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

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.