Although the exact mechanism(s) underlying endotoxin tolerance in asthma are still unclear, current evidence suggests that T-cell distributions favoring Treg (CD4+CD25+Foxp3+) or Th1 cells (which are induced by endotoxin exposure) over pathogenic Th2 (CD4+IL-4+) and Th17 (CD4+IL-17+) cells, as well as the suppression of DCs and barrier epithelial cells, may play important roles in the development of endotoxin tolerance (18). Here, CD4 is linked to asthma.