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Inhibition of natural killer cell‐mediated bone marrow graft rejection by allogeneic major histocompatibility complex class I, but not class II molecules
Author(s) -
Öhlén Claes,
Höglund Petter,
Sentman Charles L.,
Carbone Ennio,
Ljunggren HansGustaf,
Koller Beverly,
Kärre Klas
Publication year - 1995
Publication title -
european journal of immunology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.272
H-Index - 201
eISSN - 1521-4141
pISSN - 0014-2980
DOI - 10.1002/eji.1830250523
Subject(s) - major histocompatibility complex , biology , immunology , bone marrow , mhc class i , beta 2 microglobulin , natural killer cell , histocompatibility , mhc restriction , t cell , beta (programming language) , cytotoxic t cell , human leukocyte antigen , antigen , immune system , genetics , in vitro , computer science , programming language
Abstract The role of major histocompatibility complex (MHC) class I and class II molecules in natural killer (NK) cell‐mediated rejection of allogeneic, semi‐syngeneic and MHC‐matched bone marrow grafts was investigated. The use of β 2 ‐microglobulin (β 2 m) ‐/‐ and β 2 m +/‐ mice as bone marrow donors to MHC‐mismatched recipients allowed an analysis of whether the presence of semi‐syngeneic and allogeneic MHC class I gene products would be triggering, protective or neutral, in relation to NK cell‐mediated rejection. Loss of β 2 m did not allow H‐2 b bone marrow cells to escape from NK cell‐mediated rejection in allogeneic (BALB/c) or semi‐allogeneic (H‐2D d transgenic C57BL/6) mice. On the contrary, it led to stronger rejection, as reflected by the inability of a larger bone marrow cell inoculum to overcome rejection by the H‐2‐mismatched recipients. In H‐2‐matched recipients, loss of β 2 m in the graft led to a switch from engraftment to rejection. At the recipient level, loss of β 2 m led to loss of the capability to reject H‐2‐matched β 2 m‐deficient as well as allogeneic grafts. When MHC class II‐deficient mice were used as donors, the response was the same as that against donors of normal MHC phenotype: allogeneic and semi‐syngeneic grafts were rejected by NK cells, while syngeneic grafts were accepted. These data suggest a model in which allogeneic class I molecules on the target cell offer partial protection, while certain syngeneic class I molecules give full protection from NK cell‐mediated rejection of bone marrow cells. There was no evidence for a role of MHC class II molecules in this system.

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