MAJOR HISTOCOMPATIBILITY COMPLEX CONTROL OF NK-RELATED ALLOGENEIC LYMPHOCYTE CYTOTOXICITY IN RATS THE CONTRIBUTIONS OF STRONG AND MEDIAL TRANSPLANTATION ANTIGENS

1988 ◽  
Vol 46 (5) ◽  
pp. 762-767 ◽  
Author(s):  
ANN AGER ◽  
JAMES FAJUMI ◽  
SHEILA M. SPARSHOTT ◽  
WILLIAM L. FORD ◽  
GEOFFREY W. BUTCHER
Keyword(s):  
Major Histocompatibility Complex ◽  
Major Histocompatibility ◽  
Complex Control ◽  
Histocompatibility Complex ◽  
Allogeneic Lymphocyte ◽  
Lymphocyte Cytotoxicity ◽  
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.

Sign in / Sign up

Export Citation Format

Share Document