Fig. 1.

Time course of CIDP disease progression, immunotherapy and type 1 diabetes as defined by insulin need and HbA_1c (a). During the patient’s most recent flare-up of CIDP, a blood sample was drawn and analysed for T cell reactivity to the islet autoantigens PPI, IA-2 and GAD65 (GAD), as well as T cell responses to tetanus toxoid (TT) as a control for recall immunity to a vaccine antigen unrelated to type 1 diabetes (b–f). Proliferative responses to PPI were suppressed despite proinflammatory (IFN-γ, IL-17) and anti-inflammatory cytokine production in response to this islet antigen. T cells responded both to IA-2 by proliferation and cytokines, whereas no T cell responses were detectable against GAD65 despite the presence of serum autoantibodies against this protein (not shown). Dashed red arrows indicate IVIG administration. The timeline starts on September 2014 (t = 0 months) and ends on May 2016 (t = 20 months). The clinical course of CIDP is depicted as a red graded fill, in which the more intensely red areas are flare-ups and white areas are periods of remission. To convert values for HbA_1c in mmol/mol into % units, multiply by 0.0915 and add 2.15. Proliferation was normalised to the response in control wells with culture medium and human serum, i.e. without a diabetes-associated antigen (9.5 ± 1.0 [SD] cpm × 10³). Cytokine production in control wells was as follows (in ng/ml): IFN-γ, 0.059; IL-17, 0.003; IL-13, 0.006; IL-10, 0.026