Comparative and correlative assessments of cytokine, complement and antibody patterns in paediatric type 1 diabetes

Summary One of the most widespread and effective environmental factors is the infection with enteroviruses (EVs) which accelerate β cell destruction in type 1 diabetes (T1D). This study represented a comparison between diabetic EV + and EV – children as well as correlation analysis between autoantibodies, T1D markers, cytokines, complement activation products and anti‐coxsackievirus (CV) immunoglobulin (Ig)G. EV RNA was detected in Egyptian children with T1D (26·2%) and healthy controls (0%). Detection of anti‐CV IgG in T1D‐EV + resulted in 64% positivity. Within T1D‐EV + , previously diagnosed (PD) showed 74 versus 56% in newly diagnosed (ND) children. Comparisons between populations showed increased levels of haemoglobin A1c (HbA1c), C‐reactive protein (CRP), nitric oxide (NO), glutamic acid decarboxylase and insulin and islet cell autoantibodies [glutamic acid decarboxylase autoantibodies (GADA), insulin autoantibodies (IAA) and islet cell cytoplasmic autoantibodies (ICA), respectively], interferon (IFN)‐γ, tumour necrosis factor (TNF)‐α, interleukin (IL)‐1β, IL −10, IL −12, IL −17, C3d and sC5–9 in T1D‐EV + versus T1D‐EV – . Conversely, both IL‐20 and transforming growth factor (TGF‐β) decreased in T1D‐EV + versus EV – , while IL‐4, −6 and −13 did not show any changes. Correlation analysis showed dependency of accelerated autoimmunity and β cell destruction on increased IFN‐γ, IL‐12 and IL‐17 versus decreased IL‐4, −6 and −13. In conclusion, IFN‐γ, IL‐12 and IL‐17 played an essential role in exacerbating EV + ‐T1D, while C3d, sC5b −9, IL‐10 and −20 displayed distinct patterns.