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Published on: June 11, 2019
Cell death and pathological findings of the spleen in COVID-19 patients
Haiqin Ping1, Kai Zhang2, Yunyun Wang3
1Hubei AIDS Clinical Training Center, Department of Infectious Disease, Zhongnan Hospital of Wuhan University, Wuhan, PR China.
Insights
COVID-19 infection increases immune cell apoptosis and inhibits autophagy in the spleen. SARS-CoV-2 spike protein presence in immune cells suggests a link to these processes, impacting disease severity.
Area of Science:
- Immunology
- Pathology
- Virology
Background:
- Coronavirus disease 2019 (COVID-19) is a systemic inflammatory response linked to cytokine release.
- The mechanisms driving cytokine storms in COVID-19 patients remain unclear.
Purpose of the Study:
- To investigate the role of spleen immune cells in COVID-19 pathogenesis.
- To explore the association between SARS-CoV-2 infection, immune cell apoptosis, and autophagy in the spleen.
Main Methods:
- Immunofluorescence staining of spleen tissues from deceased COVID-19 patients and controls.
- Assessment of immune cell markers (CD11b, CD68), apoptosis markers (TUNEL, cleaved caspase-3), and autophagy markers (p-Akt, p62, BCL-2).
- Double immunostaining to detect SARS-CoV-2 spike protein in immune cells.
Main Results:
- Increased CD11b-positive immune cells, including macrophages, were observed in COVID-19 patient spleens.
- Higher incidence of apoptosis in spleen cells of COVID-19 patients.
- Upregulation of autophagy-related molecules and potential inhibition of autophagy in COVID-19 spleen tissues.
- SARS-CoV-2 spike protein detected in a significant percentage (67%) of splenic immune cells.
Conclusions:
- SARS-CoV-2 infection may induce apoptosis and suppress autophagy in splenic immune cells.
- These cellular dysregulations could contribute to the pathogenesis and severity of COVID-19.
- Findings enhance understanding of COVID-19 immune responses and disease mechanisms.
Abstract:
The coronavirus disease 2019(COVID-19) is recognized as systemic inflammatory response syndrome. It was demonstrated that a rapid increase of cytokines in the serum of COVID-19 patients is associated with the severity of disease. However, the mechanisms of the cytokine release are not clear. By using immunofluorescence staining we found that the number of CD11b positive immune cells including macrophages in the spleens of died COVID-19 patients, was significantly higher than that of the control patients. The incidence of apoptosis as measured by two apoptotic markers, TUNEL and cleaved caspase-3, in COVID-19 patients' spleen cells is higher than that in control patients. By double immunostaining CD11b or CD68 and SARS-CoV-2 spike protein, it was found that up to 67% of these immune cells were positive for spike protein, suggesting that viral infection might be associated with apoptosis in these cells. Besides, we also stained the autophagy-related molecules (p-Akt、p62 and BCL-2) in spleen tissues, the results showed that the number of positive cells was significantly higher in COVID-19 group. And compared with non-COVID-19 patients, autophagy may be inhibited in COVID-19 patients. Our research suggest that SARS-CoV-2 may result in a higher rate of apoptosis and a lower rate of autophagy of immune cells in the spleen of COVID-19 patients. These discoveries may increase our understanding of the pathogenesis of COVID-19.
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