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Host MHC class I gene control of NK‐cell specificity in the mouse
Author(s) -
Höglund Petter,
Sundbäck Jonas,
OlssonAlheim Mats Y.,
Johansson Maria,
Salcedo Margarita,
Öhién Claes,
Ljunggren HansGustaf,
Sentman Charles L.,
Kärre Klas
Publication year - 1997
Publication title -
immunological reviews
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 6.839
H-Index - 223
eISSN - 1600-065X
pISSN - 0105-2896
DOI - 10.1111/j.1600-065x.1997.tb00936.x
Subject(s) - biology , major histocompatibility complex , mhc class i , gene , transgene , genetics , natural killer cell , immunology , computational biology , cytotoxic t cell , in vitro
Summary: The missing self model predicts chat NK cells adapt somatically to the type as well as levels of MHC class I products expressed by their host, Transgenic and gene knock‐out mice have provided conclusive evidence chat MHC class I genes control specificity and tolerance of NK cells. The article describes this control and discusses the POSSIBLE Mechanisms behind it. starting from a genetic model to study how natural resistance to tumors is influenced by MHC class I expression in the host as well as in the target cells. Data on host gene regulation of NK‐cell functional specificity as well as Lγ49 receptor expression are reviewed, leading up to the central question: how does the system develop and maintain “useful” NK cells, while avoiding “harmful” and “useless” ones? The available data can be fitted with in each of two mutually non‐exclusive models: cellular adaptation and clonal selection. Recent studies supporting cellular adaptation bring the focus on different possibilities within this general mechanism, such as energy, receptor calibration and, most importantly, whether the specificity of each NK cell is permanently fixed or subject to continuous regulation.