Antigen-induced suppression: The role of Class I major histocompatibility antigens

1985 ◽  
Vol 5 (10-11) ◽  
pp. 1007-1014 ◽  
Author(s):  
Kathryn J. Wood ◽  
Peter J. Morris

The role of Class I major histocompatibility (MHC) antigens in the induction of specific suppression of graft rejection has been investigated. Two experimental transplantation models have been used ’ fully vascularized heterotopic Cardiac altografts in the mouse and fully vascularized orthotopic renal allografts in the rat. Preparations of ceils expressing Class I MHC antigens, for example highly purified preparations of rat erythrocytes or platelets or mouse L cells (H2k) transfected with the D locus Class I gene of the b haplotype, LDb-1 cells, were used to pretreat recipients prior to transplantation, The function of the allograft was monitored in order to assess any beneficial effects induced by Class I MHC antigens. The results obtained implicate Class I MHC as important in the induction of specific immunosuppression of vascularized allograft rejection.

Blood ◽  
1991 ◽  
Vol 77 (11) ◽  
pp. 2530-2537 ◽  
Author(s):  
NH Grana ◽  
KJ Kao

Abstract The use of 8-methoxypsoralen (8-MOP) and UV-A irradiation to inactivate contaminating donor leukocytes in platelet concentrates and to prevent primary alloimmunization against donor class I major histocompatibility (MHC) antigens in mice was investigated. CBA/CaH-T6J mice with the H2k haplotype and BALB/cByJ mice with the H2d haplotype were used as donors and recipients, respectively. The mixed leukocyte reaction between these two strains of mice showed that treatment of spleen cells with 500 ng/mL 8-MOP and 5J/cm2 UV-A inhibited 99% of responder and 92% of stimulator function. There was no measurable loss of platelet aggregating activity after the treatment. After two weekly transfusions of platelets without any treatment, 93% of control mice (n = 15) developed anti-H2k antibody. In contrast, only 33% of mice (n = 15) receiving platelets treated with 8-MOP and UV-A became alloimmunized. After six weekly platelet transfusions, all mice became alloimmunized. Nevertheless, the mean titers of anti-H2k antibody in sera of the treated groups were significantly lower than the control groups. One hour posttransfusion recoveries of 51Cr-labeled donor platelets were also higher in mice transfused with the treated platelets. Thus, the pretreatment of platelet concentrates with 8-MOP and UV-A irradiation effectively reduced the alloantigenicity of class I MHC molecules. The implication of this finding in relation to the mechanism by which donor leukocytes allosensitize recipients is discussed.


Nature ◽  
1983 ◽  
Vol 305 (5937) ◽  
pp. 771-775 ◽  
Author(s):  
P. I. Schrier ◽  
R. Bernards ◽  
R. T. M. J. Vaessen ◽  
A. Houweling ◽  
A. J. van der Eb

1983 ◽  
Vol 157 (2) ◽  
pp. 720-729 ◽  
Author(s):  
S L Swain ◽  
R W Dutton ◽  
R Schwab ◽  
J Yamamoto

Human T cells respond strongly to mouse major histocompatibility complex (MHC) antigens. The response is directed predominantly to the polymorphic determinants of the MHC antigens and there is little or no response to the nonpolymorphic determinants or to non-MHC antigens. Human cytotoxic T lymphocytes (CTL) are generated specific for the mouse class I MHC antigens and the CTL effectors are blocked by anti-Leu-2a antisera. Human interleukin 2-producing T cells are generated specific for mouse class II antigens and their induction is blocked by anti-Leu-3a antisera. These and other considerations lead us to propose a model for the T cell receptor that provides an explanation for several of the features of T cell recognition. In this model, the recognition of the "class" (I or II) of MHC antigen is separate from the recognition of the polymorphic determinants. We suggest that the initial recognition of the conserved "class" determinants positions another domain of the receptor so that it can only engage with the part of the MHC molecule carrying the polymorphic determinants.


Cell ◽  
1988 ◽  
Vol 54 (3) ◽  
pp. 413-421 ◽  
Author(s):  
Marie-Luise Blue ◽  
Kimberly A. Craig ◽  
Paul Anderson ◽  
Kenneth R. Branton ◽  
Stuart F. Schlossman

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