# Single-cell RNA-sequencing of peripheral blood mononuclear cells reveals the transcriptome profile of Microtus fortis immune cells during the early phase of infection with Schistosoma japonicum

## TL;DR

This study uses single-cell RNA sequencing to explore immune responses in reed voles infected with Schistosoma japonicum, revealing unique gene activity patterns compared to a susceptible mouse species.

## Contribution

The study identifies specific gene expression differences in immune cells of a naturally resistant host during early schistosome infection.

## Key findings

- Cxcl9 was upregulated in Microtus fortis monocytes after infection but not in Kunming mice.
- Infection induced IL2 and IL4 upregulation and Th2 cell expansion in M. fortis CD4+ T cells.
- Igha, Ighg1, and Ighg3 were upregulated in M. fortis antibody-secreting cells but not in Kunming mice.

## Abstract

The reed vole, Microtus fortis, is the only known natural non-permissive mammalian host of Schistosoma japonicum. However, the molecular mechanisms underlying this resistance have not been fully understood.

We performed single-cell RNA-seq to investigate the peripheral blood mononuclear cells (PBMCs) responses to S. japonicum in M. fortis and the susceptible host, Kunming mice. The samples were collected from uninfected animals (control group) and infected animals at 10 dpi.

The major cell types identified in the PBMCs of the two species were monocytes, dendritic cells (DCs), T cells, NK cells, B cells, and erythrocytes. We observed that the population of monocytes decreased considerably in the bloodstream after infection in both M. fortis and Kunming mice. However, differential gene expression analysis revealed that Cxcl9 was upregulated in M. fortis monocytes after infection, while it was not detected as a DEG in Kunming mice. In addition, we observed that infection induced the upregulation of IL2 and IL4 in M. fortis CD4+ T cells, and the expansion of the Th2 cell population. Regarding B cells, we did not observe any significant alteration among M. fortis B cell subpopulations after infection compared to the control. However, DEG analysis revealed that Igha, Ighg1, and Ighg3 were upregulated in M. fortis antibody secreting cells (ASCs) but not in Kunming mice.

Together, our results suggest that both the innate and adaptive immune responses were activated in the peripheral blood of M. fortis at 10 dpi, while their activation was not obvious in Kunming mice at the same moment.