在狗慢性肠病和肠道T细胞淋巴瘤中,促炎性细胞因子表达和STAT1/3通路
Kazuhiro Kojima1, James K Chambers1, Ko Nakashima2
1The University of Tokyo, Tokyo, Japan.
Veterinary pathology
|October 31, 2023
概括
亲炎性细胞因子干扰素- (IFN-γ) 和介质素-21 (IL-21) 在具有内皮细胞瘤 (IEL+CE) 的犬慢性肠病 (CE) 中被上调. STAT1和STAT3通路的激活与CE病原和肠道T细胞淋巴瘤 (ITCL) 有关.
科学领域:
- 兽医医学 兽医医学 兽医医学
- 免疫学 免疫学 免疫学
- 胃肠病学 胃肠病学
背景情况:
- 皮内淋巴细胞 (IELs) 积累是犬类慢性肠病 (CE) 的特征.
- IEL被认为是肠道T细胞淋巴瘤 (ITCL) 的起源.
- 在CE中IEL激活的致病机制尚未完全理解.
研究的目的:
- 为了研究亲炎性细胞因子和STAT途径在狗CE和ITCL中的表达.
- 阐明这些分子在IEL激活和ITCL病原体中的作用.
主要方法:
- 定量PCR测量细胞因子基因表达 (IFN-γ,IL-2,IL-12p35,IL-12p40,IL-15,IL-21) 的情况.
- 西方斑块用于评估STAT1和STAT3蛋白质水平.
- 免疫组织化学评估STAT1和STAT3激活,并与T细胞标记物和IFN-γ水平相关联.
主要成果:
- 与IEL-CE和健康对照相比,IFN-γ和IL-21表达在IEL+CE中显著更高.
- 在IEL+CE中,STAT1和STAT3得到了上调.
- 激活的STAT1 (p-STAT1) 在IEL+CE和ITCL中增加,与IFN-γ水平相关.
- 在ITCL中的新发性淋巴细胞对p-STAT1和p-STAT3.3呈阳性.
结论:
- IFN-γ和IL-21有助于IEL+CE的致病性.
- 在CE中,IFN-γ可能在T细胞激活和粘膜损伤中发挥作用.
- STAT1和STAT3激活参与了犬类ITCL的病变发生.
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