Lee and Wheeler review the interface of neuroimmune interactions, stress, and affective behaviors. They highlight anatomical and cellular mechanisms controlling immune-brain plasticity as well as ther...

Recent discoveries reveal that inflammasome signaling in neurons extends beyond host defense to influence fundamental aspects of brain function, including synaptic plasticity, axon remodeling, and exo...

Secondary lymphoid organs (SLOs) are important initiators and regulators of immunity. To carry out this function, the blood vasculature must deliver oxygen and nutrients and recruit circulating lympho...

The microbiome is receiving significant attention given its influence on a host of human diseases including cancer. Its role in response to cancer treatment is becoming increasingly apparent, with evi...

From COVID shots to cancer therapy, mRNA is changing medicine.

Cationic nanogel–based nasal therapeutic vaccine induces cancer-specific immune responses and inhibits cancer development in cervical tissue.

Job Description We are seeking a highly motivated postdoctoral researcher to join our laboratory to study the early steps of development of childhood B-cell Acute Lymphoblastic Leukemia (B-ALL). The p...

YouTube video by Centro de Biología Molecular Severo Ochoa

Sepsis, a life-threatening condition triggered by infection, disrupts the body’s immune balance and remains a major global health challenge. This forum explores the dual roles of cytokines in sepsis: their overactivation drives ‘cytokine storms,’ and dysregulation leads to immunosuppression. It also discusses regulatory mechanisms for developing targeted therapies.

Germinal center B cell–like diffuse large B cell lymphoma (GCB-DLBCL) originates from the malignant transformation of germinal center B cells. This process is driven by transcriptional and epigenetic dysregulations, frequently caused by recurrent mutations and chromosomal translocations. These changes lead to a differentiation arrest associated with unchecked proliferation and survival. This review highlights key transcriptional and epigenetic dependencies that sustain the GCB-DLBCL phenotype and identifies therapeutic vulnerabilities. Epigenetic targeting of these vulnerabilities unlocks tumor cells from their differentiation arrest, enabling further yet incomplete differentiation toward an antiproliferative, proapoptotic plasma cell–like or memory B cell–like state. We define this transition as an epigenetically programmed identity crisis, a promising therapeutic strategy to target GCB-DLBCL and potentially other malignancies.