Analysis of the transcriptome of peritoneal exudate cells (PECs) and spleen cells from Cd38 KO mice and WT mice 2, and 4 weeks after the induction of the cGVHD-lupus disease

Our research paper is a follow up our previous study showed that in the context of the chronic graft-versus-host disease (cGVHD) lupus inducible model, the transfer of B6.C-H2bm12-KhEg (bm12) spleen cells into co-isogenic Cd38 KO B6 mice causes milder lupus-like autoimmunity with lower levels of anti-ssDNA autoantibodies than the transfer of bm12 spleen cells into WT B6 mice. Then the absence of Cd38 plays a significant role in the development of the bm12cGVHD lupus model. Our experiments suggested that a B-cell subset, with the CD11c+T-bet+ B cells being the most affected by the absence of Cd38. In order to understand the role of Cd38 as a modulator receptor that controls autoimmune responses, and to identify predictive or diagnostic biomarkers of the disease, our next approach has been to analyze the transcriptomic patterns of their respective peritoneal exudate cells (PECs) and spleen cells at different time points after the adoptive cell transfer. Thus, it has been ascertained that a differential response exists between the examined tissues, as well as a varying response over time between the WT and Cd38 KO specimens. Of note are a number of KEGG pathways identified within the exclusive WT PECs samples, which are closely associated with the inflammatory response and perturbations within the immune system. Conversely, the Cd38 KO mice reveal deviations in the cell cycle, including alterations within the phagosome and MAPK signaling pathways. Both WT and Cd38 KO specimens, however, demonstrate shared pathways of interest, which includes the cytokine-cytokine receptor interaction pathway. Moreover, the functional analysis of differentially expressed genes within the spleen highlights the cytokine-cytokine receptor interaction pathway, and pathways related to oxidative phosphorylation.