Danielle Oliveira da Fonseca, Marco Antonio Moreira Puga, Vanessa T Gubert, Erica Freire de Vasconcelos Pereira, Vanessa Marcon de Oliveira, Maxlainy Tosta, Mariana Vidotti de Jesus, Inês Aparecida Tozetti
{"title":"Cellular Immune Response to High-Risk Human Papillomavirus Infection: A Systematic Review.","authors":"Danielle Oliveira da Fonseca, Marco Antonio Moreira Puga, Vanessa T Gubert, Erica Freire de Vasconcelos Pereira, Vanessa Marcon de Oliveira, Maxlainy Tosta, Mariana Vidotti de Jesus, Inês Aparecida Tozetti","doi":"10.1615/CritRevImmunol.2025057517","DOIUrl":"https://doi.org/10.1615/CritRevImmunol.2025057517","url":null,"abstract":"<p><p>The relationship between human papillomavirus (HPV) and immune cells is vital for understanding the pathophysiology of infection and its role in neoplastic progression. High-risk human papillomavirus (HR-HPV) is the main cause of cervical cancer (CC). Thus, the association between immune response cells, the virus, and its behavior according to cervical disease development could provide new ways for understanding the entire process. Since the role and the presence of the immune response cells in the uterus cervix considering HPV infection has not been elucidated so far, this study aimed to identify the immune cells involved in high-grade intraepithelial lesions (HSIL) and CC development related to uterine cervical infection caused by HR-HPV. The study population included women who had positive molecular tests for HPV. Through the databases MEDLINE, EMBASE, LILACS, Cochrane, Scopus, Web of Science, CINAHL, Science Direct, and Google Scholar we identified 6,698 studies at the beginning. After the systematic review steps, the final number of included studies was 22. Cervical lesions were distributed according to the severity of lesions in HSIL, low-grade squamous intraepithelial lesions (LSIL), and negative for intraepithelial lesions or malignancy (NILM). The cellular phenotypes presented in these publications were T lymphocytes (LT), regulatory T lymphocytes (Tregs), macrophages (MØ), natural killer cells (NK), natural killer T cells (NKT), Langerhans cells (LC), and dendritic cells (DC). Among the observed associations with cervical lesions and HR-HPV, we highlight the DC/LC and MØ being 36.4% of the cell types, followed by Tregs (31.8%) and LT CD4 / CD8 with 27.3%. The increased findings in innate and adaptive immunological response may imply both are acting together, with the innate response cells and Tregs being the most prominent. Since these cells have great importance in the maintenance and balance of the immunological system, the present study highlights the essential role of MØ and Treg cells in the process of cervical lesion severity associated with HPV, suggesting that they may be focused as prognostic markers and immunotherapeutic targets.</p>","PeriodicalId":55205,"journal":{"name":"Critical Reviews in Immunology","volume":"45 3","pages":"33-49"},"PeriodicalIF":0.8,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144217634","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"MAp44: Emerging Insights into Its Role in Disease Pathogenesis and Association with Various Diseases.","authors":"Yvonne Guithuiliu Pamei, Swekcha, Neha Sharma, Devinder Toor","doi":"10.1615/CritRevImmunol.2025057896","DOIUrl":"https://doi.org/10.1615/CritRevImmunol.2025057896","url":null,"abstract":"<p><p>The MBL-associated protein of 44 kilodaltons (MAp44) belongs to the MBL-associated serine proteases (MASP) family, which is important in regulating the complement system's alternative pathway. MAp44 has been discovered to interact with complement components in numerous autoimmune illnesses leading to complement dysregulation and amplification of inflammatory reactions. These findings imply that MAp44 could be a biomarker for disease conditions and a therapeutic target for reducing complement-mediated illness. Furthermore, recent findings reveal that MAp44 has a role in cancer genesis and progression. Its participation in tumor immune evasion, angiogenesis, and metastasis has been revealed in studies, underlining its potential as a prognostic marker and a prospective target for cancer treatment. MAp44 targeting may boost immune surveillance, decrease tumor development, and improve patient outcomes in a variety of cancers. Recent research has revealed its participation in a variety of disease processes, indicating it as a possible contributor to disease etiology. The developing understanding of MAp44's role lays the groundwork for future study and development of targeted treatment approaches. Understanding the complicated processes behind its participation in autoimmune illnesses, cancer, and cardiovascular diseases opens up new possibilities for diagnosis, prognosis, and therapy approaches. Exploiting MAp44's therapeutic potential might open the door for innovative therapies targeted at improving patient outcomes in a variety of illnesses. This review gives a comprehensive knowledge of the role of MAp44 in diseases and its therapeutic potential.</p>","PeriodicalId":55205,"journal":{"name":"Critical Reviews in Immunology","volume":"45 4","pages":"57-70"},"PeriodicalIF":0.9,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144762419","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Role of Splenocytes on T Cells and Its Cytokine Network in Rheumatoid Arthritis.","authors":"Saayaa Nazar, Yeswanth Ranganathan, Helen Antony","doi":"10.1615/CritRevImmunol.2025060175","DOIUrl":"https://doi.org/10.1615/CritRevImmunol.2025060175","url":null,"abstract":"<p><p>Rheumatoid arthritis (RA) is a chronic autoimmune condition that impacts the immune system, especially through changes in the splenic immune cell system. This review provides an overview of the role of splenocytes in T cell signaling and their immune response in RA patients. The spleen acts as a critical site for the activation and differentiation of splenic immune cells like T cells, B cells, macrophages, dendritic cells, and NK cells. In RA, splenomegaly is characterized by increased immune cell infiltration and altered architecture is often observed, contributing to the disease's pathogenesis. Antigen presentation via major histocompatibility complex (MHC) molecules, specifically HLA DRB1, mediates the contact between splenocytes and T cells, resulting in the clonal growth of autoreactive T cells. This study explains how splenocytes, in response to a pro-inflammatory cytokine, affect T cell development into pathogenic subsets including Th1, Th2, and Th17. It also emphasizes how important dendritic cells and macrophages are for digesting antigens and priming T cells and how NK cells influence T cell responses by releasing cytokines. This study highlights the role of the spleen in the immunopathology of RA and offers possible treatment approaches that target immune response modulation and systemic inflammation reduction.</p>","PeriodicalId":55205,"journal":{"name":"Critical Reviews in Immunology","volume":"45 5","pages":"35-47"},"PeriodicalIF":0.9,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145024854","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Zhengdong Guo, Hongming Zhu, Renmin Zhang, Qiang Shan, Yajing Wang
{"title":"miR-205-5p Promotes the Proliferation, Migration, and Invasion of Nasopharyngeal Carcinoma Cells by Regulating CALM1.","authors":"Zhengdong Guo, Hongming Zhu, Renmin Zhang, Qiang Shan, Yajing Wang","doi":"10.1615/CritRevImmunol.2024055296","DOIUrl":"10.1615/CritRevImmunol.2024055296","url":null,"abstract":"<p><p>Nasopharyngeal carcinoma (NPC), a malignant tumor originating from the epithelium and glands. MicroRNAs (miRNAs) play an essential role in the tumorigenesis and metastasis of NPC. They are effective biomarkers in the detection of malignant progression of NPC. In this study, we analyzed the expression profiles of miRNAs in NPC patients with Gene Expression Omnibus (GEO) database. ceRNA networks of NPC were constructed and target miRNAs were screened. MTT, colony formation and Transwell experiments were used to explore the effects of miR-205-5p on the proliferation, migration and invasion ability of NPC cells. Bioinformatics analysis combined with Double luciferase experiment verified the binding relationship between miR-205-5p and CALM1. We identified 34 long non-coding RNAs (lncRNAs), 22 miRNAs, and 145 messenger RNAs (mRNAs) and constructed a competing endogenous RNAs (ceRNA) network to explain the relationship between RNA expression profiles and NPC progression. Of which, we found that 5 miRNAs (hsa-let-7d-5p, hsa-let-7e-5p, hsa-let-7f-5p, hsa-miR-143-3p and hsa-miR-205-5p) are related to clinical features. We further found that miR-205-5p was highly expressed in NPC cell lines. In addition, MTT, colony formation and Transwell assays showed that miR-205-5p promoted the proliferation, migration and invasion of NPC cells. Double luciferase detection showed that miR-205-5p could target combined with CALM1. In addition, we found that miR-205-5p could promote the proliferation, migration and invasion of NPC cells by inhibited the expression of CALM1. Overall, the present study demonstrated that as a carcinogenic factor, miR-205-5p can affect the malignant progression of NPC by mediating CALM1.</p>","PeriodicalId":55205,"journal":{"name":"Critical Reviews in Immunology","volume":"45 2","pages":"25-38"},"PeriodicalIF":0.8,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143460859","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Shreya S Sonak, Sharda Ishwarkar, Charu Nimbarte, Vijaykumar D Nimbarte
{"title":"Caseinolytic Protease P: A Therapeutic Nexus in Infection, Inflammation, and Immunity.","authors":"Shreya S Sonak, Sharda Ishwarkar, Charu Nimbarte, Vijaykumar D Nimbarte","doi":"10.1615/CritRevImmunol.2025059878","DOIUrl":"https://doi.org/10.1615/CritRevImmunol.2025059878","url":null,"abstract":"<p><p>Caseinolytic protease P (ClpP) is a highly conserved serine protease that plays a pivotal role in protein homeostasis and quality control in bacteria, mitochondria of mammalian cells, and plant chloroplasts. As the proteolytic core of the ATP-dependent Clp protease complex, ClpP partners with regulatory ATPases (e.g., ClpX, ClpA) to degrade misfolded, damaged, or regulatory proteins. In bacteria, ClpP is crucial for survival under host-imposed stresses and modulates virulence through degradation of transcriptional regulators and signaling proteins, contributing to immune evasion, dormancy, and persistence. Particularly in pathogens like Mycobacterium tuberculosis, Staphylococcus aureus, and Listeria monocytogenes, ClpP supports intracellular adaptation and resistance, making it a promising target against antimicrobial-resistant (AMR) infections. In mammalian cells, mitochondrial ClpP ensures oxidative phosphorylation efficiency and regulates innate immunity. Loss of ClpP function can result in mitochondrial dysfunction, triggering immune activation via cytosolic leakage of mitochondrial DNA and subsequent cGAS-STING pathway stimulation. ClpP also influences cytokine production and immune cell differentiation. This dual role of ClpP in pathogen virulence and host immune modulation highlights its potential as an immunotherapeutic target. Pharmacological manipulation of ClpP activity offers novel opportunities for treating infectious diseases, inflammatory conditions, and cancer. Further investigation into ClpP's regulatory mechanisms could inform next-generation host-pathogen intervention strategies.</p>","PeriodicalId":55205,"journal":{"name":"Critical Reviews in Immunology","volume":"45 5","pages":"49-65"},"PeriodicalIF":0.9,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145024842","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Shreya S Sonak, Sharda Ishwarkar, Charu Nimbarte, Vijaykumar D Nimbarte
{"title":"Modulation of T Cell Regulation by Interleukin-2 Agonists: Mechanisms and Clinical Implications.","authors":"Shreya S Sonak, Sharda Ishwarkar, Charu Nimbarte, Vijaykumar D Nimbarte","doi":"10.1615/CritRevImmunol.2025059823","DOIUrl":"https://doi.org/10.1615/CritRevImmunol.2025059823","url":null,"abstract":"<p><p>IL-2 agonists significantly modulate T cell regulation, impacting activation, proliferation, differentiation, and immune homeostasis. Interleukin-2 (IL-2) is crucial for T cell growth and function, binding to the IL-2 receptor to trigger signaling pathways that balance immune responses. IL-2 promotes the expansion of effector T cells and enhances regulatory T cells (Tregs), preventing autoimmune responses. This review examines the mechanisms of IL-2 agonists on T cell regulation, including their roles in cytotoxic T cells and Tregs proliferation, and immune homeostasis. Clinically, IL-2 agonists show promise in treating autoimmune diseases by boosting Treg function and in cancer immunotherapy by enhancing cytotoxic T cell activity. Optimizing IL-2 therapies to balance these effects is ongoing. IL-2 agonists are pivotal in modulating T cell responses with significant therapeutic potential for autoimmunity and cancer. Understanding IL-2 signaling is crucial for developing targeted treatments leveraging this cytokine's benefits.</p>","PeriodicalId":55205,"journal":{"name":"Critical Reviews in Immunology","volume":"45 5","pages":"19-34"},"PeriodicalIF":0.9,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145024859","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Edward Sher, Meng-Wei Ko, Kawaljit Kaur, Anahid Jewett
{"title":"Processed Osteoclasts Similar to Live Osteoclasts are Capable of Supercharging Natural Killer (sNK) Cells.","authors":"Edward Sher, Meng-Wei Ko, Kawaljit Kaur, Anahid Jewett","doi":"10.1615/CritRevImmunol.2025056318","DOIUrl":"10.1615/CritRevImmunol.2025056318","url":null,"abstract":"<p><p>In this paper, we compared the ability to expand/supercharge NK cells (sNK) by either processed osteoclasts (pOCs) or live osteoclasts (OCs). pOCs induced similar levels of cell expansion in NK cells compared to live OCs. pOC-generated sNK cells exhibited lower lysis of oral squamous carcinoma stem-like cells (OSCSCs) tumors in comparison to live OC-generated sNK cells. Slightly lower levels of IFN-γ secretion were also observed in pOC-generated sNK cells when compared to live OC-generated sNK cells. Cytotoxic function and secretion levels of IFN-γ remained low in pOC-sNK cultures compared to OC-sNK cultures even after adding the supernatants harvested from live OCs to pOC-sNK cultures. pOCs were equally capable of selecting CD8+ T cells in sNK cell cultures when compared to live OCs. Overall, even though live OCs are capable of activating slightly better than the processed osteoclasts, the use of pOCs is preferable for the expansion of sNK cells due to shorter NK expansion period, higher cost-effectiveness, and faster availability for patient infusion.</p>","PeriodicalId":55205,"journal":{"name":"Critical Reviews in Immunology","volume":"45 4","pages":"31-42"},"PeriodicalIF":0.9,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144762420","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Supercharged NK Cells as a Promising Therapeutic Strategy to Target and Eliminate Aggressive DIPG Tumors in Pediatric Patients.","authors":"Anahid Jewett, Kawaljit Kaur, Naira Gharamanians","doi":"10.1615/CritRevImmunol.2025059050","DOIUrl":"https://doi.org/10.1615/CritRevImmunol.2025059050","url":null,"abstract":"<p><p>Diffuse intrinsic pontine glioma (DIPG) is the common cause of death in pediatric patients. In this report, we discussed the role of supercharged NK (sNK) cells alone or in combination with other therapies to target such aggressive pediatric brain tumors, suggesting the potential use of sNK cells alone as a therapeutic strategy in treating and preventing the recurrence of aggressive pediatric brain tumors.</p>","PeriodicalId":55205,"journal":{"name":"Critical Reviews in Immunology","volume":"45 4","pages":"13-16"},"PeriodicalIF":0.9,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144762421","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Ying Zhou, Lanying Zou, Jun Xu, Xiaoping Zhou, Huichuan Zhao
{"title":"The Overexpression of EP4 Attenuates the Killing Ability of CD8+ T Cells against Prostate Cancer Cells through the PI3K/AKT Signaling Pathway.","authors":"Ying Zhou, Lanying Zou, Jun Xu, Xiaoping Zhou, Huichuan Zhao","doi":"10.1615/CritRevImmunol.2024052115","DOIUrl":"10.1615/CritRevImmunol.2024052115","url":null,"abstract":"<p><p>Immunotherapy has shown significant promise in the clinical management of prostate cancer (PCa), and prostaglandin E receptor 4 (EP4) is a key governing factor in PCa progression. However, the molecular mechanisms by which EP4 influences immunotherapy in PCa have yet to be elucidated. This investigation was designed to unravel the specific mechanisms through which EP4 affects the killing ability of CD8+ T cells against PCa cells. Immunohistochemistry was utilized to assay the expression of EP4, programmed death ligand 1 (PD-L1), and CD8+ T cell infiltration in tissue samples, and quantitative real-time polymerase chain reaction (qRT-PCR) and Western blot (WB) were used to evaluate EP4 expression in cells. PCa cell lines with either EP4 knockdown or overexpression were co-cultured with CD8+ T cells. Lactase dehydrogenase toxicity assays were employed to measure CD8+T cell killing ability, and ELISA was employed to measure interferon-gamma (IFN-γ), tumor necrosis factor-alpha (TNF-α), and interleukin-2 (IL-2) levels. Expression of T cell exhaustion markers was detected by flow cytometry. Rescue experiments were conducted utilizing 3-methyladenine [a phosphoinositide 3-kinase (PI3K) inhibitor] and PD-L1 knockdown. The impact of EP4 overexpression on the PI3K/AKT signaling pathway-mediated PD-L1 expression and its subsequent modulation of CD8+ T cell killing ability against PCa cells was assessed through qRT-PCR, WB, flow cytometry, and immunofluorescence. EP4 exhibited a substantial upregulation in both PCa tissues and cells, displaying a positive correlation with PD-L1 expression and a converse negative correlation with the infiltration of CD8+ T cells. Knockdown of EP4 expression inhibited CD8+ T cell exhaustion, enhanced CD8+ T cell killing ability against PCa cells, increased the levels of IFN-γ, IL-2, and TNF-α, and decreased PD-L1 expression. Conversely, EP4 overexpression resulted in opposite effects, but treatment with 3-methyladenine mitigated EP4-induced promotion of PD-L1, p-AKT, and t-AKT expression. Furthermore, the knockdown of PD-L1 mitigated the inhibitory impact of EP4 overexpression on the killing ability of CD8+ T cell and the levels of IFN-γ, IL-2, and TNF-α, all while leaving the expression of p-AKT and t-AKT unaffected. EP4 was significantly overexpressed in PCa and activated PD-L1 expression via the PI3K/AKT signaling pathway, thereby suppressing the activity of CD8+ T cells.</p>","PeriodicalId":55205,"journal":{"name":"Critical Reviews in Immunology","volume":"45 2","pages":"1-13"},"PeriodicalIF":0.8,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143460869","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Assessing the Relationship among Tumor Size, Lymph Node Status, and ER/PR/HER2 Expression in Patients with Breast Cancer.","authors":"Liqin Wu, Xianghua Zhou, Fanfan Yang","doi":"10.1615/CritRevImmunol.2025055318","DOIUrl":"https://doi.org/10.1615/CritRevImmunol.2025055318","url":null,"abstract":"<p><p>This study aims to explore the relationship between tumor size, lymph node status, and ER/PR/HER2 expression in breast cancer patients. A total of 117 breast cancer patients who underwent surgery at our hospital were selected as the research objects. All patients underwent ipsilateral axillary lymph node dissection or sentinel lymph node biopsy during surgery. Pathological data and ultrasound features of primary lesions were collected. Univariate and multivariate logistic regression analyses were performed to evaluate the relationship between tumor size, lymph node status, and ER/PR/HER2 expression, as well as to identify the risk factors for lymph node metastasis in breast cancer patients. Among the 117 patients, 48 were positive for ipsilateral axillary lymph node metastasis and 69 were negative. Univariate analysis showed no significant correlation between age, PR status, molecular subtype, and lymph node metastasis (P > 0.05). Univariate analysis showed that tumor size, pathological type, menopausal status, Ki67 expression, HER2 status, and ER status were significantly associated with lymph node metastasis (P < 0.05). Logistic regression further identified tumor size [odds ratio (OR) = 1.809, 95% confidence interval (CI): 1.075-3.428, P = 0.018), pathological type (OR = 2.947, 95% CI: 1.241-7.536, P = 0.012), Ki67 expression (OR = 15.923, 95% CI: 3.219-74.512, P = 0.001), HER2 status (OR = 2.509, 95% CI: 1.586-5.769, P = 0.015), and ER status (OR = 3.226, 95% CI: 1.408-8.277, P = 0.007) as independent risk factors for lymph node metastasis. This study reveals that lymph node metastasis in breast cancer patients is significantly associated with larger tumor size (> 20 mm), invasive tumor type, higher Ki67 expression, HER2 positivity, and ER negativity. These findings emphasize the importance of incorporating these risk factors into clinical assessments to guide individualized treatment planning. By identifying patients with elevated lymph node metastasis risk, clinicians can better tailor treatment strategies to improve patient outcomes and optimize therapeutic interventions.</p>","PeriodicalId":55205,"journal":{"name":"Critical Reviews in Immunology","volume":"45 3","pages":"1-9"},"PeriodicalIF":0.8,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144217633","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}