增殖与炎症:猫慢性鼻炎和鼻腔淋巴瘤的免疫组化特征分析。
Proliferation versus inflammation: Immunohistochemical profiling of feline chronic rhinitis and nasal lymphoma.
文献信息
| PMID | 42861917 |
|---|---|
| 原文 | 在 PubMed 查看原文 ↗ |
| 发表日期 | 2026 |
| 作者 | Sandra I C V Carvalho |
| 作者单位 | CIISA, Interdisciplinary Centre of Research in Animal Health, Faculty of Veterinary Medicine, University of Lisbon, Portugal. |
| 期刊 | Veterinary pathology |
| SCI 分区 | Q2 |
| IF | 2.6 |
| 研究类型 | 基础研究 · 基础/转化 |
| 所属专科 | 鼻科 |
中文摘要
背景: 淋巴瘤是猫鼻腔最常见的肿瘤。尽管近期多数研究致力于表征猫消化道淋巴瘤的肿瘤细胞标志物,但仅有少数报道专门探讨鼻腔淋巴样肿瘤除T细胞或B细胞表型分型之外的免疫组织学特征。相比之下,猫淋巴细胞性浆细胞性慢性鼻炎代表一种慢性、进行性淋巴细胞浆细胞性炎症,导致周期性的组织损伤与修复。方法:选取65例淋巴细胞浆细胞性鼻炎和15例猫弥漫性大细胞免疫母细胞性鼻腔淋巴瘤病例,进行免疫组化检测,以检测细胞来源免疫标志物(CD3、CD20/PAX5和FOXP3)、增殖标志物(PCNA)、信号转导及转录激活因子5(STAT5)、DNA修复标志物(MLH1、MSH2和MSH6)以及凋亡标志物(BCL2)的表达。结果:我们的结果表明,肿瘤性淋巴细胞主要呈CD20+/PAX5+,提示B细胞表型。在大多数病例(n=14/15)中,肿瘤性淋巴细胞呈中度至强阳性表达STAT5、MLH1、MSH6、MSH2、PCNA和FOXP3,以及弱至中度表达BCL2。在淋巴瘤和鼻炎病例中,炎性淋巴细胞主要呈CD3+,而DNA修复标志物MLH1、MSH2和MSH6的表达为偶见,强弱不等,介于弱至中度之间。结论:我们的结果提示,MLH1、MSH2、MSH6、PCNA和FOXP3有潜力作为鉴别淋巴瘤与淋巴细胞浆细胞性鼻炎的诊断标志物,尽管对于大多数怀疑淋巴瘤的病例,包含MLH1、MSH6和PCNA的诊断组合可能已足够。这些发现有助于区分淋巴瘤与炎症,并识别潜在的治疗靶点。它们还提示鼻腔淋巴瘤中存在调节性B细胞表型,这可能有助于免疫逃逸。
英文摘要
Lymphoma is the most common nasal cavity tumor in cats. While most recent research efforts have characterized neoplastic cell markers in feline alimentary lymphoma, only few reports are dedicated to immunohistological features of nasal lymphoid tumors beyond T- or B-cell phenotyping. In comparison, feline lymphoplasmacytic chronic rhinitis represents chronic, progressive lymphoplasmacytic inflammation, causing cyclical tissue damage and repair. Sixty-five cases of lymphoplasmacytic rhinitis and 15 cases of feline diffuse, large cell, immunoblastic nasal lymphoma were selected and submitted for immunohistochemistry to detect expression of immune markers of cell origin (CD3, CD20/PAX5, and FOXP3), proliferation (PCNA), signal transducer and activator of transcription 5 (STAT5), DNA repair (MLH1, MSH2, and MSH6), and apoptosis (BCL2). Our results indicate that neoplastic lymphocytes were predominantly CD20+/PAX5+, suggesting a B-cell phenotype. Neoplastic lymphocytes were moderately to strongly STAT5+, MLH1+, MSH6+, MSH2+, PCNA+, and FOXP3+, as well as weakly or moderately BCL2+, in most cases (n = 14/15). In both lymphoma and rhinitis cases, inflammatory lymphocytes were predominantly CD3+, while expression of DNA repair markers MLH1, MSH2, and MSH6 was occasional, varying between weak and moderate. Our results suggest that MLH1, MSH2, MSH6, PCNA, and FOXP3 show potential as diagnostic markers in differentiating lymphoma from lymphoplasmacytic rhinitis, although a diagnostic panel with MLH1, MSH6, and PCNA may suffice for diagnosing most cases where lymphoma is suspected. These findings aid in distinguishing lymphoma from inflammation and identifying potential therapeutic targets. They also suggest a regulatory B-cell phenotype in nasal lymphoma, which may aid in immune evasion.