Figure 1

A schematic representation of TLR signaling via the MyD88 versus TRIF adaptors. MyD88 signaling strongly stimulates the production of pro-inflammatory interleukins, primarily via NFκB. A subset of TLRs signal via the adaptor TRIF, resulting primarily in the production of type I IFNs. The role of TRIF signaling in OM, previously unknown, is explored in this study. TLR, Toll-like receptor; MyD88, Myeloid differentiation primary response gene 88; TRIF, Tir-domain-containing adaptor inducing interferon β; TRAF, TNF-receptor-associated factor; RIP1, receptor interacting protein kinase 1; TAK1, mitogen-activated protein kinase kinase kinase 7; TBK1, TANK-binding kinase 1; IKKε, inhibitor of kappa light polypeptide gene enhancer in B-cells, kinase epsilon; p50, NFκB, nuclear factor of kappa light polypeptide gene enhancer in B-cells; p50, NFκB, subunit 1; p65, NFκB, subunit 3; JNK, Jun kinase; p38, p38 mitogen activated protein kinase IRF3, interferon regulatory factor 3; ISRE, interferon-stimulated response element; TNFα, tumor necrosis factor alpha; IL, interleukin; IFN, interferon.