Enhanced T cell-monocyte interation allievates malaria-associated acute respiratory distress syndrome : Bulk RNA-seq

Malaria-associated acute respiratory distress syndrome (MA-ARDS) is a severe manifestation of malaria with high mortality and no effective treatment. IFN-γ, a key regulator of immunity, plays a role in both promoting and suppressing malaria infection, though its effects on specific cell types remain unclear. In this study, we show that IFN-γ directly enhances CD8+ T cell proliferation, cytotoxicity, and cytokine production in a MA-ARDS mouse model. In IFNGR1-deficient T cells, IFN-γ deficiency led to increased CD8+ expression on Ly6c+ monocytes, enhancing their phagocytic ability. These findings highlight the role of T cell IFN-γ signaling in modulating monocyte function and suggest targeting this pathway could improve T cell-based therapies for MA-ARDS To investigate the mechanisms underlying the lung adaptive immune response during malaria-associated acute respiratory distress syndrome (MA-ARDS), we performed a comprehensive transcriptomic analysis of lung tissues collected from infected mice at multiple time points. A total of 28 lung samples were analyzed, representing six critical time points during the infection: 3, 5, 7, 9, 11, and 13 days post-infection (dpi). As a control, we included lung samples from naïve, uninfected mice to provide baseline comparisons. This design enables us to capture dynamic changes in gene expression associated with the progression and resolution of MA-ARDS, thereby providing insight into the immune responses involved at various stages of the disease