Immunology最新文献

{"title":"CCR5-mediated homing of regulatory T cells and monocytic-myeloid derived suppressor cells to dysfunctional endothelium contributes to early atherosclerosis","authors":"Shamima Akhtar,&nbsp;Komal Sagar,&nbsp;Ambuj Roy,&nbsp;Milind P. Hote,&nbsp;Sudheer Arava,&nbsp;Alpana Sharma","doi":"10.1111/imm.13859","DOIUrl":"10.1111/imm.13859","url":null,"abstract":"<p>A disbalance between immune regulatory cells and inflammatory cells is known to drive atherosclerosis. However, the exact mechanism is not clear. Here, we investigated the homing of immune regulatory cells, mainly, regulatory T cells (Tregs) and myeloid-derived suppressor cells (MDSCs) subsets in asymptomatic coronary artery disease (CAD) risk factor-exposed young individuals (dyslipidemia [DLP] group) and stable CAD patients (CAD group). Compared with healthy controls (HCs), Tregs frequency was reduced in both DLP and CAD groups but expressed high levels of CCR5 in both groups. The frequency of monocytic-myeloid-derived suppressor cells (M-MDSCs) was increased while polymorphonuclear myeloid-derived suppressor cells (PMN-MDSCs) were decreased in CAD patients only. Interestingly, although unchanged in frequency, M-MDSCs of the DLP group expressed high levels of CCR5. Serum levels of chemokines (CCL5, CX3CL1, CCL26) and inflammatory cytokines (IL-6, IL-1β, IFN-γ, TNF-α) were higher in the DLP group. Stimulation with inflammatory cytokines augmented CCR5 expression in Tregs and M-MDSCs isolated from HCs. Activated endothelial cells showed elevated levels of CX3CL1 and CCL5 in vitro. Blocking CCR5 with D-Ala-peptide T-amide (DAPTA) increased Treg and M-MDSC frequency in C57Bl6 mice fed a high-fat diet. In accelerated atherosclerosis model, DAPTA treatment led to the formation of smooth muscle-rich plaque with less macrophages. Thus, we show that CCR5-CCL5 axis is instrumental in recruiting Tregs and M-MDSCs to dysfunctional endothelium in the asymptomatic phase of atherosclerosis contributing to atherosclerosis progression. Drugs targeting CCR5 in asymptomatic and CAD risk-factor/s-exposed individuals might be a novel therapeutic regime to diminish atherogenesis.</p>","PeriodicalId":13508,"journal":{"name":"Immunology","volume":"173 4","pages":"712-729"},"PeriodicalIF":4.9,"publicationDate":"2024-09-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142214523","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Contributions of each of the BAFF receptors to the lymphocyte profiles in C57BL/6 mice","authors":"William Stohl,&nbsp;Ying Wu,&nbsp;Malka Stohl","doi":"10.1111/imm.13856","DOIUrl":"10.1111/imm.13856","url":null,"abstract":"<p>BAFF, a vital B cell survival and differentiation factor, has three receptors: B-cell maturation antigen (BCMA), transmembrane activator and CAML interactor (TACI) and BR3. Although B cells are greatly reduced in B6.<i>Baff</i>^−/− (which harbour no BAFF) and B6.<i>Br3</i>^−/− mice (which harbour supra-normal levels of BAFF), the distributions of B cell subsets and relationships between Foxp3⁺ and CD4⁺ cells in these mice differ. Using a large panel of B6 congenic knockout and/or transgenic mice, we demonstrate that (1) supra-normal levels of BAFF per se do not explain the phenotypic differences between B6.<i>Baff</i>^−/− and B6.<i>Br3</i>^−/− mice; (2) B cells are expanded in B6.<i>Taci</i>^−/− mice, with preferential expansion of follicular (FO) B cells at the expense of CD19⁺CD21^−/loCD23^−/lo B cells but without the preferential expansion of Foxp3⁺ cells observed in B6 mice bearing a <i>Baff</i> transgene; (3) despite no expansion in total B cells, percentages of FO B cells and marginal zone B cells are higher and percentages of CD19⁺CD21^−/loCD23^−/lo B cells are lower in young B6.<i>Bcma</i>^−/− mice, consistent with the inability of B6.<i>Br3</i>^−/−<i>.Taci</i>^−/− mice to recapitulate the B cell profile of B6.<i>Baff</i>^−/− mice; and (4) percentages of Foxp3⁺ cells in B6.<i>Br3</i>^−/−<i>.Taci</i>^−/− mice are intermediate between those in B6.<i>Br3</i>^−/− and B6.<i>Taci</i>^−/− mice despite the B cell profile of B6.<i>Br3</i>^−/−<i>.Taci</i>^−/− mice strongly resembling that of B6.<i>Br3</i>^−/− mice. Collectively, our findings point to a non-redundant role for each of the BAFF receptors in determining the ultimate lymphocyte profile of the host. This may have clinically relevant ramifications in that the degree that a candidate therapeutic agent blocks engagement of any given individual BAFF receptor may affect its clinical utility.</p>","PeriodicalId":13508,"journal":{"name":"Immunology","volume":"173 4","pages":"689-711"},"PeriodicalIF":4.9,"publicationDate":"2024-08-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1111/imm.13856","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142107021","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Towards understanding the role of nanomedicine in targeting TNFR2 in rheumatoid arthritis","authors":"Fatmawati Lambuk,&nbsp;Nor Asyikin Nordin,&nbsp;Ali Mussa,&nbsp;Lidawani Lambuk,&nbsp;Suhana Ahmad,&nbsp;Rosline Hassan,&nbsp;Ramlah Kadir,&nbsp;Rohimah Mohamud,&nbsp;Nurul Khaiza Yahya","doi":"10.1111/imm.13855","DOIUrl":"10.1111/imm.13855","url":null,"abstract":"<p>Rheumatoid arthritis (RA) is a chronic autoimmune disease characterized by inflammation of the synovium and progressive joint destruction which significantly affects both quality of life and socioeconomic status. Admittedly, various treatments are available, but they are usually accompanied by various side effects, from mild to severe, and potentially with adverse events. Tumour necrosis factor-alpha (TNF-α) plays a crucial role in the pathophysiology of RA. It promotes inflammatory, apoptosis and necroptosis via TNF receptor-1 (TNFR1) but elicit anti-inflammatory effects via TNFR2. Herein, targeting TNFR2 has gained attention in RA studies. Understanding the role of nanomedicine in modulating TNFR2 signalling may be the instrument in development of RA therapies. Nanotechnology has made a significant progress in treating various conditions of diseases since its inception. Due to this, nanomedicine has emerged as a promising therapeutics approach for RA. Recent studies have demonstrated the potential of nanomedicine in RA theranostics, combining therapy and diagnostics for improved treatment outcomes. Owing to the challenges and advancements in the field of nanotechnology, nanoparticles are seen as an applicable candidate in the treatment of RA. In this review, we provide an overview of the role of nanomedicine in targeting TNFR2 for the treatment of RA and highlight the limitations of current therapies as well as the potential of nanocarriers with controlled drug release and active targeting abilities.</p>","PeriodicalId":13508,"journal":{"name":"Immunology","volume":"173 4","pages":"622-633"},"PeriodicalIF":4.9,"publicationDate":"2024-08-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1111/imm.13855","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142080196","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Hypoxic tumour-derived exosomal miR-1290 exacerbates the suppression of CD8+ T cells by promoting M2 macrophage polarization","authors":"Yeni Yang,&nbsp;Tiansong Wu,&nbsp;Youpeng Wang,&nbsp;Dingan Luo,&nbsp;Ziyin Zhao,&nbsp;Hongfa Sun,&nbsp;Mao Zhang,&nbsp;Bin Zhang,&nbsp;Bing Han","doi":"10.1111/imm.13853","DOIUrl":"10.1111/imm.13853","url":null,"abstract":"<p>Hypoxia plays an important role in the metastasis of hepatocellular carcinoma (HCC). Exosomes have been widely studied as mediators of communication between tumours and immune cells. However, the specific mechanism by which hypoxic HCC cell-derived exosomes suppress antitumor immunity is unclear. Hypoxia scores were determined for The Cancer Genome-Liver Hepatocellular Carcinoma (TCGA-LIHC) dataset patients, and HCC patients in the hyperhypoxic group had a higher degree of M2 macrophage infiltration. Patients in the M2 high-invasion group had a lower probability of survival than those in the low-invasion group. In vivo and in vitro experiments demonstrated that exosomes secreted by hypoxic HCC cells promote M2 macrophage polarization. This polarization induces apoptosis in CD8+ T cells. Additionally, it encourages epithelial–mesenchymal transition (EMT), which increases HCC migration. Exosomal miRNA sequencing revealed that miR-1290 was highly expressed in exosomes secreted by hypoxic HCC cells. Mechanistically, miR-1290 in macrophages inhibited Akt2 while upregulating PD-L1 to promote M2 polarization, induce apoptosis in CD8⁺ T cells, and enhance EMT in HCC. Animal studies found that the miR-1290 antagomir in combination with the immune checkpoint inhibitor produced better antitumor effects than the monotherapies. In conclusion, the secretion of exosome-derived miR-1290 from HCC cells in a hypoxic environment supported immune escape by HCC cells by promoting M2 macrophage polarization to induce apoptosis in CD8⁺ T cells and enhance EMT that promoted HCC metastasis. Therefore, miR-1290 is an important molecule in antitumor immunity in HCC, and inhibition of miR-1290 could provide a novel immunotherapeutic approach for HCC treatment.</p>","PeriodicalId":13508,"journal":{"name":"Immunology","volume":"173 4","pages":"672-688"},"PeriodicalIF":4.9,"publicationDate":"2024-08-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142055476","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Microscopic marvels: Decoding the role of micropeptides in innate immunity","authors":"Praveena Naidu,&nbsp;Mandë Holford","doi":"10.1111/imm.13850","DOIUrl":"10.1111/imm.13850","url":null,"abstract":"<p>The innate immune response is under selection pressures from changing environments and pathogens. While sequence evolution can be studied by comparing rates of amino acid mutations within and between species, how a gene's birth and death contribute to the evolution of immunity is less known. Short open reading frames, once regarded as untranslated or transcriptional noise, can often produce micropeptides of &lt;100 amino acids with a wide array of biological functions. Some micropeptide sequences are well conserved, whereas others have no evolutionary conservation, potentially representing new functional compounds that arise from species-specific adaptations. To date, few reports have described the discovery of novel micropeptides of the innate immune system. The diversity of immune-related micropeptides is a blind spot for gene and functional annotation. Immune-related micropeptides represent a potential reservoir of untapped compounds for understanding and treating disease. This review consolidates what is currently known about the evolution and function of innate immune-related micropeptides to facilitate their investigation.</p>","PeriodicalId":13508,"journal":{"name":"Immunology","volume":"173 4","pages":"605-621"},"PeriodicalIF":4.9,"publicationDate":"2024-08-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1111/imm.13850","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142072704","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Altered epitopes enhance macrophage-mediated anti-tumour immunity to low-immunogenic tumour mutations","authors":"Qiumin Yu,&nbsp;Tingran Zhang,&nbsp;Tiandi He,&nbsp;Yifan Yang,&nbsp;Wanli Zhang,&nbsp;Yanliang Kang,&nbsp;Zijie Wu,&nbsp;Wenbin Xie,&nbsp;Jiaxue Zheng,&nbsp;Qianqian Qian,&nbsp;Guozhi Li,&nbsp;Di Zhang,&nbsp;Qiuli Mao,&nbsp;Zheng Gao,&nbsp;Xiaoning Wang,&nbsp;Xupeiyao Shi,&nbsp;Shitong Huang,&nbsp;Hanlin Guo,&nbsp;Haoyu Zhang,&nbsp;Lingxiao Chen,&nbsp;Ximing Li,&nbsp;Danni Deng,&nbsp;Li Zhang,&nbsp;Yue Tong,&nbsp;Wenbing Yao,&nbsp;Xiangdong Gao,&nbsp;Hong Tian","doi":"10.1111/imm.13854","DOIUrl":"10.1111/imm.13854","url":null,"abstract":"<p>Personalized neoantigen therapy has shown long-term and stable efficacy in specific patient populations. However, not all patients have sufficient levels of neoantigens for treatment. Although somatic mutations are commonly found in tumours, a significant portion of these mutations do not trigger an immune response. Patients with low mutation burdens continue to exhibit unresponsiveness to this treatment. We propose a design paradigm for neoantigen vaccines by utilizing the highly immunogenic unnatural amino acid p-nitrophenylalanine (pNO₂Phe) for sequence alteration of somatic mutations that failed to generate neoepitopes. This enhances the immunogenicity of the mutations and transforms it into a suitable candidate for immunotherapy. The nitrated altered epitope vaccines designed according to this paradigm is capable of activating circulating CD8⁺ T cells and inducing immune cross-reactivity against autologous mutated epitopes in different MHC backgrounds (H-2K^b, H-2K^d, and human HLA-A02:01), leading to the elimination of tumour cells carrying the mutation. After immunization with the altered epitopes, tumour growth was significantly inhibited. It is noteworthy that nitrated epitopes induce tumour-infiltrating macrophages to differentiate into the M1 phenotype, surprisingly enhancing the MHC II molecule presenting pathway of macrophages. Nitrated epitope-treated macrophages have the potential to cross-activate CD4⁺ and CD8⁺ T cells, which may explain why pNO₂Phe can enhance the immunogenicity of epitopes. Meanwhile, the immunosuppressive microenvironment of the tumour is altered due to the activation of macrophages. The nitrated neoantigen vaccine strategy enables the design of vaccines targeting non-immunogenic tumour mutations, expanding the pool of potential peptides for personalized and shared novel antigen therapy. This approach provides treatment opportunities for patients previously ineligible for new antigen vaccine therapy.</p>","PeriodicalId":13508,"journal":{"name":"Immunology","volume":"173 4","pages":"654-671"},"PeriodicalIF":4.9,"publicationDate":"2024-08-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142035754","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Advancement in the development of mRNA-based vaccines for respiratory viruses","authors":"Tays Troncoso-Bravo,&nbsp;Mario A. Ramírez,&nbsp;Ricardo A. Loaiza,&nbsp;Carolina Román-Cárdenas,&nbsp;Georgios Papazisis,&nbsp;Daniel Garrido,&nbsp;Pablo A. González,&nbsp;Susan M. Bueno,&nbsp;Alexis M. Kalergis","doi":"10.1111/imm.13844","DOIUrl":"10.1111/imm.13844","url":null,"abstract":"<p>Acute respiratory infections are the leading cause of death and illness in children under 5 years old and represent a significant burden in older adults. Primarily caused by viruses infecting the lower respiratory tract, symptoms include cough, congestion, and low-grade fever, potentially leading to bronchiolitis and pneumonia. Messenger ribonucleic acid (mRNA)-based vaccines are biopharmaceutical formulations that employ mRNA molecules to induce specific immune responses, facilitating the expression of viral or bacterial antigens and promoting immunization against infectious diseases. Notably, this technology had significant relevance during the COVID-19 pandemic, as these formulations helped to limit SARS-CoV-2 virus infections, hospitalizations, and deaths. Importantly, mRNA vaccines promise to be implemented as new alternatives for fighting other respiratory viruses, such as influenza, human respiratory syncytial virus, and human metapneumovirus. This review article analyzes mRNA-based vaccines' main contributions, perspectives, challenges, and implications against respiratory viruses.</p>","PeriodicalId":13508,"journal":{"name":"Immunology","volume":"173 3","pages":"481-496"},"PeriodicalIF":4.9,"publicationDate":"2024-08-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1111/imm.13844","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142004164","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Featured Cover","authors":"","doi":"10.1111/imm.13852","DOIUrl":"https://doi.org/10.1111/imm.13852","url":null,"abstract":"<p>Cover illustration: The cover image is based on the article <i>Immunotherapy and the ovarian cancer microenvironment: Exploring potential strategies for enhanced treatment efficacy</i> by Zhi-Bin Wang et al., https://doi.org/10.1111/imm.13793.\u0000 <figure>\u0000 <div><picture>\u0000 <source></source></picture><p></p>\u0000 </div>\u0000 </figure></p>","PeriodicalId":13508,"journal":{"name":"Immunology","volume":"173 1","pages":"i"},"PeriodicalIF":4.9,"publicationDate":"2024-08-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1111/imm.13852","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141986070","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The role and therapeutic strategies for tissue-resident memory T cells, central memory T cells, and effector memory T cells in psoriasis","authors":"Guoshu Deng,&nbsp;Yulin Zhang,&nbsp;Jiankun Song,&nbsp;Ying Zhang,&nbsp;Qi Zheng,&nbsp;Yue Luo,&nbsp;Xiaoya Fei,&nbsp;Yang Yang,&nbsp;Le Kuai,&nbsp;Bin Li,&nbsp;Ying Luo","doi":"10.1111/imm.13843","DOIUrl":"10.1111/imm.13843","url":null,"abstract":"<p>Psoriasis is a skin disease that is inflammatory and persistent, causing a high rate of recurrence, poor quality of life, and significant socioeconomic burden. Its main pathological manifestations are abnormal activation and infiltration of T cells and excessive proliferation of keratinocytes (KCs). The great majority of patients with psoriasis will relapse after remission. It usually lasts a lifetime and necessitates long-term treatment strategies. During periods of activity and remission, one of the main cell types in psoriasis is memory T cells, which include tissue-resident memory T (TRM) cells, central memory T (TCM) cells, and effector memory T (TEM) cells. They work by releasing inflammatory factors, cytotoxic particles, or altering cell subpopulations, leading to increased inflammation or recurrence. This review summarizes the role of memory T cells in the pathology and treatment of psoriasis, with a view to potential novel therapies and therapeutic targets.</p>","PeriodicalId":13508,"journal":{"name":"Immunology","volume":"173 3","pages":"470-480"},"PeriodicalIF":4.9,"publicationDate":"2024-08-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1111/imm.13843","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141971043","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Mast cells contribute to T-cell accumulation in the bronchoalveolar space in mice with IL-33-induced airway inflammation","authors":"P. Abigail Alvarado-Vazquez,&nbsp;Erika Mendez-Enriquez,&nbsp;Lisa Pähn,&nbsp;Aleksandra Dondalska,&nbsp;Diego Pazos-Castro,&nbsp;Jenny Hallgren","doi":"10.1111/imm.13849","DOIUrl":"10.1111/imm.13849","url":null,"abstract":"<p>Interleukin (IL)-33 released from airway epithelial cells plays a vital role in shaping type 2 immune responses by binding to the ST2 receptor present in many immune cells, including mast cells (MCs). Intranasal administration of IL-33 in mice induces type 2 lung inflammation, an increase in lung MC progenitors, and transepithelial migration of leukocytes to the bronchoalveolar space. The aim of this study was to determine the contribution of MCs in IL-33-induced lung pathology. Four daily intranasal administrations of IL-33 reduced spirometry-like lung function parameters, induced airway hyperresponsiveness, and increased leukocytes in bronchoalveolar lavage fluid (BAL) in an ST2-dependent manner. MC-deficient (Cpa3^cre/+) mice, which lack MCs, had intact spirometry-like lung function but slightly reduced airway hyperresponsiveness, possibly related to reduced IL-33 or serotonin. Strikingly, Cpa3^cre/+ mice exposed to IL-33 had 50% reduction in BAL T-cells, and CXCL1 and IL-33 were reduced in the lung. Intranasal IL-33 induced CXCR2 expression in T-cells in a MC-independent fashion. Furthermore, IL-33-induced lung MCs were immunopositive for CXCL1 and localized in the epithelium of wild-type mice. These results suggest that MCs are required to sustain intact lung IL-33 and CXCL1 levels in mice with IL-33-induced airway inflammation, thereby facilitating T-cell accumulation in the bronchoalveolar space.</p>","PeriodicalId":13508,"journal":{"name":"Immunology","volume":"173 3","pages":"590-602"},"PeriodicalIF":4.9,"publicationDate":"2024-08-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1111/imm.13849","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141916527","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}