Mice treated with anti-IL-1R blocking mAb at the time of infection showed no change in total cells in the dLN compared with control IgG-treated mice (Fig 5M), but had reduced neutrophils (percentage and total number; Fig 5N–5P), indicating that the MyD88-IL-1R signaling axis regulates the rapid accumulation of neutrophils in the dLN during pathogenic CHIKV infection. The gene discussed is IL1R1; the disease is infection.