Issues

Esther Obeng is an attending physician and associate professor at Emory University School of Medicine, where she leads a research group focused on myelodysplastic syndromes (MDS). Esther’s team is investigating how normal hematopoietic stem cells develop into cancerous cells as well as developing targeted therapies for MDS patients.

Mtb drives expression of type I IFN–mediated neutrophil accumulation, which limits interaction between CD4 T cells and macrophages. Failure to limit type I IFN very early in the interaction between Mtb and immune cells allows rapid progression of disease.

In MEPs heterozygous for JAK2V617F, heterodimers composed of wild-type and mutant JAK2 selectively activate STAT1, while elevated kynurenine levels activate the aryl hydrocarbon receptor; together, these pathways bias MEP differentiation toward megakaryopoiesis, leading to thrombocythemia. In MEPs homozygous for JAK2V617F, homodimers of mutant JAK2 preferentially activate STAT5, driving erythropoiesis and resulting in polycythemia.

Florescu et al. investigate the temporal accumulation of immune cells within distinct meningeal compartments in an animal model of progressive MS and uncover a population of anti-CD20–resistant dural B cells that remain in the brain parenchyma at disease remission.

Chang et al. identify lymphatic vasculature on the outer surface of the skull but not inside the skull bone marrow, and reveal skull channel and bone marrow heterogeneity varying by region and age.

Although S2-reactive antibodies are often non-neutralizing, Changrob et al. identify OC43-primed S2 antibodies that demonstrate greater breadth and neutralizing potential compared with SARS-CoV-2–primed S2 antibodies. This study suggests that OC43-based priming strategies could inform next-generation vaccine design for enhanced pan-coronavirus immunity.

Human trophoblasts activate a DUX4-driven antiviral program in response to herpesvirus infection. This defense pathway, distinct from canonical immune responses, induces a coordinated set of antiviral genes and highlights DUX4 as a key regulator of placental protection at the maternal-fetal interface.

Effective tuberculosis control requires CD4⁺ T cell recognition of infected macrophages. The authors show that TCR clonotypes from latently infected individuals demonstrate dominant but not exclusive recognition of infected macrophages, specificity for type VII secretion system substrates, and expression of canonical effector programs.

The early immune mechanisms determining M. tuberculosis infection outcome are unclear. Type I signaling early during M. tuberculosis infection favors neutrophil swarming and limits CD4⁺ T cell–macrophage interactions in TB lesions, impeding TB disease control.

This study demonstrates that the cGAS-TREX1 axis forms a critical negative feedback loop, enabling immune evasion in MSI-H/dMMR tumors. They revealed that Trex1 loss amplifies tumor-intrinsic cGAS–STING signaling and activates CD8⁺ T cell–mediated antitumor immunity, thereby highlighting TREX1 inhibition’s therapeutic potential.

This study reveals that heterozygous JAK2V617F variant in megakaryocyte-erythroid progenitors drives ET via STAT1-IDO1-AhR-RUNX1, whereas the homozygous JAK2V617F variant promotes polycythemia vera through the activation of STAT5. Blocking IDO1 or AhR in humanized ET mice shows therapeutic potential.

Zhu et al. show that CD2 and its ligands, CD48 in mice and CD58 in humans, regulate MAIT cell development and antigen responses by enhancing TCR signaling. A natural subset of human MAIT cells lacking CD2 exhibits reduced activation responses to antigen.

Han et al. unravel that RIPK1 S161 autophosphorylation promotes further autophosphorylation and is sufficient to substitute for RIPK1 kinase activity in TNF-induced necroptosis-mediated cecal damage and mouse death.

Koerner et al. show that RIPK1 autophosphorylation at S161 is crucial for regulating cell death and inflammation. S161N mutation reduces RIPK1 kinase activity and prevents RIPK1-dependent keratinocyte death and skin inflammation, with combined mutations revealing functional interplay between S161 and S166 phosphorylation.

The signaling pathway linking invariant TCR to PLZF during iNKT cell development is not completely understood. Ishikawa et al. find that PKD plays a pivotal role in this pathway through a transcription factor Ikaros.