-transparent.png){kind=logo}
Current interpretation based on analytical in vitro works that actions of Ia antigens and accessory cells such as macrophages and dendritic cells are crucial for inducing cytotoxic T cell responses to class I major histocompatibility complex (MHC) alloantigens has been challenged by experiments performed in a newly developed system handling in vivo cytotoxic T cell immunity. We first characterized the transplantation immunity for second-set rejection of ascitic tumor allografts as principally induced by allogeneic stimulator cells via direct pathway, and as exclusively mediated by class I MHC alloantigen-specific in vivo cytotoxic T cell activity. By comparison of activities of limiting effective doses (10(4)-10(5) cells per mouse) of various stimulator cells in this defined system, we could demonstrate that genetic disparity at the D region of H-2 to the recipient is just enough for inducing the immunity, and presence of allogeneic or syngeneic Ia antigens in addition to H-2D alloantigens on stimulator cells does not give any premium effect. Further study revealed that allogeneic peritoneal cells rich in macrophages or glass-adherent spleen cells enriched for dendritic cells are not stronger stimulators than allogeneic adherent cell-depleted spleen cells and semi-allogeneic thymocytes. These results fit with the alternative concept that the physiological pathway inducing in vivo cytotoxic T cell immunity for graft rejection entirely depends on class I MHC antigens on live lymphocytes as self-supported stimulators, and does not crucially involve additional stimulator activities of Ia antigens and special accessory cell types, which must be in vivo concerned with induction of other types of transplantation immunity.
K Mizoguchi, and
I Nakashima, and
K Isobe, and
K Ando, and
F Nagase, and
N Kato, and
K Kawashima, and
K Shimokata, and
Y Hasegawa
October 1993,
European journal of immunology,
K Mizoguchi, and
I Nakashima, and
K Isobe, and
K Ando, and
F Nagase, and
N Kato, and
K Kawashima, and
K Shimokata, and
Y Hasegawa
June 1993,
The Journal of experimental medicine,
K Mizoguchi, and
I Nakashima, and
K Isobe, and
K Ando, and
F Nagase, and
N Kato, and
K Kawashima, and
K Shimokata, and
Y Hasegawa
November 1994,
European journal of immunology,
K Mizoguchi, and
I Nakashima, and
K Isobe, and
K Ando, and
F Nagase, and
N Kato, and
K Kawashima, and
K Shimokata, and
Y Hasegawa
November 1994,
The Journal of infectious diseases,
K Mizoguchi, and
I Nakashima, and
K Isobe, and
K Ando, and
F Nagase, and
N Kato, and
K Kawashima, and
K Shimokata, and
Y Hasegawa
August 1994,
The Journal of experimental medicine,
K Mizoguchi, and
I Nakashima, and
K Isobe, and
K Ando, and
F Nagase, and
N Kato, and
K Kawashima, and
K Shimokata, and
Y Hasegawa
November 1995,
The Journal of experimental medicine,
K Mizoguchi, and
I Nakashima, and
K Isobe, and
K Ando, and
F Nagase, and
N Kato, and
K Kawashima, and
K Shimokata, and
Y Hasegawa
April 1993,
The Journal of general virology,
K Mizoguchi, and
I Nakashima, and
K Isobe, and
K Ando, and
F Nagase, and
N Kato, and
K Kawashima, and
K Shimokata, and
Y Hasegawa
July 1995,
Annals of the New York Academy of Sciences,
K Mizoguchi, and
I Nakashima, and
K Isobe, and
K Ando, and
F Nagase, and
N Kato, and
K Kawashima, and
K Shimokata, and
Y Hasegawa
April 2004,
Poultry science,
K Mizoguchi, and
I Nakashima, and
K Isobe, and
K Ando, and
F Nagase, and
N Kato, and
K Kawashima, and
K Shimokata, and
Y Hasegawa
November 1996,
Proceedings of the National Academy of Sciences of the United States of America,
