinity maturation. This mechanism converted germinal center B cells into supercompetitors that rapidly outstrip their normal counterparts. This effect was conferred by a small shift in MYC protein induction kinetics but resulted in aggressive invasive lymphomas, which in humans are linked to dire clinical outcomes. Our findings reveal a delicate evolutionary trade-off between natural selection of B cells to provide immunity and potentially dangerous features that recall the more competitive nature of unicellular organisms.
Asunto(s)
Linfocitos B , Transformación Celular Neoplásica , Linfoma de Células B Grandes Difuso , Proteínas de Neoplasias , Animales , Humanos , Ratones , Afinidad de Anticuerpos/genética , Linfocitos B/patología , Centro Germinal , Mutación , Proteínas de Neoplasias/genética , Linfoma de Células B Grandes Difuso/genética , Transformación Celular Neoplásica/genética , Selección GenéticaRESUMEN
Highlights from the Science family of journals.
RESUMEN
Highlights from the Science family of journals.
RESUMEN
Endogenous retroviruses (ERVs) are fossils left in our genome from retrovirus infections of the past. Their sequences are part of every vertebrate genome and their random integrations are thought to have contributed to evolution. Although ERVs are mainly silenced by the host genome, they have been found to be activated in multiple disease states, such as auto-inflammatory disorders and neurological diseases. However, the numerous copies in mammalian genomes and the lack of tools to study them make defining their role in health and diseases challenging. In this study, we identified eight copies of the zebrafish endogenous retrovirus zferv. We created and characterised the first in vivo ERV reporter line in any species. Using a combination of live imaging, flow cytometry and single-cell RNA sequencing, we mapped zferv expression to early T cells and neurons. Thus, this new tool identified tissues expressing ERV in zebrafish, highlighting a potential role of ERV during brain development and strengthening the hypothesis that ERV play a role in immunity and neurological diseases. This transgenic line is therefore a suitable tool to study the function of ERV in health and diseases.
Asunto(s)
Retrovirus Endógenos , Infecciones por Retroviridae , Animales , Animales Modificados Genéticamente , Retrovirus Endógenos/genética , Mamíferos , Neuronas , Infecciones por Retroviridae/genética , Pez Cebra/genéticaRESUMEN
Highlights from the Science family of journals.
RESUMEN
Highlights from the Science family of journals.
RESUMEN
Highlights from the Science family of journals.