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AUGMENTATION BY CORYNEBACTERIUM LIQUEFACIENS OF ERYTHROCYTE SURFACE H-2 EXPRESSION AND ALLOIMMUNOGENICITY FOR ANTIBODY RESPONSES
Author(s) -
Tomoaki Yoshida,
Izumi Nakashima,
Takashi Yokochi,
Kenji Mizoguchi,
Ru Ding,
Naoya Kato,
K Isobe,
Fumihiko Nagase,
Kazuhiko Andō,
Toshiyuki Iwamoto
Publication year - 1988
Publication title -
transplantation
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.45
H-Index - 204
eISSN - 1534-6080
pISSN - 0041-1337
DOI - 10.1097/00007890-198808000-00015
Subject(s) - antigen , immunogenicity , microbiology and biotechnology , biology , bone marrow , population , antibody , lipopolysaccharide , corynebacterium , bacteria , immunology , chemistry , medicine , genetics , environmental health
Intravenous injection of killed Corynebacterium liquefaciens induced a population of red blood cells that expressed both H-2K and H-2D antigens at exceptionally high density and displayed augmented immunogenicity for H-2 alloantigen-specific B cell activation. Injection of killed Escherichia coli or E. coli lipopolysaccharide was ineffective for the generation of such RBC. RBC that express H-2 antigens at high density first appeared at 7 days after injection of C. liquefaciens. These RBC persisted for more than 50 days, although they lost H-2 antigens gradually with time. The observed phenomenon was not due to enhanced erythropoiesis and peripheral release of immature RBC (reticulocytes); populations of both mature and immature RBC of mice injected with C. liquefaciens expressed H-2 antigens at high density, whereas those from normal mice or mice injected with phenyl hydrazine did not. Appearance of RBC expressing H-2 antigens at high density was preceded by a temporal increase in H-2 expression of bone marrow cells that included precursors of RBC. It was concluded that RBC expressing H-2 antigens at high density were descendants of bone marrow cells whose H-2 expression was augmented by C. liquefaciens. The present communication would be the 1st report of the bacteria-mediated augmentation of cell surface expression and activity of major-histocompatibility-complex class I antigens on host cells in vivo.

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