While IFNγ signaling within T cells may lead to this outcome [44], our results suggest that IFNγ-signalling in TRC and DC leading to NO production early after infection might not only control the expansion, but also the contraction phase of CD8+ T cells, such as by nitrosylating and thereby altering key proteins of the IL-2 or TCR signaling pathway [42], [45]. The gene discussed is CD8A; the disease is infection.