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We probed the mechanisms of T\u00a0cell adaptation using an experimental autoimmune encephalomyelitis (EAE) model in which the fate of autopathogenic T\u00a0cells could be followed. We demonstrated that immunisation with a high dose of myelin basic protein (MBP) peptide and complete Freund's adjuvant failed to effectively initiate EAE, in contrast to low dose MBP peptide immunisation which readily induced disease. The proportion of autopathogenic CD4<jats:sup>+<\/jats:sup> T\u00a0cells in the central nervous system (CNS) of mice immunised with a high dose of MBP peptide was not significantly different to mice immunised with a low dose. However, autopathogenic T\u00a0cells in mice immunised with high dose MBP peptide had an unresponsive phenotype in ex vivo recall assays. Importantly, whilst expression of PD\u20101 was increased on adapted CD4<jats:sup>+<\/jats:sup> T\u00a0cells within the CNS, loss of PD\u20101 function did not prevent the development of the unresponsive state. The lack of a role for PD\u20101 in the acquisition of the adapted state stands in striking contrast to the reported functional importance of PD\u20101 in T\u00a0cell unresponsiveness in other disease models.<\/jats:p>","DOI":"10.1002\/eji.201847868","type":"journal-article","created":{"date-parts":[[2018,11,28]],"date-time":"2018-11-28T19:06:23Z","timestamp":1543431983000},"page":"112-120","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":5,"title":["PD\u20101 expression is upregulated on adapted T\u00a0cells in experimental autoimmune encephalomyelitis but is not required to maintain a hyporesponsive state"],"prefix":"10.1002","volume":"49","author":[{"given":"Iris","family":"Mair","sequence":"first","affiliation":[{"name":"MRC Centre for Inflammation Research Centre for Multiple Sclerosis Research Centre for Immunity, Infection and Evolution The University of Edinburgh  Edinburgh 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