Type 1 diabetes proceeds through well-defined stages, from autoantibody positivity in early-stage disease to progressive loss of insulin secretion after diagnosis. Disease-modifying therapies aiming t...

Type 1 diabetes proceeds through well-defined stages, from autoantibody positivity in early-stage disease to progressive loss of insulin secretion after diagnosis. Disease-modifying therapies aiming t...

Cell Death Discovery - Immunoregulatory role of quercetin in lung cancer

The immune system balances protective immunity against pathogens with tolerance to self and selected foreign antigens. Emerging evidence identifies erythropoietin (EPO) as a systemic immunoregulatory signal that links physiological stress to immune adaptation. Beyond its canonical role in erythropoiesis, EPO–EPO receptor (EPOR) signaling reprograms specialized myeloid cells, including macrophages and type 1 conventional dendritic cells (cDC1s), promoting efferocytosis, inflammatory restraint, and maturation-associated cDC1 fate. Through these mechanisms, EPO shapes antigen-specific T-cell responses across transplantation and cancer. We propose that the EPO–EPOR axis functions as a systemic regulator of immune adaptation through myeloid-cell programming.

The persistent HIV reservoir constitutes the main obstacle to curing HIV/AIDS disease. Our understanding of how non-productive HIV infections are established in primary human CD4+ T cells during the first round of infection is still incomplete. In this study, we leverage the HIV reporter virus pMorpheus-V5 to delineate cellular expression patterns upregulated in non-productively infected stem cell memory (TSCM) CD4+ T cells. We find that CD4+ TSCM harboring non-productive proviruses display a distinct transcriptomic signature comprising 118 upregulated genes, distinct from that of productively infected cells as well as from negative-exposed and mock-infected cells. Among the cellular genes most upregulated in CD4+ TSCM cells harboring non-productive proviruses are CCR4-binding migratory chemokines (CCL22, CCL17), tryptophan catabolic enzymes (IDO1, KYNU), and genes encoding cytoskeletal rearrangement proteins (BASP1, TNFAIP2). Flow cytometry-based analyses confirm that non-productively

This systematic review synthesised evidence from 65 studies examining >65 helminth-derived immunomodulatory proteins (HDIPs) across animal models of inflammatory disease. HDIPs consistently reduced disease severity, decreased pro-inflammatory cytokines and increased anti-inflammatory cytokines, highlighting their broad disease-modifying potential and promise as novel immunoregulatory therapeutics.

The idea of immune privilege has reshaped our understanding of how the immune system is regulated across tissues. It is viewed as a state of selective immune tolerance characterized by tissue- and organ-specific immune regulation. Classic examples include the central nervous system (CNS), eyes and testes, where immune surveillance is present but constrained. These sites maintain a highly regulated immunological milieu through cellular barriers, local immunoregulatory mediators and context-dependent modulation of antigen presentation. While this restrained inflammatory tone is essential to preserve the function and integrity of indispensable tissues, it comes at a cost: the same features that limit immunopathology can also reduce pathogen clearance. As a result, immune-privileged niches may be co-opted by pathogens as long-term reservoirs and enable persistence despite systemic immune surveillance. Understanding how viruses exploit these specialized environments is therefore critical for defining the mechanisms underlying chronic infection and relapse. Numerous studies have characterized viral replication dynamics, transmission and evolution during acute Ebola virus (EBOV) infection. However, increasing evidence indicates that EBOV can persist during the chronic phase, with ongoing viral replication in survivors supporting the concept that persistence represents an active infection within immune-privileged reservoirs1. Among these niches, the CNS has emerged as a particularly...

A new Northwestern Medicine study has uncovered how a key immunoregulatory receptor plays an unexpected dual role in promoting T-cell exhaustion during chronic infection and cancer, according to findi...

Wang et al. identify an immunoregulatory subset of IGFBP2+ NK cells in liver cancer, driven by hypoxia-induced histone lactylation. NK-secreted IGFBP2 helps tumors evade immunity by suppressing stress ligand expression. Blocking IGFBP2 restores tumor sensitivity to cytotoxicity and synergizes with checkpoint therapy, revealing a therapeutic target.

A new Northwestern Medicine study has uncovered how a key immunoregulatory receptor plays an unexpected dual role in promoting T-cell exhaustion during chronic infection and cancer, according to findi...

A new Northwestern Medicine study has uncovered how a key immunoregulatory receptor plays an unexpected dual role in promoting T-cell exhaustion during chronic infection and cancer, according to findings published in the Proceedings of the National Academy of Sciences.

A new Northwestern Medicine study has uncovered how a key immunoregulatory receptor plays an unexpected dual role in promoting T-cell exhaustion during chronic infection and cancer, according to findings published in the Proceedings of the National Academy of Sciences. The research sheds light on why targeted cancer therapies have shown limited efficacy in recent clinical trials for a variety of solid tumors, according to Bin Zhang, MD, Ph.D., the Johanna Dobe Professor of Cancer Immunology and senior author of the study.

Read the full paper: Immunoregulatory properties of the human acellular amniotic membrane for diabetic wound healing

Clinical trial related to Multiple Sclerosis.