Interestingly, while many changes were entirely absent in plg−/− mice, indicating a plasmin-dependent process (e.g., lymphopenia, the increase in pro-inflammatory plasma cytokines, as well as the proportional alterations of cDC and macrophages in the cLN), others were present in plg−/− mice to a comparable extent as wild-type mice, suggesting a truly t-PA-mediated, plasmin-independent activity as the underlying mechanism (for example splenic cDC proportions). This evidence concerns the gene PLG and lymphopenia.