Critical Reviews in Immunology最新文献

{"title":"Study of TNF-α, IFN-γ, IL-10, TGF-β and IL-6 Gene Polymorphisms in a Cohort of Professionals Who Worked in the First Pandemic Wave in the Brazilian Amazon.","authors":"Beatriz Dos Reis Marcelino, Marcelo Cleyton da Silva Vieira, Marcos Jessé Abrahão Silva, Lilian Cristina Santos Sinfronio da Silva, Ellen Polyana da Costa Gurrão, Everaldina Cordeiro Dos Santos, Jeanne Gonçalves Cabral, Alex Brito Souza, Daniele Melo Sardinha, Rebecca Lobato Marinho, Sebastião Kauã de Sousa Bispo, Karla Valéria Batista Lima, Luana Nepomuceno Gondim Costa Lima","doi":"10.1615/CritRevImmunol.2024055001","DOIUrl":"10.1615/CritRevImmunol.2024055001","url":null,"abstract":"<p><p>Genetic polymorphisms in genes that enable the production of an effective host immune response, such as single nucleotide polymorphisms (SNPS) in the IL-6, INF-alpha, IFN-gamma, IL-10, TGF-beta genes can cause unfavorable clinical conditions or susceptibility to pathologies. The objective of this work is to evaluate the epidemiological and genetic profile of professionals from health institutions during the first pandemic wave. A case-control study was performed with convenience sampling from health institutions (HI) workers from Belém-PA, Northern Brazil (N = 213), divided into symptomatology groups (Asymptomatic-AS, n = 91; and Symptomatic-SI, n = 122); and severity groups classified by chest computerized tomography-CCT data (symptomatic with pulmonary involvement-SCP, n = 37; symptomatic without pulmonary involvement-SSP, n = 8). Genotyping was performed by sanger sequencing for SNP TNF-α -308 G/A (rs1800629), IFN-γ +874 T/A (rs2430561), TGF-β codon 10 (rs1982073), codon 25 (rs1800471), IL-6 - 174 G/C (rs180079), IL-10 - 1082 A/T (rs1800896), -819 C/T (rs1800871), and -592 A/C (rs1800872), and statistical analysis through the Epilfo program. Significant association was observed between the presence of comorbidities and poor prognosis of COVID-19 (especially between COVID-19 and overweight and obesity). Only the TNF-α 308 G/A snp was significantly associated with the symptoms and severity of COVID-19. These findings about this TNF-α SNP passed in the multiple testing correction at a false discovery rate (FDR)< 0.05. These data can help medicine and the scientific community understand the influence of genetics and epidemiological parameters in combating COVID-19.</p>","PeriodicalId":55205,"journal":{"name":"Critical Reviews in Immunology","volume":"45 2","pages":"39-61"},"PeriodicalIF":0.8,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143460861","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":"Neonatal Immunity to Candida: Current Understanding and Contributions of Murine Models.","authors":"Angel Palacios, Ajay Kumar, Fides Myles C Caliwag, Miguel A Becerril-Garcia","doi":"10.1615/CritRevImmunol.2024055053","DOIUrl":"10.1615/CritRevImmunol.2024055053","url":null,"abstract":"<p><p>Neonatal candidiasis poses significant clinical challenges due to its potential for severe morbidity and mortality in vulnerable infants. Due to their underdeveloped immune system, neonates are at a higher risk for infections caused by Candida species. They can vary from mild to severe, including penetrating deep tissues, bloodstream spread, and dissemination to organs. The immune system of newborns is marked by a limited innate immune response, with lower levels of pro-inflammatory cytokines. Adaptive immunity, important for lasting protection, also experiences delayed maturation with weakened Th1 and Th17 responses. These shortcomings result in a higher vulnerability to Candida infections during infancy. Murine models have been crucial in understanding the reasons behind this susceptibility. These models assist in examining how different immune elements, like neutrophils, macrophages, and T cells, and their interactions are involved in Candida infections. Moreover, they offer an understanding of how early-life exposure to Candida affects immune responses and may aid in developing possible therapeutic plans. In this article we review current results from research to provide a thorough summary and critical insights into neonatal immune response to Candida, highlighting the importance of using murine models in this field of study. Understanding these immune dynamics is essential for creating specific treatments and preventive strategies to prevent newborns from Candida infections, ultimately improving neonatal health outcomes.</p>","PeriodicalId":55205,"journal":{"name":"Critical Reviews in Immunology","volume":"45 2","pages":"63-76"},"PeriodicalIF":0.8,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143460860","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":"Combination therapy of supercharged NK cells and ONC201 or ONC206 to target aggressive K27M brain tumor.","authors":"Kawaljit Kaur, Anahid Jewett","doi":"10.1615/CritRevImmunol.2025058345","DOIUrl":"10.1615/CritRevImmunol.2025058345","url":null,"abstract":"<p><p>High-grade glioma tumors are the common cause of death in pediatric patients. K27M cell line is regularly used as tumor model to study diffuse intrinsic pontine glioma (DIPG) since they harbor genetic mutation in which the lysine of the histone H3 protein is replaced with a methionine. The objective of this study is to demonstrate the significance of supercharged NK (sNK) cells alone or in combination with ONC201 or ONC206 to target such aggressive pediatric brain tumor K27M. We have observed increased secretion of IFN-γ by sNK cells compared to primary IL-2-activated NK cells. Combining sNK cells with ONC201 or ONC206 further increased IFN-γ in sNK cells. When primary NK cells and sNK cells were used as effectors against the glioma tumor cell line K27M, tumor cells were found to be highly susceptible to sNK cell-mediated cytotoxicity compared to primary NK cell-mediated cytotoxicity. sNK cell-mediated cytotoxicity against K27M was significantly increased when sNK cells were combined with ONC201 and ONC206. This study suggests the potential use of sNK cells alone or in combination with ONC201 or ONC206 as therapeutic strategies in treating and preventing the recurrence of aggressive pediatric brain tumors.</p>","PeriodicalId":55205,"journal":{"name":"Critical Reviews in Immunology","volume":"45 3","pages":"0"},"PeriodicalIF":0.8,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144217635","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":"The Role of FGFR2 on Proliferation, Apoptosis and Glucose Metabolism of Breast Cancer Cells.","authors":"Yuan Liang, Tian-Cheng Ma, Junhui Qin, Yuwei Li, RuiAn Wang","doi":"10.1615/CritRevImmunol.2025054378","DOIUrl":"https://doi.org/10.1615/CritRevImmunol.2025054378","url":null,"abstract":"<p><p>The present study investigated the expression of miR-598 in both breast cancer tissues and cells. Overexpression systems were established by introducing miR-598 mimics and pcDNA- Fibroblast Growth Factor Receptor 2(FGFR2) plasmids, either individually or in combination, into breast cancer cells. Four groups were constituted for probing purposes: control group, miR-598 mimics group, pcDNA-FGFR2 group, and mimics+FGFR2 group. Quantitative real-time polymerase chain reaction (qRT-PCR) was employed to measure the expression of miR-598 and FGFR2. Furthermore, bioinformatics software was used to predict and identify the possible binding sites between miR-598 and FGFR2. To validate the predicted binding sites, a dual-luciferase reporter gene experiment was carried out. A clone formation assay was used to evaluate cell proliferation, while glucose consumption and lactic acid production assays were conducted using a kit. Moreover, Western blot analysis was done to ascertain the expression of Bcl-2, Bax, Caspase-3, and Caspase-9 proteins. The expression of miR-598 in breast cancer tissues and cell lines was found to be significantly lower than that in normal breast tissues and cell lines, respectively (P < 0.05). It was also revealed that FGFR2 is the target gene of miR-598 and there is an inverse correlation between the two. Overexpression of miR-598 led to a decrease in clonal formation rate caused by high FGFR2 levels. Moreover, the overexpression of miR-598 reversed the effects induced by high FGFR2 levels, such as increased mitochondrial membrane potential and reduced expression of apoptosis-associated proteins. The microRNA miR-598 has been found to decrease the proliferation of breast cancer cells by targeting FGFR2, inducing apoptosis, and suppressing glucose consumption.</p>","PeriodicalId":55205,"journal":{"name":"Critical Reviews in Immunology","volume":"45 3","pages":"51-62"},"PeriodicalIF":0.8,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144217638","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":"Pathogenesis, Diagnosis, Treatment, and Prognosis of CD20-Positive T and NK Cell Lymphoma: A Review.","authors":"Yang Liu, Bo Li, Xiaomin Chen, Hao Xiong, Chunlan Huang","doi":"10.1615/CritRevImmunol.2025051500","DOIUrl":"https://doi.org/10.1615/CritRevImmunol.2025051500","url":null,"abstract":"<p><p>T and NK cell lymphoma with abnormal CD20 expression is a condition that primarily seen in Asians. Due to the variable expression of CD20, it is difficult to generalize its origin, leading to controversial conclusions about the role of CD20. In this review, we provide an overview of CD20 localization and function in three cell types. In NK/T-cell lymphoma (NKTCL), CD20 was discovered to be confined to B cells, presenting a mature active phenotype and having an inert course. However, in T-cell lymphoma (TCL), variable expression of CD20 antigen on T cells and NK cells correlates with tumor transformation and rituximab efficacy. We highlight the fact that CD20 expression is stage-specific and further classify CD20 antigen assignment, which contributes to understanding the variety of outcome and the function of CD20 during various phases of tumor development.</p>","PeriodicalId":55205,"journal":{"name":"Critical Reviews in Immunology","volume":"45 3","pages":"11-18"},"PeriodicalIF":0.8,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144217637","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":"Dual Inhibition of IRE1α and YAP Signaling as a Potential Therapy for Epithelial Ovarian Carcinoma.","authors":"Fei Liu, Chunhua Tu, Buzhen Tan, Linsheng He, Yuan Wen","doi":"10.1615/CritRevImmunol.2025057246","DOIUrl":"10.1615/CritRevImmunol.2025057246","url":null,"abstract":"<p><p>Epithelial ovarian carcinoma (EOC) is a highly lethal gynecological malignancy with limited treatment options. This study aimed to explore the regulatory roles of IRE1α and YAP1 in EOC progression and identify potential therapeutic targets. Blood and tissue samples were collected from 26 EOC patients and 10 patients with ovarian cysts. The expression of inflammatory factors in the blood was measured using ELISA. The proliferation, migration, invasion, and cell cycle of human ovarian cancer cell lines SK-OV-3, SW626, and Anglene were evaluated using MTT assays, scratch tests, Transwell assays, and flow cytometry. The effects of IRE1α inhibition on EOC cell proliferation, migration, and apoptosis were investigated using pharmacological inhibitors and shRNA knockdown. IRE1α was highly expressed in EOC patients and was negatively correlated with patient survival rates. Additionally, IRE1α scores in EOC patients were positively correlated with serum levels of TNF-α and VEGF-a. Compared to normal controls, significantly higher expressions of IRE1α and XBP1 were observed in ovarian cancer tissues and cells. Knockdown of IRE1α in ovarian cancer cells led to a significant reduction in the expression of IRE1α and XBP1s, as well as inhibited cell proliferation and survival. The IRE1α inhibitors STF-083100 and 4μ8C suppressed the proliferation, invasion, and migration of SK-OV-3 cells and reduced the expression levels of related factors. 4μ8C inhibited the degradation of YAP within SK-OV-3 cells while downregulating the expression of Cyclin D1 protein. Compared to the group treated with 4μ8C alone, the combined intervention of 4μ8C and a YAP inhibitor showed a more pronounced inhibitory effect on the proliferation of SK-OV-3 cells.This study first reveals that the IRE1α/YAP signal drives the malignant progression of EOC through the regulation of cell proliferation, migration, and invasion. The dual-targeted synergistic inhibition of IRE1α/YAP1 offers an innovative therapeutic paradigm for the treatment of EOC.</p>","PeriodicalId":55205,"journal":{"name":"Critical Reviews in Immunology","volume":"45 3","pages":"19-32"},"PeriodicalIF":0.8,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144217636","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":"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":"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}

{"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}