| Target Validation Information | |||||
|---|---|---|---|---|---|
| Target ID | T96627 | ||||
| Target Name | Macrophage inflammatory protein-2-alpha | ||||
| Target Type | Clinical Trial |
||||
| Action against Disease Model | Laquinamod | Experimental evidence to date, derived mostly from animal models of multiple sclerosis, suggests that laquinimod may mediate its effects via modulating pro-inflammatory immune responses and interfering with cell trafficking, as well as potentially acting directly in the central nervous system to limit demyelination and axonal injury. | [553095] | Drug Info | |
| The Effect of Target Knockout, Knockdown or Genetic Variations | This study seeks to further investigate the mechanisms involved in acetaminophen-induced hepatotoxicity and the role of chemokine (C-X-C motif) receptor 2 (CXCR2) receptor/ligand interactions in the liver's response to and recovery from acetaminophen toxicity. The CXC chemokines and their receptor, CXCR2, are important inflammatory mediators and are involved in the control of some types of cellular proliferation. CXCR2 knockout mice exposed to a median lethal dose of acetaminophen had a significantly lower mortality rate than wild-type mice. This difference was at least partially attributable to a significantly decreased rate of apoptosis in CXCR2 knockout mice versus wild-type mice; there were no differences seen in hepatocyte proliferation in wild-type mice versus knockout mice after this injury. Conclusion: The decreased rate of apoptosis in the knockout mice correlated with an almost undetectable and significantly decreased level of activated caspase-3 and significantly increased levels of X-linked inhibitor of apoptosis protein, which also correlated with increased levels of nuclear factor kappa B p52 and decreased levels of c-Jun N-terminal kinase; thisprovides a possible mechanism for the decrease in apoptosis seen in CXCR2 knockout mice | [553095] | |||
| References | |||||
| Ref 553095 | Laquinimod in multiple sclerosis. Clin Immunol. 2012 Jan;142(1):38-43. doi: 10.1016/j.clim.2011.02.021. Epub 2011 Mar 4. | ||||
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