MYD88 and type 1 diabetes mellitus: The same authors also found that colonization of GF mice with a variety of intestinal bacteria reduced the occurrence of T1D in MyD88-negative but not wild-type NOD mice, favoring the balanced signal hypothesis: i.e., that both inflammatory and regulatory responses are induced by the microbiota and that TLR4-mediated Trif signaling causes a tolerizing immune response, which protects against T1D development [48].