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A Novel Receptor on Allograft (H‐2d)‐Induced Macrophage (H‐2 b ) toward an Allogeneic Major Histocompatibility Complex Class I Molecule, H‐2D d , in Mice
Author(s) -
TashiroYamaji Junko,
EinagaNaito Kuniko,
Kubota Takahiro,
Yoshida Ryotaro
Publication year - 2006
Publication title -
microbiology and immunology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.664
H-Index - 70
eISSN - 1348-0421
pISSN - 0385-5600
DOI - 10.1111/j.1348-0421.2006.tb03775.x
Subject(s) - major histocompatibility complex , microbiology and biotechnology , biology , complementary dna , cd8 , monoclonal antibody , receptor , cytotoxic t cell , antibody , antigen , biochemistry , immunology , in vitro , gene
The generation of knockout mice demonstrated that noncytotoxic CD4 + , but not cytotoxic CD8 + , T cells were essential for the rejection of skin or organ allografts. Earlier we reported that allograft‐induced macrophages (AIM) in mice lysed allografts with H‐2 haplotype specificity, implying screening of grafts by AIM. Here, we isolated a cDNA clone encoding a novel receptor on AIM (H‐2D b ) for an allogeneic major histocompatibility complex (MHC) class I molecule, H‐2D d , by using H‐2D d tetramer and a monoclonal antibody (mAb; R15) specific for AIM. The cDNA (1,181‐bp) encoded a 342‐amino acid polypeptide with a calculated molecular mass of 45 kDa and was found to be expressed on AIM, but not on resident macrophages or other cells, infiltrating into the rejection site. HEK293T cells transfected with this cDNA reacted with R15 mAb and H‐2D d , but not H‐2L d , H‐2K d , H‐2D b , H‐2K b , H‐2D k , or H‐2K k , molecules; and the H‐2D d binding was suppressed by the addition of R15 or anti‐H‐2D d mAb. AIM yielded a specific saturation isotherm in the presence of increasing concentrations of H‐2D d , but not H‐2D b or H‐2D k , molecules. The dissociation constant of AIM toward H‐2D d tetramers was 1.9×10 –9 M ; and the binding was completely inhibited by the addition of R15 or anti‐H‐2D d mAb. These results reveal that a novel receptor for an allogeneic H‐2D d molecule was induced on effector macrophages responsible for allograft (H‐2 d ) rejection in H‐2 b mice.