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MyD88s Innate Powers

Infection or tissue injury causes innate immune cells, such as dendritic cells, macrophages, and neutrophils, to recognize pathogen-associated molecular patterns (PAMPs) or host derived damage-associated molecular patterns (DAMPs) via pattern recognition receptors (PRRs) on the cell surface and in the cytoplasm. Toll-like receptors are major PRRs in cells. TLRs dimerize upon ligand binding and their cytoplasmic domain called Toll/IL-1 (TIR, due to similarities to the IL-1 receptor) serve as a docking site for TIR containing adaptor proteins. Out of the TIR containing proteins such as TRIF, TIRAP and TRAM, MyD88 acts a central player in innate immune signaling by being the canonical adaptor for inflammatory signaling pathways downstream of TLRs (except TLR3, which signals via TRIF) as well as IL-1 receptor families. BioLegend provides several antibodies and reagents to aid your study of both TLRs and innate signaling pathways.

After ligation, TLR initiates signaling by recruiting MyD88 followed by the recruitment of kinases IRAK1 and IRAK4 and an adaptor ubiquitin ligase TRAF6. IRAK1-TRAF6 then dissociates from the complex and further activates the IKK complex for NF-ÎºB and MAPK dependent gene transcription and production of pro-inflammatory cytokines such as IL-1b, IL-6, IL-8, and IL-12, and TNF-a. In addition, via the activation of interferon regulatory factor (IRF), MyD88 can also stimulate type 1 IFN genes leading to the production of anti viral interferons such as IFN-a and IFN-b.

Related Products

Human Antibodies

ERK2	IkB-α	IRF3	IRF7	JNK1
MKK6	MyD88	NF-κB	pERK	pJNK
TLR1	TLR2	TLR3	TLR4	TLR6
TLR9	TLR10	TRAM	TRAF6	TRIF

Mouse Antibodies

ERK2	IkB-α	IRF3	JNK1	MKK6
MyD88	NF-κB	pERK	TLR2	TLR3
TLR4	TLR5	TRAF6	TRIF

Rat Antibodies

LEGENDplex™ Panels

Human Inflammation Panel

Mouse Inflammation Panel

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