scholarly journals Evidence that major histocompatibility complex restriction of foreign transplantation antigens occurs when tolerance is induced in neonatal mice and rats.

1985 ◽  
Vol 82 (18) ◽  
pp. 6265-6267 ◽  
Author(s):  
L. Desquenne-Clark ◽  
H. Kimura ◽  
W. K. Silvers
Keyword(s):  
Major Histocompatibility Complex ◽  
Major Histocompatibility ◽  
Neonatal Mice ◽  
Histocompatibility Complex ◽  
Transplantation Antigens

scholarly journals Immune response genes controlling responsiveness to major transplantation antigens. Specific major histocompatibility complex-linked defect for antibody responses to class I alloantigens.

1982 ◽  
Vol 155 (1) ◽  
pp. 303-320 ◽  
Author(s):  
G W Butcher ◽  
J R Corvalán ◽  
D R Licence ◽  
J C Howard
Keyword(s):  
Major Histocompatibility Complex ◽  
Antibody Response ◽  
Antibody Responses ◽  
Class I ◽  
Control Analysis ◽  
Major Histocompatibility ◽  
Histocompatibility Complex ◽  
Transplantation Antigens ◽  
Ir Genes

We have identified two major histocompatibility complex (MHC)-linked Ir genes that control the antibody response made by rats against class I major alloantigens. We have named these genes Ir-RT1Aa and Ir-RT1Ac. These Ir genes determine responsiveness of the immunized animal in a typical codominant fashion. There is no evidence so far for trans-complementation between low-responder haplotypes. Detailed studies of Ir-RT1Aa indicate that it controls the antibody response to at least two distinct alloantigenic determinants on RT1Aa molecules. These class I molecules thus behave like hapten-carrier conjugates when the response against the carrier is under Ir gene control. Analysis of the origin of alloantibody-forming cells in tetraparental radiation chimeras indicates that Ir-RT1Aa must control the provision of effective help to B cells. In many respects therefore, the properties of Ir-RT1Aa are broadly similar to those described for Ir genes controlling antibody responses to conventional antigens. The existence of apparently conventional Ir genes controlling the antibody response to major alloantigens strongly suggest that the processing of these transmembrane molecules by host antigen-presenting cells is a prerequisite for immune induction, and that it is the MHC of the responder rather than that of the allograft to which T helper cells are restricted in alloimmune responses in vivo.

Rejection of B16 melanoma induced by expression of a transfected major histocompatibility complex class I gene

1988 ◽  
Vol 8 (4) ◽  
pp. 1857-1861
Author(s):  
K Tanaka ◽  
E Gorelik ◽  
M Watanabe ◽  
N Hozumi ◽  
G Jay
Keyword(s):  
Major Histocompatibility Complex ◽  
Major Histocompatibility Complex Class ◽  
Tumor Cells ◽  
Human Cancer ◽  
Class I ◽  
Complex Class ◽  
Major Histocompatibility ◽  
Histocompatibility Complex ◽  
Transplantation Antigens ◽  
I Gene

Transfection of a functional major histocompatibility complex class I gene into certain tumor cells, induced by oncogenic viruses or chemical carcinogens, can effectively abrogate their tumorigenic activity. Since experimentally induced tumors possess strong tumor-specific transplantation antigens, expression of cell surface class I antigens may present the tumor cells to appropriate immune effector cells. Most spontaneously arising tumors do not possess tumor-specific transplantation antigens, and their tumorigenicity may not be affected by the expression of a transfected class I gene. We demonstrate that the poorly immunogenic B16-BL6 melanoma can be rendered nontumorigenic in syngeneic mice by the expression of the class I H-2K antigen but not the class II I-A antigen. Furthermore, the poorly tumorigenic, class I-expressing B16-BL6-transfected cells can effectively immunize syngeneic C57BL/6 mice against the highly tumorigenic, class I-deficient B16-BL6 parental cells. Our success in experimentally manipulating the tumorigenicity of a spontaneously derived neoplasm offers hope for a potential modality for the effective treatment of human cancer.

Genetic Consideration: The major histocompatibility complex of primates: evolutionary aspects and comparative histogenetics

1981 ◽  
Vol 292 (1057) ◽  
pp. 109-119 ◽  
Keyword(s):  
Major Histocompatibility Complex ◽  
Chromosomal Region ◽  
Mammalian Species ◽  
Biological Significance ◽  
Basic Structure ◽  
Biological Traits ◽  
Major Histocompatibility ◽  
Histocompatibility Complex ◽  
Transplantation Antigens ◽  
Evolutionary Aspects

All mammalian species investigated have a chromosomal region designated as the major histocompatibility complex or m.h.c. The biological significance of the m.h.c. goes far beyond controlling the most important histocompatibility or transplantation, antigens; the capacity to respond immunologically, the susceptibility to disease (including cancer), the serum level of several complement factors and numerous other biological traits are regulated by genetic systems closely linked within that chromosomal region. While the basic structure of the m.h.c. seems to be rather similar for all mammalian species, the similarities among the m.h.c. of human and non-human primates are particularly impressive. In this communication, m.h.c. gene products of rhesus monkey, chimpanzee and man are compared and reviewed. Evolutionary aspects of the persistence of the m.h.c. region or 'supergene’ throughout the animal kingdom are discussed.

scholarly journals Rejection of B16 melanoma induced by expression of a transfected major histocompatibility complex class I gene.

1988 ◽  
Vol 8 (4) ◽  
pp. 1857-1861 ◽  
Author(s):  
K Tanaka ◽  
E Gorelik ◽  
M Watanabe ◽  
N Hozumi ◽  
G Jay
Keyword(s):  
Major Histocompatibility Complex ◽  
Major Histocompatibility Complex Class ◽  
Tumor Cells ◽  
Human Cancer ◽  
Class I ◽  
Complex Class ◽  
Major Histocompatibility ◽  
Histocompatibility Complex ◽  
Transplantation Antigens ◽  
I Gene

Transfection of a functional major histocompatibility complex class I gene into certain tumor cells, induced by oncogenic viruses or chemical carcinogens, can effectively abrogate their tumorigenic activity. Since experimentally induced tumors possess strong tumor-specific transplantation antigens, expression of cell surface class I antigens may present the tumor cells to appropriate immune effector cells. Most spontaneously arising tumors do not possess tumor-specific transplantation antigens, and their tumorigenicity may not be affected by the expression of a transfected class I gene. We demonstrate that the poorly immunogenic B16-BL6 melanoma can be rendered nontumorigenic in syngeneic mice by the expression of the class I H-2K antigen but not the class II I-A antigen. Furthermore, the poorly tumorigenic, class I-expressing B16-BL6-transfected cells can effectively immunize syngeneic C57BL/6 mice against the highly tumorigenic, class I-deficient B16-BL6 parental cells. Our success in experimentally manipulating the tumorigenicity of a spontaneously derived neoplasm offers hope for a potential modality for the effective treatment of human cancer.

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