Genetic Causes of Human NK Cell Deficiency and Their Effect on NK Cell Subsets
Identifieur interne : 001042 ( Main/Exploration ); précédent : 001041; suivant : 001043Genetic Causes of Human NK Cell Deficiency and Their Effect on NK Cell Subsets
Auteurs : Emily M. Mace [États-Unis] ; Jordan S. Orange [États-Unis]Source :
- Frontiers in Immunology [ 1664-3224 ] ; 2016.
Abstract
Human NK cells play critical roles in human host defense, particularly the control of viral infection and malignancy, and patients with congenital immunodeficiency affecting NK cell function or number can suffer from severe illness. The importance of NK cell function is particularly underscored in patients with primary immunodeficiency in which NK cells are the primary or sole affected population (NK cell deficiency, NKD). While NKD may lead to the absence of NK cells, we are also gaining an increasing appreciation of the effect that NKD may have on the generation of specific NK cell subsets. In turn, this leads to improved insights into the requirements for human NK cell subset generation, as well as their importance in immune homeostasis. The presence of inherently abnormally developed or functionally impaired NK cells, in particular, appears to be problematic in the way of interfering with normal human host defense and may be more impactful than low numbers of NK cells alone. Here, we review the known genetic causes of NKD and the insight that is derived by these into the requirements for human subset generation and, by extension, for NK cell-mediated immunity.
Url:
DOI: 10.3389/fimmu.2016.00545
PubMed: 27994588
PubMed Central: 5133264
Affiliations:
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Le document en format XML
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<front><div type="abstract" xml:lang="en"><p>Human NK cells play critical roles in human host defense, particularly the control of viral infection and malignancy, and patients with congenital immunodeficiency affecting NK cell function or number can suffer from severe illness. The importance of NK cell function is particularly underscored in patients with primary immunodeficiency in which NK cells are the primary or sole affected population (NK cell deficiency, NKD). While NKD may lead to the absence of NK cells, we are also gaining an increasing appreciation of the effect that NKD may have on the generation of specific NK cell subsets. In turn, this leads to improved insights into the requirements for human NK cell subset generation, as well as their importance in immune homeostasis. The presence of inherently abnormally developed or functionally impaired NK cells, in particular, appears to be problematic in the way of interfering with normal human host defense and may be more impactful than low numbers of NK cells alone. Here, we review the known genetic causes of NKD and the insight that is derived by these into the requirements for human subset generation and, by extension, for NK cell-mediated immunity.</p>
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<author><name sortKey="Forbes, Lr" uniqKey="Forbes L">LR Forbes</name>
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<author><name sortKey="Monaco Shawver, L" uniqKey="Monaco Shawver L">L Monaco-Shawver</name>
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<author><name sortKey="Oshinsky, J" uniqKey="Oshinsky J">J Oshinsky</name>
</author>
<author><name sortKey="Atkinson, Tp" uniqKey="Atkinson T">TP Atkinson</name>
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<author><name sortKey="Moody, C" uniqKey="Moody C">C Moody</name>
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<biblStruct><analytic><author><name sortKey="Liu, Ll" uniqKey="Liu L">LL Liu</name>
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<author><name sortKey="Landskron, J" uniqKey="Landskron J">J Landskron</name>
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<author><name sortKey="Ask, Eh" uniqKey="Ask E">EH Ask</name>
</author>
<author><name sortKey="Enqvist, M" uniqKey="Enqvist M">M Enqvist</name>
</author>
<author><name sortKey="Sohlberg, E" uniqKey="Sohlberg E">E Sohlberg</name>
</author>
<author><name sortKey="Traherne, Ja" uniqKey="Traherne J">JA Traherne</name>
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<affiliations><list><country><li>États-Unis</li>
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<tree><country name="États-Unis"><noRegion><name sortKey="Mace, Emily M" sort="Mace, Emily M" uniqKey="Mace E" first="Emily M." last="Mace">Emily M. Mace</name>
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<name sortKey="Orange, Jordan S" sort="Orange, Jordan S" uniqKey="Orange J" first="Jordan S." last="Orange">Jordan S. Orange</name>
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