These include relating antigen specificity to expansion and expression phenotypes of Tfh populations during chronic infection, quantifying repertoire dynamics relating to Tfh and Tfr during GC collapse, exploring consequences of prolonged T-cell exhaustion and effector phenotypes persisting beyond the peaks of neurological disease (déjà vu) and latent viral infections, or revisiting previously reported differences between MOG peptide and protein models of EAE in terms of the adaptive immune response [56]. The gene discussed is MOG; the disease is nervous system disorder.