Trends in Immunology最新文献

Parity and lactation have long been recognised as protective factors in breast cancer, with notable risk reduction in triple negative breast cancer (TNBC). Recent work by Virassamy et al. suggests a tissue-specific, persistent immune surveillance underpins this effect, particularly in women who have also breastfed.

Traumatic brain injury (TBI) is a leading cause of neurological disability, associated with higher rates of cognitive complications that negatively affect recovery. Myriad cytokine and chemokine pathways propagate the secondary responses to injury. This review discusses the integration of peripheral and central immune cytokine and chemokine signaling cascades after TBI and recovery, with a focus on preclinical work. We first discuss key cytokine and chemokine interactions influencing recovery and long-term deficits. Next, we discuss the major cell types that propagate and respond to the inflammatory process after TBI. Understanding neuroimmune signaling, utilizing recent advances in transcriptomics and immune profiling, with a focus on cytokines and chemokine after TBI reveals therapeutic targets and informs strategies to improve long-term recovery and outcomes.

Chi and colleagues revealed that dietary cysteine enhances intestinal stem cell (ISC) regeneration, driving coenzyme A (CoA) synthesis and expansion of intraepithelial (IEL) CD8αβ⁺ T cells that secrete IL-22. This epithelial-immune crosstalk potentiates ISC repair after injury, highlighting a metabolism-immune axis linking cysteine sensing to tissue regeneration.

Estrogen receptor (ER)⁺ breast malignancies are poorly infiltrated by immune cells, hence exhibiting limited sensitivity to immune checkpoint inhibitors (ICIs). Recent data from Palomeque et al. demonstrate that ER signaling actively contributes to such an immunoevasive phenotype by preventing the nuclear factor LCOR from establishing an ICI-sensitive tumor microenvironment.

The SARS-CoV-2 pandemic has drawn global attention to post-acute infection syndromes (PAIS), with millions affected by post-acute sequelae of COVID-19 (PASC, or Long COVID). While Long COVID is newly defined, PAIS have been described for over a century following epidemic infections. Multiple pathogens - including influenza, Epstein-Barr virus, and Borrelia burgdorferi, among others - can precipitate persistent, poorly understood symptoms. Chronic illnesses such as myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS) have long been linked to infectious triggers. This recurring association highlights critical knowledge gaps and underscores the need for systematic investigation. Unlike prior pandemics, the current era offers advanced technologies and analytic tools to address these gaps. Defining the biology of Long COVID may yield broader insights into host-pathogen interactions and mechanisms of chronic illness.

The advancement of immunotherapy faces significant challenges, including extending its benefits to a growing number of patients and enhancing its efficacy across different tumor types. In this context, γδ T cells emerge as particularly promising candidates owing to their distinctive biological features such as MHC-independent activation, potent cytotoxicity, and capacity to bridge innate and adaptive immunity. Recently, advanced single-cell techniques have allowed detailed γδ T cell characterization in the tumor microenvironment (TME) and have emphasized their heterogeneity, mechanisms of activation, and response to immune checkpoint blockade (ICB). This review provides a comprehensive summary of recent advances in understanding γδ T cells in colorectal cancer (CRC), with a particular emphasis on their prognostic and therapeutic relevance in both primary tumors and metastatic disease.

Intestinal homeostasis is crucial for overall health, and its maintenance relies on a complex and delicate interplay between intestinal epithelial cells, the gut microbiota, and the immune system. Among immune components, group 3 innate lymphoid cells (ILC3s), which primarily reside in the intestinal microenvironment, play a crucial role in maintaining gut homeostasis. Through the expression of multiple effector molecules such as interleukin (IL)-22 and major histocompatibility complex class II (MHCII), ILC3s orchestrate intestinal epithelial responses and regulate innate and adaptive immunity, thereby collectively promoting a symbiotic host-microbiota relationship, supporting immune tolerance, and providing protection against pathogens. This review summarizes current understanding of ILC3 functions in gut homeostasis, highlights their interactions with the microbiota and other cell types, and outlines how aberrant ILC3 activity contributes to disease pathogenesis.

Pregnancy requires dynamic immune adaptations that balance tolerance, homeostasis, and defense at the maternal-fetal interface. Recent advances integrating findings from human placental samples with those from refined animal models now enable a detailed analysis of how cellular responses in mid and late gestation contribute to major obstetrical complications - with distinct clinical manifestations - such as preterm birth, fetal growth restriction, and pre-eclampsia. In this Opinion article we propose a unifying paradigm: the breakdown of maternal-fetal immune homeostasis. We highlight regulatory T cells and decidual macrophages as complementary regulators of antigen-specific tolerance and nonspecific homeostasis, whereas effector T cell infiltration in chronic placental inflammation and neutrophil-driven inflammation in acute chorioamnionitis exemplify pathological immune activation. Together, these examples illustrate how immune programs that sustain mid-to-late pregnancy, when dysregulated, drive pathology and open new therapeutic opportunities.

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 exosome-mediated intercellular communication. This review explores how basal neuronal inflammasome activity contributes to central nervous system (CNS) homeostasis and how heightened signaling in neurons drives neuroinflammatory and degenerative processes. Understanding these dual roles of neuronal inflammasomes provides new insights into neuroimmune crosstalk and identifies potential targets for modulating repair and inflammation in CNS injury and disease.

The developmental origins of health and diseases concept posits that early-life exposure to environmental adversities increases risks for diverse noncommunicable and infectious diseases. Among these adversities, maternal malnutrition is a critical determinant of offspring health trajectories. Maternal malnutrition from preconception to lactation can durably alter cellular and tissue function in the offspring. We propose that tissue-resident macrophages (TRMs) act as central mediators of this developmental programming. Seeding tissues during embryogenesis, integrating metabolic and hormonal signals, and persisting throughout life, TRMs can encode maternal nutritional states into lasting tissue adaptations. We summarize how specific maternal diets program distinct TRM subsets and how programmed TRMs link maternal nutritional statuses to disease susceptibility. TRMs may offer early intervention targets to improve offspring health.