Collaborative Action of Toll-Like and Nod-Like Receptors as Modulators of the Inflammatory Response to Pathogenic Bacteria

<div><i>NOD1 and NOD2 signaling.</i> Bacteria or their components reach the cytosol by several mechanisms. The interaction between NOD2 and NIK (<i>blue arrows</i>) activates the noncanonical NF-<i>κ</i>B pathway (p100/p52-dependent). While binding of PGN to LRR domain of NLRs leads to recruitment of RIP-2 through CARD-CARD interaction (<i>black arrows</i>). Ubiquitination of RIP-2 favors, on the one hand, the activation of the MAPKs p38/JNK, and on the other hand activates IKK complex, which induces the activation of NF-<i>κ</i>B.</div>

Mediators of Inflammation

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Figure 2

Figure 2: Collaborative Action of Toll-Like and Nod-Like Receptors as Modulators of the Inflammatory Response to Pathogenic Bacteria 