我们报告了一例SARS-CoV-2感染后的炎症性结肠炎,该患者在住院后三周内死亡,没有其他合并症。随着SARS-CoV-2感染可引起免疫学改变,我们研究了抑制性检查点PD-1及其配体PD-L1的表达,以探讨该轴在自身耐受破坏中的潜在作用.通过qRT-PCR和核衣壳蛋白的免疫组织化学定位证明了SARS-CoV-2病毒在结肠组织中的存在。淋巴细胞标志物的表达,通过IHC研究结肠组织中的PD-1和PD-L1。在溃疡和非溃疡粘膜区域均检测到SARS-CoV-2免疫反应性细胞。与健康组织相比,PD-1弱表达,PD-L1缺失,PD-1和PD-L1表达出现在发炎的粘膜组织中,正如预期的那样,但主要局限于非溃疡区。同时,这些标记物在粘膜溃疡部位几乎检测不到.我们的数据显示PD-1/PD-L1轴的改变,并提示SARS-CoV-2感染与伴随PD-1/PD-L1相互作用破坏导致患者早期死亡的异常自身炎症反应之间存在联系。
We report a
case of inflammatory colitis after SARS-CoV-2 infection in a patient with no additional co-morbidity who died within three weeks of hospitalization. As it is becoming increasingly clear that SARS-CoV-2 infection can cause immunological alterations, we investigated the expression of the inhibitory checkpoint PD-1 and its ligand PD-L1 to explore the potential role of this axis in the break of self-tolerance. The presence of the SARS-CoV-2 virus in colon tissue was demonstrated by qRT-PCR and immunohistochemical localization of the nucleocapsid protein. Expression of lymphocyte markers, PD-1, and PD-L1 in colon tissue was investigated by IHC. SARS-CoV-2-immunoreactive cells were detected both in the ulcerated and non-ulcerated mucosal areas. Compared to healthy tissue, where PD-1 is weakly expressed and PD-L1 is absent, PD-1 and PD-L1 expression appears in the inflamed mucosal tissue, as expected, but was mainly confined to non-ulcerative areas. At the same time, these markers were virtually undetectable in areas of mucosal ulceration. Our data show an alteration of the PD-1/PD-L1 axis and suggest a link between SARS-CoV-2 infection and an aberrant autoinflammatory response due to concomitant breakdown of the PD-1/PD-L1 interaction leading to early death of the patient.