Influenza A virus‐induced thymus atrophy differentially affects dynamics of conventional and regulatory T‐cell development in mice

Foxp3+ Treg cells, which are crucial for maintenance of self-tolerance, mainly develop within the thymus, where they arise from CD25+ Foxp3- or CD25- cell precursors. Although it is known that infections can cause transient thymic involution, impact infection-induced thymus atrophy on (tTreg) development unknown. Here, we infected mice with influenza A virus (IAV) and studied thymocyte population dynamics post infection. IAV infection caused a massive, but dominated by loss CD4+ CD8+ double-positive (DP) thymocytes, was accompanied significant increase in frequency tTreg cells. Differential apoptosis susceptibility could be experimentally excluded as reason relative increase, mathematical modeling suggested enhanced generation cannot explain increased Yet, an death DP thymocytes augmented exit single-positive (SP) to causative. Interestingly, IAV-induced resulted significantly reduced T-cell receptor (TCR) repertoire diversity newly produced Taken together, substantially altering major populations, finally resulting cells altered TCR repertoire.