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溃疡性结肠炎患者袋炎炎症区域中CD3+CD56+自然杀伤性T淋巴细胞减少及人类白细胞抗原-DR+细胞增加。

Decreased CD3+CD56+ Natural Killer T Lymphocytes and Increased Human Leukocyte Antigen-DR+ Cells in the Inflamed Area of Pouchitis in Ulcerative Colitis Patients.

作者信息

Iwamuro Masaya, Tanaka Takehiro, Takahara Masahiro, Inokuchi Toshihiro, Hiraoka Sakiko

机构信息

Department of Gastroenterology and Hepatology, Okayama University Graduate School of Medicine, Dentistry, and Pharmaceutical Sciences, Okayama, JPN.

Department of Pathology, Okayama University Hospital, Okayama, JPN.

出版信息

Cureus. 2024 Sep 24;16(9):e70066. doi: 10.7759/cureus.70066. eCollection 2024 Sep.

DOI:10.7759/cureus.70066
PMID:39449918
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11499896/
Abstract

BACKGROUND

Pouchitis is an inflammatory condition that affects the ileal pouch during ileal pouch-anal anastomosis surgery. Despite its clinical significance, precise immunological mechanisms underlying pouchitis remain unclear. This study aimed to investigate the lymphocyte profile in the ileal pouch of patients with pouchitis compared to those with familial adenomatous polyposis (FAP) and ulcerative colitis without pouchitis using flow cytometry and immunohistochemical techniques.

METHODS

We prospectively analyzed endoscopic biopsy specimens from the ileal pouches of 15 patients and categorized them into three groups: FAP, ulcerative colitis with an inflammation-free pouch (UC-I), and ulcerative colitis with ulcers and/or erosions in the pouch (UC-UE). Flow cytometry was used to assess various T-lymphocyte markers, including cluster of differentiation (CD) 4, CD8, CD56, and human leukocyte antigen (HLA)-DR. Immunohistochemistry was performed to visualize the spatial distribution of CD3+, CD56+, and HLA-DR+ cells in the pouch mucosa.

RESULTS

We observed significantly reduced CD56+/CD3+ and CD8+/CD3+ ratios in the UC-UE group compared to those in the FAP group, indicating a disruption in natural killer T-cell populations. Immunohistochemical analysis revealed that the spatial distribution of lymphocytes differed among the non-inflamed mucosa, dense lymphocyte infiltration, and lymphoid follicles, with these components frequently intermingling. CD56 + cells were less abundant in areas with dense lymphocyte infiltration, whereas HLA-DR+ cells were more abundant.

CONCLUSION

Our study revealed a decrease in CD56+ natural killer T cells and an increase in HLA-DR+-activated T cells in areas with dense lymphocyte infiltration, suggesting an association between these cells and pouchitis in ulcerative colitis. The distinct patterns observed in non-inflamed mucosa, areas with dense lymphocyte infiltration, and lymphoid follicles underscore the need for further analyses of these three segments to elucidate the immunological mechanisms underlying pouchitis.

摘要

背景

袋炎是一种在回肠袋肛管吻合术期间影响回肠袋的炎症性疾病。尽管其具有临床意义，但袋炎潜在的精确免疫机制仍不清楚。本研究旨在通过流式细胞术和免疫组织化学技术，调查患有袋炎的患者与患有家族性腺瘤性息肉病（FAP）以及无袋炎的溃疡性结肠炎患者的回肠袋中的淋巴细胞谱。

方法

我们前瞻性地分析了15例患者回肠袋的内镜活检标本，并将其分为三组：FAP、无炎症袋状的溃疡性结肠炎（UC-I）以及袋中有溃疡和/或糜烂的溃疡性结肠炎（UC-UE）。流式细胞术用于评估各种T淋巴细胞标志物，包括分化簇（CD）4、CD8、CD56和人类白细胞抗原（HLA）-DR。进行免疫组织化学以观察回肠袋黏膜中CD3 +、CD56 +和HLA-DR +细胞的空间分布。

结果

我们观察到，与FAP组相比，UC-UE组中CD56 + /CD3 +和CD8 + /CD3 +比率显著降低，表明自然杀伤T细胞群体受到破坏。免疫组织化学分析显示，淋巴细胞的空间分布在无炎症黏膜、密集淋巴细胞浸润和淋巴滤泡之间存在差异，这些成分经常相互交织。在密集淋巴细胞浸润区域，CD56 +细胞较少，而HLA-DR +细胞较多。

结论

我们的研究显示，在密集淋巴细胞浸润区域，CD56 +自然杀伤T细胞减少，HLA-DR +活化T细胞增加，提示这些细胞与溃疡性结肠炎中的袋炎之间存在关联。在无炎症黏膜、密集淋巴细胞浸润区域和淋巴滤泡中观察到的不同模式强调了对这三个部分进行进一步分析以阐明袋炎潜在免疫机制的必要性。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2386/11499896/0974bd6aac88/cureus-0016-00000070066-i07.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2386/11499896/416acb4b414e/cureus-0016-00000070066-i01.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2386/11499896/a656e1308ff4/cureus-0016-00000070066-i02.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2386/11499896/ac208fa264e4/cureus-0016-00000070066-i03.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2386/11499896/b18dbb812836/cureus-0016-00000070066-i05.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2386/11499896/69e1482faeef/cureus-0016-00000070066-i06.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2386/11499896/0974bd6aac88/cureus-0016-00000070066-i07.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2386/11499896/416acb4b414e/cureus-0016-00000070066-i01.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2386/11499896/a656e1308ff4/cureus-0016-00000070066-i02.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2386/11499896/ac208fa264e4/cureus-0016-00000070066-i03.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2386/11499896/4463dd5703d1/cureus-0016-00000070066-i04.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2386/11499896/b18dbb812836/cureus-0016-00000070066-i05.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2386/11499896/69e1482faeef/cureus-0016-00000070066-i06.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2386/11499896/0974bd6aac88/cureus-0016-00000070066-i07.jpg

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