Pub Date : 2024-12-01Epub Date: 2024-11-27DOI: 10.1016/j.it.2024.10.003
Rosalie W M Kempkes, Rab K Prinjha, Menno P J de Winther, Annette E Neele
The polycomb repressive complex 2 (PRC2) is an established therapeutic target in cancer. PRC2 catalyzes methylation of histone H3 at lysine 27 (H3K27me3) and is known for maintaining eukaryote cell identity. Recent discoveries show that modulation of PRC2 not only impacts cell differentiation and tumor growth but also has immunomodulatory properties. Here, we integrate multiple immunological fields to understand PRC2 and its subunits in epigenetic canonical regulation and non-canonical mechanisms within innate immunity. We discuss how PRC2 regulates hematopoietic stem cell proliferation, myeloid cell differentiation, and shapes innate immune responses. The PRC2 catalytic domain EZH2 is upregulated in various human inflammatory diseases and its deletion or inhibition in experimental mouse models can reduce disease severity, emphasizing its importance in regulating inflammation.
{"title":"Novel insights into the dynamic function of PRC2 in innate immunity.","authors":"Rosalie W M Kempkes, Rab K Prinjha, Menno P J de Winther, Annette E Neele","doi":"10.1016/j.it.2024.10.003","DOIUrl":"10.1016/j.it.2024.10.003","url":null,"abstract":"<p><p>The polycomb repressive complex 2 (PRC2) is an established therapeutic target in cancer. PRC2 catalyzes methylation of histone H3 at lysine 27 (H3K27me3) and is known for maintaining eukaryote cell identity. Recent discoveries show that modulation of PRC2 not only impacts cell differentiation and tumor growth but also has immunomodulatory properties. Here, we integrate multiple immunological fields to understand PRC2 and its subunits in epigenetic canonical regulation and non-canonical mechanisms within innate immunity. We discuss how PRC2 regulates hematopoietic stem cell proliferation, myeloid cell differentiation, and shapes innate immune responses. The PRC2 catalytic domain EZH2 is upregulated in various human inflammatory diseases and its deletion or inhibition in experimental mouse models can reduce disease severity, emphasizing its importance in regulating inflammation.</p>","PeriodicalId":54412,"journal":{"name":"Trends in Immunology","volume":" ","pages":"1015-1030"},"PeriodicalIF":13.1,"publicationDate":"2024-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142740853","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Effector-triggered immunity (ETI) enables hosts to react to pathogens by monitoring few key cellular processes. ETI responses are assumed to be similar toward related pathogen effectors. However, recent evidence from the invertebrate model Caenorhabditis elegans and pore-forming toxins indicates a much more complex and specific ETI than previously anticipated.
{"title":"Unanticipated specificity in effector-triggered immunity.","authors":"Alejandra Zárate-Potes, Hinrich Schulenburg, Katja Dierking","doi":"10.1016/j.it.2024.10.008","DOIUrl":"10.1016/j.it.2024.10.008","url":null,"abstract":"<p><p>Effector-triggered immunity (ETI) enables hosts to react to pathogens by monitoring few key cellular processes. ETI responses are assumed to be similar toward related pathogen effectors. However, recent evidence from the invertebrate model Caenorhabditis elegans and pore-forming toxins indicates a much more complex and specific ETI than previously anticipated.</p>","PeriodicalId":54412,"journal":{"name":"Trends in Immunology","volume":" ","pages":"939-942"},"PeriodicalIF":13.1,"publicationDate":"2024-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142645207","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2024-12-01Epub Date: 2024-11-18DOI: 10.1016/j.it.2024.10.004
Valentino D'Onofrio, Rafick Pierre Sékaly
Men are at higher risk for developing severe COVID-19 than women, while women are at higher risk for developing post-acute sequelae of COVID-19 (PASC). This highlights the impact of sex differences on immune responses and clinical outcomes of acute COVID-19 or PASC. A dynamic immune-endocrine interface plays an important role in the development of effective immune responses impacting the control of viral infections. In this opinion article we discuss mechanisms underlying the transcriptional and epigenetic regulation of immune responses by sex hormones during viral infections. We propose that disruption of this delicate immune-endocrine interplay can result in worsened outcomes of viral disease. We also posit that insights into these immune mechanisms can propel the development of novel immunomodulatory interventions that leverage immune-endocrine pathways to treat viral infections.
{"title":"The immune-endocrine interplay in sex differential responses to viral infection and COVID-19.","authors":"Valentino D'Onofrio, Rafick Pierre Sékaly","doi":"10.1016/j.it.2024.10.004","DOIUrl":"10.1016/j.it.2024.10.004","url":null,"abstract":"<p><p>Men are at higher risk for developing severe COVID-19 than women, while women are at higher risk for developing post-acute sequelae of COVID-19 (PASC). This highlights the impact of sex differences on immune responses and clinical outcomes of acute COVID-19 or PASC. A dynamic immune-endocrine interface plays an important role in the development of effective immune responses impacting the control of viral infections. In this opinion article we discuss mechanisms underlying the transcriptional and epigenetic regulation of immune responses by sex hormones during viral infections. We propose that disruption of this delicate immune-endocrine interplay can result in worsened outcomes of viral disease. We also posit that insights into these immune mechanisms can propel the development of novel immunomodulatory interventions that leverage immune-endocrine pathways to treat viral infections.</p>","PeriodicalId":54412,"journal":{"name":"Trends in Immunology","volume":" ","pages":"943-958"},"PeriodicalIF":13.1,"publicationDate":"2024-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142677812","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2024-12-01Epub Date: 2024-11-15DOI: 10.1016/j.it.2024.10.005
Mohammed N Ullah, Nicholas R Rowan, Andrew P Lane
While primarily a sensory organ, the mammalian olfactory epithelium (OE) also plays a critical role as an immune barrier. Mechanisms governing interactions between the immune system and this specialized chemosensory tissue are gaining interest, in part sparked by the COVID-19 pandemic. Regulated inflammation is intrinsic to normal mucosal healing and homeostasis, but prolonged OE inflammation is associated with persistent loss of smell, belying the intertwining of local mucosal immunology and olfactory function. Evidence supports bidirectional communication between OE cells and the immune system in health and disease. Recent investigations suggest that neuro-immune cross-talk modulates olfactory stem cell behavior and neuronal regeneration dynamics, prioritizing the epithelial-like non-neuronal framework with immune barrier function at the expense of the neurosensory organ in chronic inflammation.
{"title":"Neuroimmune interactions in the olfactory epithelium: maintaining a sensory organ at an immune barrier interface.","authors":"Mohammed N Ullah, Nicholas R Rowan, Andrew P Lane","doi":"10.1016/j.it.2024.10.005","DOIUrl":"10.1016/j.it.2024.10.005","url":null,"abstract":"<p><p>While primarily a sensory organ, the mammalian olfactory epithelium (OE) also plays a critical role as an immune barrier. Mechanisms governing interactions between the immune system and this specialized chemosensory tissue are gaining interest, in part sparked by the COVID-19 pandemic. Regulated inflammation is intrinsic to normal mucosal healing and homeostasis, but prolonged OE inflammation is associated with persistent loss of smell, belying the intertwining of local mucosal immunology and olfactory function. Evidence supports bidirectional communication between OE cells and the immune system in health and disease. Recent investigations suggest that neuro-immune cross-talk modulates olfactory stem cell behavior and neuronal regeneration dynamics, prioritizing the epithelial-like non-neuronal framework with immune barrier function at the expense of the neurosensory organ in chronic inflammation.</p>","PeriodicalId":54412,"journal":{"name":"Trends in Immunology","volume":" ","pages":"987-1000"},"PeriodicalIF":13.1,"publicationDate":"2024-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11624989/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142645206","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2024-12-01Epub Date: 2024-11-22DOI: 10.1016/j.it.2024.11.002
Alexandra Tabachnikova, Akiko Iwasaki
Innate immune cells that are epigenetically reprogrammed by infection can modify host responses to subsequent infections. Lercher et al. have identified epigenetic reprogramming of murine airway-resident macrophages following recovery from SARS-CoV-2 infection, conferring protection from pathology and lethality following secondary influenza A virus (IAV) challenge without reducing viral titers.
{"title":"SARS-CoV-2 reprograms murine alveolar macrophages to dampen flu.","authors":"Alexandra Tabachnikova, Akiko Iwasaki","doi":"10.1016/j.it.2024.11.002","DOIUrl":"10.1016/j.it.2024.11.002","url":null,"abstract":"<p><p>Innate immune cells that are epigenetically reprogrammed by infection can modify host responses to subsequent infections. Lercher et al. have identified epigenetic reprogramming of murine airway-resident macrophages following recovery from SARS-CoV-2 infection, conferring protection from pathology and lethality following secondary influenza A virus (IAV) challenge without reducing viral titers.</p>","PeriodicalId":54412,"journal":{"name":"Trends in Immunology","volume":" ","pages":"925-927"},"PeriodicalIF":13.1,"publicationDate":"2024-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142696202","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2024-12-01Epub Date: 2024-11-19DOI: 10.1016/j.it.2024.10.007
Ravi Bharadwaj, Swati Jaiswal, Neal Silverman
Solute carrier proteins (SLCs) are pivotal for maintaining cellular homeostasis by transporting small molecules across cellular membranes. Recent discoveries have uncovered their involvement in modulating innate immunity, particularly within the cytosol. We review emerging evidence that links SLC transporters to cytosolic innate immune recognition and highlight their role in regulating inflammation. We explore how SLC transporters influence the activation of endosomal Toll-like receptors, cytosolic NODs, and STING sensors. Understanding the contribution of SLCs to innate immune recognition provides insight into their fundamental biological functions and opens new avenues to develop possible therapeutic interventions for autoimmune and inflammatory diseases. This review aims to discuss current knowledge and identify key gaps in this rapidly evolving field.
{"title":"Cytosolic delivery of innate immune agonists.","authors":"Ravi Bharadwaj, Swati Jaiswal, Neal Silverman","doi":"10.1016/j.it.2024.10.007","DOIUrl":"10.1016/j.it.2024.10.007","url":null,"abstract":"<p><p>Solute carrier proteins (SLCs) are pivotal for maintaining cellular homeostasis by transporting small molecules across cellular membranes. Recent discoveries have uncovered their involvement in modulating innate immunity, particularly within the cytosol. We review emerging evidence that links SLC transporters to cytosolic innate immune recognition and highlight their role in regulating inflammation. We explore how SLC transporters influence the activation of endosomal Toll-like receptors, cytosolic NODs, and STING sensors. Understanding the contribution of SLCs to innate immune recognition provides insight into their fundamental biological functions and opens new avenues to develop possible therapeutic interventions for autoimmune and inflammatory diseases. This review aims to discuss current knowledge and identify key gaps in this rapidly evolving field.</p>","PeriodicalId":54412,"journal":{"name":"Trends in Immunology","volume":" ","pages":"1001-1014"},"PeriodicalIF":13.1,"publicationDate":"2024-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11624987/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142683570","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2024-12-01Epub Date: 2024-11-21DOI: 10.1016/j.it.2024.11.006
C J E Metcalf, B Koskella
Following on from the discovery that innate immune pathways are shared widely across the tree of life comes another surprise: Hobbs et al. show that viruses targeting animals and bacteria also use highly conserved tools to fight back. Why such mechanisms remain seemingly unchanged despite the rapid coevolution among hosts and pathogens is now a key open question for the field.
{"title":"Weapon of choice: viruses share cross-kingdom tools.","authors":"C J E Metcalf, B Koskella","doi":"10.1016/j.it.2024.11.006","DOIUrl":"10.1016/j.it.2024.11.006","url":null,"abstract":"<p><p>Following on from the discovery that innate immune pathways are shared widely across the tree of life comes another surprise: Hobbs et al. show that viruses targeting animals and bacteria also use highly conserved tools to fight back. Why such mechanisms remain seemingly unchanged despite the rapid coevolution among hosts and pathogens is now a key open question for the field.</p>","PeriodicalId":54412,"journal":{"name":"Trends in Immunology","volume":" ","pages":"937-938"},"PeriodicalIF":13.1,"publicationDate":"2024-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142694014","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2024-12-01Epub Date: 2024-11-12DOI: 10.1016/j.it.2024.10.002
Chih-Chung 'Jerry' Lin, Yuyao Tian, Rudolph E Tanzi, Mehdi Jorfi
Peripheral immune cells play an important role in the pathology of Alzheimer's disease (AD), impacting processes such as amyloid and tau protein aggregation, glial activation, neuronal integrity, and cognitive decline. Here, we examine cutting-edge strategies - encompassing animal and cellular models - used to investigate the roles of peripheral immune cells in AD. Approaches such as antibody-mediated depletion, genetic ablation, and bone marrow chimeras in mouse models have been instrumental in uncovering T, B, and innate immune cell disease-modifying functions. However, challenges such as specificity, off-target effects, and differences between human and mouse immune systems underscore the need for more human-relevant models. Emerging multicellular models replicating critical aspects of human brain tissue and neuroimmune interactions increasingly offer fresh insights into the role of immune cells in AD pathogenesis. Refining these methodologies can deepen our understanding of immune cell contributions to AD and support the development of novel immune-related therapeutic interventions.
外周免疫细胞在阿尔茨海默病(AD)的病理过程中发挥着重要作用,影响着淀粉样蛋白和 tau 蛋白聚集、神经胶质细胞活化、神经元完整性和认知能力下降等过程。在此,我们将探讨用于研究外周免疫细胞在阿尔茨海默病中的作用的前沿策略--包括动物和细胞模型。小鼠模型中的抗体介导耗竭、基因消融和骨髓嵌合体等方法有助于发现T、B和先天性免疫细胞的疾病调节功能。然而,特异性、脱靶效应以及人类和小鼠免疫系统之间的差异等挑战突出表明,我们需要更多与人类相关的模型。新出现的多细胞模型复制了人类脑组织和神经免疫相互作用的关键方面,越来越多地提供了免疫细胞在艾滋病发病机制中作用的新见解。完善这些方法可以加深我们对免疫细胞在艾滋病中的作用的了解,并支持开发新型免疫相关治疗干预措施。
{"title":"Approaches for studying neuroimmune interactions in Alzheimer's disease.","authors":"Chih-Chung 'Jerry' Lin, Yuyao Tian, Rudolph E Tanzi, Mehdi Jorfi","doi":"10.1016/j.it.2024.10.002","DOIUrl":"10.1016/j.it.2024.10.002","url":null,"abstract":"<p><p>Peripheral immune cells play an important role in the pathology of Alzheimer's disease (AD), impacting processes such as amyloid and tau protein aggregation, glial activation, neuronal integrity, and cognitive decline. Here, we examine cutting-edge strategies - encompassing animal and cellular models - used to investigate the roles of peripheral immune cells in AD. Approaches such as antibody-mediated depletion, genetic ablation, and bone marrow chimeras in mouse models have been instrumental in uncovering T, B, and innate immune cell disease-modifying functions. However, challenges such as specificity, off-target effects, and differences between human and mouse immune systems underscore the need for more human-relevant models. Emerging multicellular models replicating critical aspects of human brain tissue and neuroimmune interactions increasingly offer fresh insights into the role of immune cells in AD pathogenesis. Refining these methodologies can deepen our understanding of immune cell contributions to AD and support the development of novel immune-related therapeutic interventions.</p>","PeriodicalId":54412,"journal":{"name":"Trends in Immunology","volume":" ","pages":"971-986"},"PeriodicalIF":13.1,"publicationDate":"2024-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11624993/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142632132","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2024-12-01Epub Date: 2024-11-21DOI: 10.1016/j.it.2024.10.006
Malcolm J W Sim, Eric O Long
Combinations of the highly polymorphic KIR and HLA-I genes are associated with numerous human diseases. Interpreting these associations requires a molecular understanding of the multiple killer-cell immunoglobulin-like receptor (KIR)-human leukocyte antigen-1 (HLA-I) receptor-ligand interactions on natural killer (NK) cells and identifying the salient features that underlie disease risk. We hypothesize that a critical discriminating factor in KIR-HLA-I interactions is the selective detection of HLA-I-bound peptides by KIRs. We propose a 'peptide selectivity model', where high-avidity KIR-HLA-I interactions reflect low selectivity for peptides conferring consistent NK cell inhibition across different tissue immunopeptidomes. Conversely, lower-avidity interactions (including those with activating KIRs) are more dependent on HLA-I-bound peptide sequence, requiring an appreciation of how HLA-I immunopeptidomes influence KIR binding and regulate NK cell function. Relevant to understanding NK cell function and pathology, we interpret known KIR-HLA-I combinations and their associations with certain human diseases in the context of this 'peptide selectivity model'.
高度多态的 KIR 和 HLA-I 基因组合与许多人类疾病相关。解读这些关联需要从分子角度了解自然杀伤(NK)细胞上的多种杀伤细胞免疫球蛋白样受体(KIR)-人类白细胞抗原-1(HLA-I)受体-配体的相互作用,并确定疾病风险的显著特征。我们假设,KIR-HLA-I 相互作用的一个关键鉴别因素是 KIR 对 HLA-I 结合肽的选择性检测。我们提出了一个 "肽选择性模型",即高活性的 KIR-HLA-I 相互作用反映了对肽的低选择性,从而在不同组织免疫肽组中产生一致的 NK 细胞抑制作用。相反,低度相互作用(包括与激活型 KIR 的相互作用)则更依赖于 HLA-I 结合的肽序列,因此需要了解 HLA-I 免疫肽组如何影响 KIR 结合并调节 NK 细胞功能。为了了解 NK 细胞的功能和病理学,我们将在这种 "肽选择性模型 "的背景下解释已知的 KIR-HLA-I 组合及其与某些人类疾病的关联。
{"title":"The peptide selectivity model: Interpreting NK cell KIR-HLA-I binding interactions and their associations to human diseases.","authors":"Malcolm J W Sim, Eric O Long","doi":"10.1016/j.it.2024.10.006","DOIUrl":"10.1016/j.it.2024.10.006","url":null,"abstract":"<p><p>Combinations of the highly polymorphic KIR and HLA-I genes are associated with numerous human diseases. Interpreting these associations requires a molecular understanding of the multiple killer-cell immunoglobulin-like receptor (KIR)-human leukocyte antigen-1 (HLA-I) receptor-ligand interactions on natural killer (NK) cells and identifying the salient features that underlie disease risk. We hypothesize that a critical discriminating factor in KIR-HLA-I interactions is the selective detection of HLA-I-bound peptides by KIRs. We propose a 'peptide selectivity model', where high-avidity KIR-HLA-I interactions reflect low selectivity for peptides conferring consistent NK cell inhibition across different tissue immunopeptidomes. Conversely, lower-avidity interactions (including those with activating KIRs) are more dependent on HLA-I-bound peptide sequence, requiring an appreciation of how HLA-I immunopeptidomes influence KIR binding and regulate NK cell function. Relevant to understanding NK cell function and pathology, we interpret known KIR-HLA-I combinations and their associations with certain human diseases in the context of this 'peptide selectivity model'.</p>","PeriodicalId":54412,"journal":{"name":"Trends in Immunology","volume":" ","pages":"959-970"},"PeriodicalIF":13.1,"publicationDate":"2024-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142694013","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2024-12-01Epub Date: 2024-11-20DOI: 10.1016/j.it.2024.11.005
Michal A Stanczak, Erika L Pearce
Tissue-resident memory (TRM) T cells not only control infection and cancer, but also contribute to inflammatory disease. In a recent study, Obers et al. demonstrate that retinoic acid (RA) and TGF-β direct TRM residency in mice, with RA uniquely retaining cells in the intestine by limiting migration. This discovery highlights the potential for harnessing local residency cues to enhance tissue-specific TRM responses.
{"title":"Please don't go: retinoic acid 'retains' tissue-specific memory.","authors":"Michal A Stanczak, Erika L Pearce","doi":"10.1016/j.it.2024.11.005","DOIUrl":"10.1016/j.it.2024.11.005","url":null,"abstract":"<p><p>Tissue-resident memory (T<sub>RM</sub>) T cells not only control infection and cancer, but also contribute to inflammatory disease. In a recent study, Obers et al. demonstrate that retinoic acid (RA) and TGF-β direct T<sub>RM</sub> residency in mice, with RA uniquely retaining cells in the intestine by limiting migration. This discovery highlights the potential for harnessing local residency cues to enhance tissue-specific T<sub>RM</sub> responses.</p>","PeriodicalId":54412,"journal":{"name":"Trends in Immunology","volume":" ","pages":"920-921"},"PeriodicalIF":13.1,"publicationDate":"2024-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142689665","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}