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We have had a long-standing standing interest in chemokines and their receptors and have been working in this field for 18 years. Currently, we have a number of projects that relate to various aspects of chemokine and chemokine receptor function:Studies into the biological function of the D6-chemokine decoy receptor
In 1997 we reported the cloning of the D6 chemokine receptor. D6 is an atypical receptor and can bind many chemokines with high affinity. Interestingly it does not signal following ligand binding and is thus not a typical chemokine receptor. The chemokines that D6 binds are those that are involved in inflammatory responses. D6 internalises ligand and targets it for intracellular degradation. We have thus proposed a role for D6 as a ‘decoy’ or ‘scavenging’ receptor which is capable of internalising and degrading a range of inflammatory chemokines. We have generated D6-nul mice in collaboration with Dr. Don Cook and Prof Sergio Lira and have shown that these mice display an altered ability to resolve inflammation in both the lung and skin. In the skin, following application of a chemical irritant, these D6-null mice develop a pathology which is similar to human psoriasis. Overall our conclusion is that D6 is an indispensable regulator of the in vivo inflammatory response. We are now undertaking a more detailed investigation of the inflammatory response of the D6 null mice using a range of models. We are also generating D6-GFP reporter mice to help us to detail the key cells that express D6 in the inflamed context and the dynamics of expression of D6 during an inflammatory response.
In 1997 we reported the cloning of the D6 chemokine receptor. D6 is an atypical receptor and can bind many chemokines with high affinity. Interestingly it does not signal following ligand binding and is thus not a typical chemokine receptor. The chemokines that D6 binds are those that are involved in inflammatory responses. D6 internalises ligand and targets it for intracellular degradation. We have thus proposed a role for D6 as a ‘decoy’ or ‘scavenging’ receptor which is capable of internalising and degrading a range of inflammatory chemokines. We have generated D6-nul mice in collaboration with Dr. Don Cook and Prof Sergio Lira and have shown that these mice display an altered ability to resolve inflammation in both the lung and skin. In the skin, following application of a chemical irritant, these D6-null mice develop a pathology which is similar to human psoriasis. Overall our conclusion is that D6 is an indispensable regulator of the in vivo inflammatory response. We are now undertaking a more detailed investigation of the inflammatory response of the D6 null mice using a range of models. We are also generating D6-GFP reporter mice to help us to detail the key cells that express D6 in the inflamed context and the dynamics of expression of D6 during an inflammatory response.
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Brain, Behavior, and Immunity (2016): e28
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