In the case of NKT cells, the researchers found that the mice genetically rendered deficient in CXCR6 showed reduced survival of their NKT cells, but no change in the speed or pattern of their patrolling. The studies showed that the presence of CXCR6 prolonged the NKT cells' survival. The researchers also found that the NKT cells of CXCR6-deficient mice showed a reduced patrolling, as well as a decreased severity of artificially induced hepatitis.
“So, all the evidence we can obtain so far points to CXCR6 being involved in promoting survival of these NKT cells when they get into the environment of the liver, and that's how the cells tend to accumulate there,?said Littman. “Our data don't support a critical role of CXCR6 in crawling behavior of the cells.?/p>
Evidence for the role of CXCR6 in the survival of NKT cells ?as well as the cells' involvement in triggering hepatitis ?suggests a possible clinical implication of the findings, said Littman. “In general, these NKT cells could have an important inflammatory role, particularly in the case of chronic hepatitis,?he said. “If that is the case, we speculate that it may be possible to manipulate the NKT cell, perhaps by interfering with CXCR6 function, to ameliorate the inflammatory process,?he said.
Still unknown, said Littman, is which antigens alert NKTs to infections, as well as the nature of the regulatory machinery of crawling and stopping. The chemical the researchers used in their experiment is a general immune activator and does not reflect what occurs during an actual infection, he noted. Such knowledge would offer important insights into the me
Source:Howard Hughes Medical Center