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. 2016 Apr 1;149(1):1–12. doi: 10.1111/imm.12605

Figure 2.

Figure 2

Carbon monoxide (CO) reduces the expression of the Toll like receptor 4/ myeloid differentiation factor 2 (TLR4/MD2) complex receptor in the surface of myeloid cells. TLR4 and MD2 form a glycosylation‐dependent complex in the Golgi apparatus, which is then transported to the cell surface. Once in the surface, this complex can recognize lipopolysaccharide (LPS) and trigger an intracellular inflammatory cascade, which will lead to the activation of innate immune responses. After haem oxygenase 1 (HO‐1) expression and CO production, a blockade in the glycosylation is produced in the Golgi apparatus and the standard generation and assembly of the TLR4/MD2 complex is compromised. Then, a non‐well assembled complex is transported to the cell surface. Normal levels of TLR4 and MD2 are placed in the cell surface but its geometric association lack of effectiveness to recognize LPS. The innate immune response is compromised and reduced.