At steady-state, we and others have shown that, upon engagement of Toll like receptor (TLR)4 (i.e., the main receptor for LPS) and the adaptor molecule MYD88, bulk IM could fulfill important tolerogenic tasks by inhibiting DC functions via IL-10-dependent mechanisms, thus preventing the development of asthma in animal models12,18. This evidence concerns the gene TLR4 and asthma.