shannah
Senior Member
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For the scientists amongst us, would this new research hold any implications for ME?
From Montreal & France
Nature Immunology Published online 15 February 2016
Abstract
Activation of natural killer (NK) cells by hematopoietic target cells is controlled by the SLAM family of receptors and by the associated SAP family of adaptors. Here we found that SLAM receptors also enhanced NK cell activation by nonhematopoietic target cells, which lack ligands for SLAM receptors. This function was mediated by SLAMF6, a homotypic SLAM receptor found on NK cells and other hematopoietic cells, and was regulated by SAP adaptors, which uncoupled SLAM receptors from phosphatase SHP-1 and diminished the effect of SLAMF6 on NK cell responsiveness toward nonhematopoietic cells. Thus, in addition to their role in NK cell activation by hematopoietic cells, the SLAM-SAP pathways influence responsiveness toward nonhematopoietic targets by a process akin to NK cell 'education'.
http://www.nature.com/ni/journal/v17/n4/full/ni.3369.html#affil-auth
And an additional article about it with an excerpt:
"Now knowing that NK cells improve their defences through learning, Dr. Veillette hopes to pave the way for the development of innovative therapies against cancer and certain viral infections.
The discovered mechanism could also contribute to a better understanding of Duncan's syndrome. This rare disease, also known as the XLP syndrome, affects only young boys and occurs when they come into contact with the Epstein-Barr virus, which causes mononucleosis. It is estimated that, without treatment, 70 per cent of patients with Duncan’s syndrome die before they reach the age of 10.
“Our research group had previously shown that the SAP adaptor does not react normally in patients with XLP syndrome,” reports Dr. Veillette. “Therefore, NK cells are unable to kill infected cells. Now that we know that SAP interacts with the SLAMF6 receptor and the SHP-1 enzyme, we hope to clarify what leads to the onset of Duncan's syndrome.”
https://www.ircm.qc.ca/Medias/Nouvelles/Pages/Detail.aspx?pID=467&PFLG=1033&lan=1033
From Montreal & France
Nature Immunology Published online 15 February 2016
Abstract
Activation of natural killer (NK) cells by hematopoietic target cells is controlled by the SLAM family of receptors and by the associated SAP family of adaptors. Here we found that SLAM receptors also enhanced NK cell activation by nonhematopoietic target cells, which lack ligands for SLAM receptors. This function was mediated by SLAMF6, a homotypic SLAM receptor found on NK cells and other hematopoietic cells, and was regulated by SAP adaptors, which uncoupled SLAM receptors from phosphatase SHP-1 and diminished the effect of SLAMF6 on NK cell responsiveness toward nonhematopoietic cells. Thus, in addition to their role in NK cell activation by hematopoietic cells, the SLAM-SAP pathways influence responsiveness toward nonhematopoietic targets by a process akin to NK cell 'education'.
http://www.nature.com/ni/journal/v17/n4/full/ni.3369.html#affil-auth
And an additional article about it with an excerpt:
"Now knowing that NK cells improve their defences through learning, Dr. Veillette hopes to pave the way for the development of innovative therapies against cancer and certain viral infections.
The discovered mechanism could also contribute to a better understanding of Duncan's syndrome. This rare disease, also known as the XLP syndrome, affects only young boys and occurs when they come into contact with the Epstein-Barr virus, which causes mononucleosis. It is estimated that, without treatment, 70 per cent of patients with Duncan’s syndrome die before they reach the age of 10.
“Our research group had previously shown that the SAP adaptor does not react normally in patients with XLP syndrome,” reports Dr. Veillette. “Therefore, NK cells are unable to kill infected cells. Now that we know that SAP interacts with the SLAMF6 receptor and the SHP-1 enzyme, we hope to clarify what leads to the onset of Duncan's syndrome.”
https://www.ircm.qc.ca/Medias/Nouvelles/Pages/Detail.aspx?pID=467&PFLG=1033&lan=1033