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PubMed1986

Skin graft and kidney transplantation in rats. Relation between circulatory condition of the transplanted organ and histocompatibility.

To determine the relationship between histocompatibility and circulation in the transplanted graft, which are the major factors influencing graft survival, the survival of the skin grafts and kidney transplants were compared between strong (ACI to Lewis) and weak (Fisher to Lewis) histocompatible strains, because rats given skin graft receive poor blood supply from a recipient, and the rats given kidney transplants receive immediate blood supply after transplant. In the group with a weak histocompatibility barrier circulation of the engrafted organ was better and the survival period longer. In the group with a strong histocompatibility barrier graft survival was little influenced by the circulatory disorder, and the degree of histocompatibility overwhelmed the circulatory condition.

Animals↗
PubMedDate not supplied

Ovarian hormones, antiestrogen and pregnancy effects on the expression of class II histocompatibility antigens by N-nitroso-N-methylurea-induced rat mammary carcinomas.

Hormonal modulation of Class II histocompatibility antigen expression was studied in female Sprague-Dawley rats with N-nitroso-N-methylurea-induced mammary tumors. The effects of ovarian hormones, pregnancy and lactation were examined when cancers appeared. At this time, rats with tumors were divided into several groups. Different groups received respectively 17 beta-estradiol alone, 17 beta-estradiol in association with progesterone, and tamoxifen alone. Other groups were selected to undergo pregnancy. The control group received carcinogenic treatment only. For all removed tumors, Class II histocompatibility antigens were radiolabeled, specifically immunoprecipitated with monoclonal antibody and quantified by chromatofocusing. The amount of Class II histocompatibility antigens measured in NMU-induced rat mammary tumors without any hormonal treatment decreased significantly after treatment with estrogen alone or in association with antiestrogen and during the pregnancy. Nevertheless, Class II histocompatibility antigen expression was not changed in mammary carcinoma from rats receiving progesterone, but increased significantly during the lactation. These results demonstrated clearly that ovarian hormones change the Class II histocompatibility antigen expression of NMU-induced mammary tumors in female Sprague-Dawley rats.

Animals↗
PubMed2005

Immunotherapy of cancer through targeting of minor histocompatibility antigens.

Minor histocompatibility antigens are allogeneic targets of T-cell mediated graft-versus-tumour effects following allogeneic stem cell transplantation. Recent research has identified several minor histocompatibility antigens as tumour proteins and has also disclosed their unique properties in both the induction and the effector phase of graft-versus-tumour effects. Targeting tumour-specific minor histocompatibility antigens by adoptive immunotherapy will battle against tumour tolerance and evoke allo-immune responses, thereby enhancing graft-versus-tumour effects against leukaemia and solid tumours. Recently acquired knowledge of the role of donor immunisation status, new techniques in the generation of minor histocompatibility antigen-specific cytotoxic T lymphocytes in vitro, and innovative principles in vaccination will help to design clinical trials that exploit minor histocompatibility antigens in the immunotherapy of cancer.

Animals↗
PubMed1978

Modulation of mixed lymphocyte culture reactivity following alloimmunization between H-1 (Ag-B)-histocompatible rat strains.

H-1 (Ag-B)-histocompatible rats were cross-immunized to study the effects of presensitization on the mixed lymphocyte culture (MLC) reactivity in normally nonresponsive MLC interactions. Lewis (LEW) rats, H-1 (Ag-B), were given s.c. injections of Fischer (F), H-1 (Ag-B), lymhocytes at weekly intervals for 3 weeks. Immunized LEW (Lew-iF) and F lymphocytes showed increased proliferative responses in MLC after the third immunization. The augmented proliferative responses in the MLC between these H-1 (Ag-B)-histocompatible rat strains following immunization may reflect minor histocompatibility antigenic differences. On the other hand, decreased proliferative responses in MLC between Lew-iF and Ag-B (H-1)-disparate rat strains were demonstrated. Alloimmunization across minor histocompatibility differences led to different types of regulatory effects on the MLC interactions. With low MLC responses, e.g., minor histocompatibility differences, the regulation tends to be positive; whereas for strong MLC responses, e.g., major H-1 (Ag-B) differences, the regulation tends to be negative or suppression.

Animals↗
PubMed2002

Minor histocompatibility antigens as targets of graft-versus-leukemia reactions.

The main advantage of allogeneic stem cell transplantation over autologous stem cell transplantation for hematologic malignancies is the ability to perform cellular immunotherapy using donor-derived immune effector cells after transplantation. In HLA-matched allogeneic stem cell transplantation, the beneficial graft-versus-leukemia effect of donor lymphocytes appears to be caused mainly by alloreactive T cells that are capable of recognizing minor histocompatibility antigens on the malignant cell population from the patient. The tissue distribution of minor histocompatibility antigens probably determines the clinical result of T-cell responses against these antigens. Whereas T cells recognizing broadly expressed antigens cause not only graft-versus-leukemia but also graft-versus-host disease, T cells recognizing minor histocompatibility antigens specifically expressed on hematopoietic cells may mainly eliminate hematopoietic cells from the recipient, including the malignant cells, without affecting donor hematopoiesis or normal nonhematopoietic tissues. Graft-versus-host disease may still occur because of the induction of inflammatory responses against hematopoietic cells in the tissues. Vaccination of patients after transplantation or vaccination of stem cell donors before transplantation using minor histocompatibility antigen-specific peptides, production of minor histocompatibility antigen-specific T cells, and redirection of T-cell specificity by gene transfer of T-cell receptors may be strategies to eradicate specifically the malignant cells after allogeneic stem cell transplantation.

Antigens, Neoplasm↗
PubMedDate not supplied

Evidence for a histocompatibility locus probably linked to but distinct from Mls and H-25.

BALB/c (Mlsb) and BALB.D2-Mlsa strains of mice, both H-2d, are congenic and differ for the Mls locus (and linked genes) located on chromosome 1. The BALB.D2-Mlsa strain was obtained by introducing the Mlsa allele of DBA/2 mice into BALB/c mice. In previous studies we showed that BALB.D2-Mlsa recipients reject, relatively rapidly, all skin grafts from BALB/c donors. We and other groups have questioned whether the rejections observed were indeed due to the incompatibility for Mlsb products or for products of a histocompatibility (non-H-2) locus linked to, but distinct from, Mlsb. To answer this question, several hybrids carrying either Mlsa or Mlsb in various genetic contexts were grafted with skin from Mls-compatible BALB/c or BALB.D2-Mlsa donors; in the genetic combinations selected, any rejection which might occur would reflect the effects of a non-Mls incompatibility between BALB/c and BALB.D2-Mlsa strains. In certain of the donor-recipient combinations studied, the skin grafts were tolerated for greater than 200 days, but a relatively rapid rejection of BALB/c skin grafts was observed in (B10.D2 x BALB.D2-Mlsa)F1 and (B10.BR x BALB. D2-Mlsa)F1 hybrid recipients. These results indicated that in addition to Mls, the BALB/c and BALB.D2-Mlsa strains differ for at least one other non-H-2 histocompatibility locus. The possible involvement of H-25 was then investigated. Indeed, disparity for H-25, which maps on chromosome 1 close to Mls, can induce relatively rapid skin graft rejection. The H-25 allele of the DBA/2 strain has not been defined: we considered, therefore, that BALB/c and DBA/2 could be disparate at the H-25 locus, and that H-25 (transmitted by DBA/2 to the BALB.D2-Mlsa strain, together with the Mlsa allele) could be responsible for the skin graft rejection we observed. Our results showed, however, that DBA/2, BALB/c and BALB.D2-Mlsa strains of mice all share the H-25c allele; they therefore ruled out a role for H-25 incompatibility in the skin graft rejections we observed, and indicated that these rejections are due to the effects of a yet undefined histocompatibility locus (locus 'x'), probably linked to, but distinct from, the Mls locus. Further experiments showed that the histocompatibility effect of locus 'x' cumulates with that exhibited by Mlsb (or by a putative histocompatibility locus linked to Mlsb).

Animals↗
PubMed2003

Importance of minor histocompatibility antigen expression by nonhematopoietic tissues in a CD4+ T cell-mediated graft-versus-host disease model.

Minor histocompatibility antigens with expression restricted to the recipient hematopoietic compartment represent prospective immunological targets for graft-versus-leukemia therapy. It remains unclear, however, whether donor T cell recognition of these hematopoietically derived minor histocompatibility antigens will induce significant graft-versus-host disease (GVHD). Using established bone marrow irradiation chimeras across the multiple minor histocompatibility antigen-disparate, C57BL/6-->BALB.B combination, we studied the occurrence of lethal GVHD mediated by CD4+ T cells in recipient mice expressing only hematopoietically derived alloantigens. Even substantial dosages of donor C57BL/6 CD4+ T cells were unable to elicit lethal GVHD when transplanted into [BALB.B-->C57BL/6] chimeras. Instead, chimeric mice displayed transient cachexia with reduced target-tissue injury over time, reflecting an early, limited, graft-versus-host response. On the other hand, the importance of minor histocompatibility antigens derived from nonhematopoietic tissues was demonstrated by the finding that [C57BL/6-->BALB.B] chimeric mice succumbed to C57BL/6 CD4+ T cell-mediated GVHD. These data suggest that severe acute CD4+ T cell-mediated GVHD across this minor histocompatibility antigen barrier depends on the expression of nonhematopoietically rather than hematopoietically derived alloantigens for maximal target-tissue infiltration and injury.

Animals↗
PubMed1980

The major histocompatibility complex in the turkey: do erythrocytes bear serologically detectable H antigens?

An attempt was made to identify erythrocyte cell surface antigens associated with the major histocompatibility complex in the turkey. Two turkey lines, A and B, from the University of Minnesota, putatively homozygous for different major histocompatibility complex alleles, were used for this study. A total of 79 birds were immunized either by skin grafting or by injection of homogenized skin preparation in Freund's incomplete adjuvant. Antisera produced with skin grafts and homogenized skin inoculated intramuscularly both contained red cell agglutinins of low titer. Because agglutination reactions were weak, no sera were suitable for use as line-specific typing fluids. Thus, we were unable to demonstrate that turkey erythrocytes contain serologically detectable major histocompatibility antigens corresponding to the B major histocompatibility system in the chicken or the H-2 system in mice. Rather, the turkey major histocompatibility complex is more like that in rabbits, dogs, monkeys and humans.

Animals↗
PubMed1993

Interferon-gamma inhibits liver regeneration by stimulating major histocompatibility complex class II antigen expression by regenerating liver.

The effects of interferon-gamma and interleukin-2 on liver regeneration after 70% hepatectomy in rats was studied immunohistologically, with special attention paid to major histocompatibility complex class II antigen expression. Liver regeneration 2 days after partial hepatectomy as assessed on the basis of bromodeoxyuridine labeling index revealed that regeneration was inhibited significantly in rats given a single dose of interleukin-2 or interferon-gamma compared with rats that underwent only partial hepatectomy. Simultaneous administration of interleukin-2 and interferon-gamma inhibited liver regeneration more markedly than administration of either drug. In rats subjected to partial hepatectomy, Kupffer cells around the portal vein expressed slightly more major histocompatibility complex class II antigen than did sham-operated controls. In the group given interferon-gamma, major histocompatibility complex class II antigen expression was markedly increased. Major histocompatibility complex class II antigen expression was greatest in most Kupffer cells of rats given both interleukin-2 and interferon-gamma. These results suggest that interferon-gamma activates (proliferating) Kupffer cells, in turn leading to suppression of liver regeneration. These major histocompatibility complex class II antigen-positive Kupffer cells act as antigen-presenting cells and present hepatocyte as antigen, the so-called abnormal self, to helper and cytotoxic T cells. Both types of T cells, in turn, may suppress hepatocyte proliferation. The various cytokines induced by the activated Kupffer cells and helper T cells seem to form a network with interferon-gamma to regulate liver regeneration.

Animals↗
PubMed1988

The distribution of human C4 DNA variants in relation to major histocompatibility complex alleles and extended haplotypes.

A C4 DNA polymorphism that can subdivide C4 allotypes and major histocompatibility complex-linked complement gene cluster allele combinations (complotypes) that are not distinguishable by standard electrophoretic means was used to assess further the distribution and linkage association of C4 variants. Segregation of the DNA polymorphism in family studies allowed assignment of particular variants to particular major histocompatibility complex haplotypes. These studies revealed that some complotypes were exclusively correlated with a particular C4 DNA variant, whereas others were not and could be subdivided according to which particular C4 DNA variant was observed. When complotypes that could be subdivided at the DNA level were considered in relation to flanking major histocompatibility complex markers, it was apparent that complotypes associated with major histocompatibility complex "extended haplotypes" had an exclusive correlation with a particular C4 DNA variant. This finding supports the hypothesis that "extended haplotypes" are unique associations of major histocompatibility complex allele combinations and are genetically similar, stably inherited units.

Alleles↗
PubMed1986

Current trends in histocompatibility: clinical relevance versus laboratory phenomena.

The role of conventionally analyzed data in tissue typing is decreasing in clinical transplantation. Improved immunosuppression seems increasingly capable of overcoming the immune response to known histocompatibility differences. The introduction of the concept of public specificities may improve the correlation between matching and graft outcome. The further understanding of the roles of cell-specific antigen systems, particularly those on the vascular endothelial cells, may also improve the clinical relevance of matching. The VEC antigens are becoming more important both in our understanding of histocompatibility and of sensitization. The sensitization of potential transplant candidates needs to be prevented by new protocols for transfusion. The amelioration of sensitization to histocompatibility antigens similar to that achieved in transplantation across the ABO barrier seems theoretically possible and should be an important research effort. Most importantly, sensitization needs to be more accurately defined. Sensitization to specific antigens (cell-specific as well as HLA) must be more carefully correlated with graft survival, and the quantitative aspects of sensitization must be better understood. Thus, there are new trends in the field of histocompatibility that hold promise for further improving the results of clinical transplantation and our understanding of the rejection process.

Antilymphocyte Serum↗
PubMed1985

Maternal-fetal disparity at multiple minor histocompatibility loci affects the weight of the feto-placental unit in mice.

Inbred mice from selected unrelated and congenic strains were mated to determine the relative effects of maternal-fetal disparity at major histocompatibility complex (H-2) and non-H-2 minor histocompatibility antigens on the feto-placental unit at 14 days of gestation. A significant increase in weight of the feto-placental unit was observed only when mother and fetus differed at multiple minor histocompatibility loci. No increase in the weight of the feto-placental unit was observed when mother and fetus differed only at H-2. These results suggest that immunostimulation of the fetus results from a maternal response to minor histocompatibility antigens and not to H-2 antigens.

Animals↗
PubMed2000

HLA class I-minor histocompatibility antigen tetramers select cytotoxic T cells with high avidity to the natural ligand.

INTRODUCTION: Cytotoxic T cells specific for the hematopoietic system-restricted minor histocompatibility antigens HA-1 and HA-2 are potential tools for the treatment of relapsed leukemia after minor histocompatibility antigen mismatched bone marrow transplantation. HA-1/HA-2-specific cytotoxic T cells with strong cytotoxic activity against HA-1/HA-2 positive target cells can be generated in vitro using HA-1 and HA-2 peptide-pulsed dendritic cells as antigen presenting cells. MATERIAL AND METHODS: We used HLA-A2 HA-1/HA-2 tetramers (HA-1(A2)/HA-2(A2) tetramers) to monitor the in vitro generation of HA-1- or HA-2-specific cytotoxic T cells. RESULTS: We show that the intensity of the tetramer-staining of the HA-1/HA-2-specific cytotoxic T cells strongly correlates with their capability to recognize mHag positive target cells. The bright tetramer-staining cytotoxic T cells lyse target cells expressing the natural ligand. The dim tetramer-staining cytotoxic T cells fail to lyse natural ligand positive target cells and lyse peptide-pulsed target cells only. The frequency of bright tetramer-staining, high avidity minor histocompatibility antigen-specific CTLs increases significantly upon appropriate antigen-specific restimulations. CONCLUSION: Our results demonstrate that HLA class I-minor histocompatibility antigen tetramers are useful tools for monitoring and selection of high avidity HA-1- and HA-2-specific cytotoxic T cells for adoptive immunotherapy.

Antigen Presentation↗
PubMed2002

Recipient cytokine genotypes for TNF-alpha and IL-10 and the minor histocompatibility antigens HY and CD31 codon 125 are not associated with occurrence or severity of acute GVHD in unrelated cord blood transplantation: a retrospective analysis.

BACKGROUND: In HLA-identical sibling bone marrow transplantation, certain recipient cytokine gene polymorphism genotypes and minor histocompatibility differences influence the occurrence and severity of acute graft-versus-host disease (aGvHD). The present study investigated the role of cytokine tumor necrosis factor (TNF)-alpha and interleukin (IL)-10 gene polymorphisms HY, HA-1, and CD31 minor histocompatibility antigen (mHag) mismatch in the development of aGvHD after unrelated cord blood (CB) transplant (CBT). METHODS: DNA samples of 115 CB recipients and their unrelated CB grafts were analyzed for genotype associated with TNF-alpha (TNFd3/d3) and IL-10 (IL-10(-1064), 11-16) and for disparities in major and three minor histocompatibility antigens, HY, HA-1, and CD31 codon 125. Results were correlated with the incidence of aGvHD grades II to IV. RESULTS: Neither the donor nor the recipient GvHD risk alleles TNFd3/d3 and IL-10(-1064) (11-16) were associated with the development of aGvHD grades II to IV and I to IV. Because of the heterogeneity of CBTs, the data were reanalyzed separately for patients with malignancies (n=83) or with inborn errors (n=24). No significant association was observed between the severity of aGvHD and the possession of either TNFd3/d3 or IL-10 (11-16) genotypes. Mismatches for the mHags HY, HA-1, and CD31 exon 125 between donor and recipient did not associate with aGvHD grades II to IV. CONCLUSIONS: In contrast to HLA-identical sibling bone marrow transplantation, in mismatched unrelated CBT, neither the cytokine genotypes TNFd3/d3 alone or in combination with IL-10(-1064) alleles nor the minor histocompatibility antigens HY, HA-1, and CD31 exon 125 were associated with aGvHD grades II to IV. Further determination of the cytokine gene polymorphism genotypes in CBTs compared with bone marrow transplants may identify those polymorphisms that could be potential predictive markers for the occurrence of aGvHD.

Acute Disease↗
PubMed1986

The NOD mouse: recessive diabetogenic gene in the major histocompatibility complex.

Examination of the histocompatibility region of the nonobese diabetic (NOD) mouse with antibodies against class II glycoproteins (products of immune response genes of the major histocompatibility complex I-A and I-E), hybrid T-cell clones, and mixed-lymphocyte cultures and analysis of restriction fragment length polymorphisms indicate that the NOD mouse has a unique class II major histocompatibility complex with no expression of surface I-E, no messenger RNA for I-E alpha, and an I-A not recognized by any monoclonal antibodies or hybrid T-cell clones studied. In crosses of NOD mice with control C3H mice, the development of diabetes was dependent on homozygosity for the NOD mouse's unique major histocompatibility region.

Animals↗
PubMed1981

The quantitative effects of the B blood group locus and sex linked histocompatibility antigen in chickens on G-v-H reaction.

The major histocompatibility locus in the chicken is the B locus with a minor histocompatibility antigen controlled by a gene (s) on the W chromosome. This study was designed to determine the quantitative effects of the B locus and the sex linked histocompatibility gene on splenomegaly of chick embryos after inoculation with adult male lymphocytes. The embryos and male lymphocyte donors had blood group genotypes designed B9/B9, B9/B11 so that nine donor-host combinations were used. When the donor and host were homozygous for different B alleles (B9 and B11) or different by one B allele (B9 or B11) the splenomegaly was 4 and 2 times greater, respectively, than the compatible donor and host. A greater splenomegaly was produced in male to female injections than in male to male injections. However, the histocompatibility antigen controlled by a gene(s) on the W chromosome was weaker than the controlled by the B locus.

ABO Blood-Group System↗
PubMed1994

Localization and characterization of major histocompatibility complex class II-positive cells in the posterior segment of the eye: implications for induction of autoimmune uveoretinitis.

PURPOSE: To identify potential antigen-presenting cells in the choroid and retina of the normal rat eye, with a view to proposing a role for such cells in the induction and perpetuation of experimental autoimmune uveoretinitis, a model of human uveoretinal inflammation. METHODS: Immunohistochemical and electron microscopic studies using a panel of monoclonal antibodies were performed on frozen sections of the perfused-fixed normal Lewis rat eye, choroid whole mounts, and cytospin preparations of cells harvested from choroid/ciliary body explant cultures. In addition, time-lapse video recordings of migratory uveal tract cells in culture were taken. RESULTS: No major histocompatibility complex class II-positive cells were found in the normal Lewis rat retina. However, at least three populations of potential antigen-presenting cells were found in the uveal tissues of the eye: classical dendritic cells expressing high levels of major histocompatibility complex class II antigen; resident dendritiform macrophages, which were negative for major histocompatibility complex class II antigen, but expressed specific macrophage markers (ED2); and blood-borne macrophages (ED1) that had emigrated from the vasculature into the tissue compartment. In addition there were small numbers of cells expressing novel markers such as markers usually found only on macrophage subsets in splenic tissue (ED3) and a recently described marker for veiled dendritic cells (OX62). Dendritic cells and resident dendritiform macrophages closely interacted with each other and with tissue cells, particularly retinal pigment epithelial cells. CONCLUSIONS: The posterior uveal tract is richly populated with classical dendritic cells expressing constitutive high levels of major histocompatibility complex class II antigen. There are also several types of macrophages with the potential to modulate immune responses in the posterior segment. Interactions among these cells and with resident tissue cells such as retinal pigment epithelial cells are probably central to the initiation of (auto)immune responses in the posterior segment of the eye.

Animals↗
PubMed1993

Effect of donor and recipient gender disparities on fatal graft-vs.-host disease in a mouse model for major histocompatibility complex-matched unrelated-donor bone marrow transplantation.

Sex chromosome-linked minor histocompatibility determinants have been shown to affect the incidence and severity of graft-vs.-host disease (GVHD) in both humans and animals. On the basis of earlier studies done in mice and humans, it has often been assumed that this effect is due to a simple response of female donor cells recognizing recipient male HY antigens as foreign and reacting against them. However, the data of various clinical groups have not always supported this assumption. Moreover, since most of the earlier mouse studies focused only on the single transplant direction of female into male and/or were done under totally syngeneic conditions, the possibility of a GVHD response based on donor recognition of the recipient female HX antigen as foreign was never fully addressed. We have therefore reexamined the question in a more clinically relevant allogeneic transplantation setting, using a major histocompatibility complex (MHC)-matched, unrelated-donor mouse model. Five different donor/recipient sets were paired in all four possible gender combinations. The results indicated that, in addition to GVHD reaction against male HY, reaction against female HX was also possible. The results also showed that when the total level of GVHD due to autosomal chromosome minor histocompatibility disparities is extensive, it may masks the influence of gender-related factors on GVHD. Finally, the data also suggest the possibility that the sex chromosome-linked minor histocompatibility determinants may be polymorphic and thus capable of multiple allele expression.

Alleles↗