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All rights reserved. http://resource.belframework.org/belframework/1.0/knowledge/large_corpus.bel http://purl.org/dc/elements/1.1/title BEL Framework Large Corpus Document http://resource.belframework.org/belframework/1.0/knowledge/large_corpus.bel http://purl.org/pav/authoredBy http://www.tkuhn.ch/bel2nanopub/RAUAAum59FiSDa4c_iY8aWjV8dwF2MI7DkuqgY_R3ggbA#_6 http://resource.belframework.org/belframework/1.0/knowledge/large_corpus.bel http://purl.org/pav/version 1.4 http://www.tkuhn.ch/bel2nanopub/RAUAAum59FiSDa4c_iY8aWjV8dwF2MI7DkuqgY_R3ggbA#_5 http://www.w3.org/ns/prov#value Fig. 6 Model of TLR4 and chemokine receptor crosstalk. MIP-2 binding to CXCR2 induces PMN migration, as well as GRK2 and GRK5 expression, through PI3K-? signaling. Increased GRK2 and GRK5 expression results in chemokine receptor internalization and desensitization, thereby negatively regulating PMN migration. Thus, PI3K-?-activated signaling is postulated to be a feedback mechanism regulating PMN migration. Because persistent infection requires continued PMN infiltration, LPS acting through the TLR4 signaling pathway transcriptionally downregulates expression of GRK2 and GRK5 in response to MIP-2. This decreases chemokine receptor desensitization by preventing CXCR2 internalization and thus augments PMN migration. MEK kinase is involved in mediating the crosstalk between TLR4 and chemokine receptors. 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