| Type I IFNs modulate the onset of immune responses against viruses through the activation of numerous rapid signaling pathways. Although beneficial on specific infected cells, administered IFNs were shown to decrease thymic cellularity. Herein, we developed a murine model treated with polyinosinic:polycytidylic acid (Poly IC) to dissect the mechanisms and the role of in vivo produced IFNs on the thymus. Treatment induced thymic atrophy, while having no effect on the lymph nodes. However, under chronic conditions, we observed a complete thymic replenishment. These findings should be the result of a LPS contamination, since the use of a new certified LPS-free Poly IC induced a maintained thymic atrophy in time. DP (CD4+CD8+) cells were mostly affected, where part of this decrease was contributed by apoptosis. T cell receptor excision circle (TREC) levels, produced during T cell receptor (TCR) rearrangements, were unaffected, suggesting no alteration of this diversity factor. Additionally, measured up-regulation of MHC class I expression could result in aberrant thymic selections with a modification of selection ranges. Finally, using Caspase 3 KO mice, we showed that DP apoptosis was Caspase-3 independent. |
