SEMINARS IN IMMUNOLOGY免疫学专题综述
SEMINARS IN IMMUNOLOGY(英文缩写 SEMIN IMMUNOL),ISSN 1044-5323,eISSN 1096-3618,中文译名:免疫学专题综述 是一本学术期刊。本页汇总该期刊的最新影响因子、分区信息以及最新收录于 PubMed 的文献,帮助您快速了解期刊全貌。
发文量统计区间：2025-11-01 至 2026-10-31，按本站收录文献的发表日期统计。
期刊介绍
历年影响因子趋势
| JCR 数据年份 | 影响因子 | JCR 分区 |
|---|---|---|
| 2021 | 10.671 | Q1 |
| 2022 | 7.800 | Q1 |
| 2023 | 7.400 | Q1 |
| 2024 | 7.800 | Q1 |
| 2025 | 11.500 | Q1 |
SEMINARS IN IMMUNOLOGY 最新收录文献
-
1. IL-1 signaling in cancer-associated fibroblasts: shaping fibroblast heterogeneity, tumor immunity, and therapeutic resistance.
1. 癌症相关成纤维细胞中的IL-1信号传导：塑造成纤维细胞异质性、肿瘤免疫及治疗耐药性PMID:日期:2026-10-02IL-1 signaling is a central regulator of inflammation and immune responses within the tumor microenvironment, with IL-1α and IL-1β acting as key mediators. Tumors exploit IL-1 signaling through complex autocrine and paracrine interactions among malignant cells, immune cells, and cancer-associated fibroblasts (CAFs) to promote growth and progression. CAFs comprise a heterogeneous population of stromal cells with critical roles in extracellular matrix remodeling, angiogenesis, and immune response modulation. Within the broader spectrum of CAFs exhibiting inflammatory and immunomodulatory programs, inflammatory CAFs (iCAFs) represent a distinct and well-characterized polarized fibroblast state. IL-1 is a key driver of iCAF polarization, acting primarily through NF-κB and JAK/STAT3 signaling to promote the secretion of pro-inflammatory cytokines and chemokines. These factors can enhance malignant tumor-cell phenotypes and establish self-reinforcing stromal-immune circuits that foster immunosuppression and treatment resistance. Although IL-1 signaling represents an attractive therapeutic target, the clinical efficacy of IL-1-targeted approaches has been variable. These divergent outcomes may reflect differences in tumor and patient context, treatment timing, and the functional heterogeneity of the CAF compartment, in which distinct CAF states may differentially contribute to tumor-promoting activities and responses to IL-1 inhibition. Here, we discuss the spatiotemporal dynamics of IL-1 signaling across the tumor-immune-CAF axis and evaluate emerging therapeutic strategies targeting IL-1 signaling and pro-tumorigenic CAF states to overcome immunosuppression and treatment resistance in cancer.
-
2. Latin American immunology: struggles, gaps, and global perspectives.
2. 拉丁美洲免疫学：困境、差距与全球视角PMID:日期:2026-09-19该文献暂无摘要。
-
3. I am me and my circumstance - Context dictates the outcome of IL-1 signaling in and around T cells.
PMID:日期:2026-09-11该文献暂无摘要。
-
4. Diabetes and immunity: Decoding immunometabolism for precision intervention.
4. 糖尿病与免疫：解码免疫代谢以实现精准干预PMID:日期:2026-09-03该文献暂无摘要。
-
5. Food antigen-driven immune disorders: From tolerance breakdown to precision therapeutics.
5. 食物抗原驱动的免疫紊乱：从免疫耐受破坏到精准治疗PMID:日期:2026-08-25该文献暂无摘要。
-
6. IL-1-mediated cancer-adapted hematopoiesis in aging and clonal hematopoiesis.
PMID:日期:2026-08-25A defining and evolutionary-selected feature of hematopoiesis is its capacity to adapt to organismal cellular needs. This demand-adapted hematopoiesis relies on a complex peripheric immune system capable of sensing minute amounts of damage and pathogen molecular patterns and trigger an inflammation-based reaction that sets the organism on alert. At a receiver-end of this response are bone marrow (BM) hematopoietic stem and progenitor cells (HSPCs) which rapidly sense inflammatory messages and engage in differentiating divisions to replenish the consumed innate immune cells, bringing the organism back into homeostasis. Cancer can elicit such systemic inflammatory-immune response, possibly as an initial attempt to contain tumor progression, which pushes HSPC differentiation towards myeloid cells production (myelopoiesis) in a process here termed cancer-adapted hematopoiesis (CAH). CAH leads to proliferation and mobilization of HSPCs, causing extramedullary hematopoiesis (EMH) and increased myelopoietic output that, due to its accelerated nature, generates immature myeloid cells with immunosuppressive functions that support tumor progression, generally termed myeloid-derived suppressor cells (MDSC). While multiple inflammatory pathways are implicated in CAH, here we focus on the impact of IL-1 pathway, which is a well-established modulator of HSPC biology in contexts of sterile inflammation, infection and myeloablation. We present evidence for the IL-1 pathway as a central driver of CAH acting both as a direct and indirect agent between tumors and HSPCs. Moreover, we highlight recent models on how IL-1-mediated CAH is impacted by age and clonal disorders of the hematopoietic system, further highlighting its pathological and thus targetable role in cancer progression.
-
7. Complement in tumor immunology: From a circulating cascade to a therapeutic target in the tumor microenvironment.
7. 肿瘤免疫学中的补体：从循环级联到肿瘤微环境中的治疗靶点PMID:日期:2026-08-22该文献暂无摘要。
-
8. The multifaceted roles of cellular senescence in liver pathophysiology: from tissue repair to tumor progression.
PMID:日期:2026-08-17Cellular senescence is a stress-response program that coordinates cell-autonomous growth arrest and non-cell autonomous remodeling of the tissue environment. Initially defined through its role in aging and tumor suppression, senescence is now recognized as a highly complex program shaped by cell-intrinsic and environmental factors. This complexity places senescence as a broad stress response mechanism operating at the intersection of metabolic dysfunction, chronic inflammation and tissue repair. Given its constant exposure to metabolic, inflammatory and toxic stress alongside its high regenerative demands, the liver is particularly prone to engage senescence as a protective mechanism to maintain tissue integrity. In this context, senescence exerts dual and often opposing effects. This review discusses the multifaceted roles of senescence along the liver disease trajectory, from its early protective functions in tissue repair to its later pathologic contributions to chronic liver disease and tumor progression, underscoring how cell type, stage of senescence program, disease stage and microenvironmental cues shape these divergent outcomes. We highlight the potential of emerging therapeutic interventions that modulate senescence, including pro-senescence, senolytic, senomorphic, and immune-modulating strategies. Advancing our understanding of the multifaceted roles of cellular senescence will be essential to translate this knowledge into therapies that selectively modulate senescent cell states, harnessing their beneficial effects while limiting their detrimental roles in chronic liver disease and cancer.
-
9. The burden of tuberculosis in Latin America: Immunogenetic and socioepidemiological determinants.
9. 拉丁美洲的结核病负担：免疫遗传学和社会流行病学决定因素PMID:日期:2026-08-13Tuberculosis (TB), caused by Mycobacterium tuberculosis (Mtb), remains a major global health challenge and the leading cause of death from a single infectious agent. Despite diagnostic and therapeutic advances, the COVID-19 pandemic reversed progress in TB control, with a notable rise in incidence across Latin America. This region bears a disproportionate burden of the disease due to socioeconomic inequality, limited access to healthcare, and high rates of multidrug-resistant TB. Interactions among pathogen genetics, host susceptibility, immune response, and environmental determinants critically shape disease outcomes. Several key questions remain about the higher incidence of TB in the Americas, including the roles of genetic predisposition, environmental factors, and social determinants such as poverty and migration. Addressing these issues is essential to refining control strategies. Accordingly, this review provides an updated overview of TB in Latin America, integrating immunological, genetic, and socio-epidemiological perspectives that could be useful for future research and policy discussions toward more region-specific interventions against Mtb.
-
10. The IL-1 system in inflammation and cancer.
10. 炎症和癌症中的IL-1系统PMID:日期:2026-08-08Inflammation is a pathogenetic driver of several pathological conditions, including cancer. The tumor microenvironment, which includes cellular, molecular, and structural components, is an essential component of cancer, involved in tumor promoting or controlling processes. In particular, inflammatory players contribute to the establishment of a tumor-promoting microenvironment, which affects all stages of tumor development, from initiation to metastasis, as well as response to therapy. The IL-1 system includes two large sets of structurally related ligands and receptors, with agonist or regulatory activity, playing non-redundant roles in inflammation and immunity. Each of them has specific functions in tissue homeostasis, inflammation, innate and adaptive immune responses, and potentially contributes to processes related to carcinogenesis and metastasis, or immune-mediated control of cancer cells. Depending on the context and cellular target, IL-1 family members may play dual roles in cancer, driving both pro- or anti-tumor processes. IL-1α and IL-1β can directly promote cancer cell proliferation, survival, and plasticity, in addition to contribute to the establishment of a pro-inflammatory environment that promotes tissue remodeling, cellular stress responses, and genomic instability. On the other hand, IL-1 is a lymphoproliferative and activating molecule in innate and adaptive responses, thus contributing to anti-tumor immune mediated responses. In addition, members of the IL-1 system act as regulators of mechanisms involved in cancer, including emergency hematopoiesis, trained immunity, and metabolism. Here, we will provide an overview of the IL-1 system in cancer and discuss the functional complexity of IL-1 family cytokines, which orchestrate both protective and pro-tumorigenic responses, by directly acting on cancer cells and by driving environmental stimuli which indirectly act on cancer cells.