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PubMed1985

Analysis of immunological tolerance to major histocompatibility complex antigens. I. High frequencies of tolerogen-specific cytotoxic T lymphocyte precursors in mice neonatally tolerized to class I major histocompatibility complex antigens.

Injection of (CBA X A)F1 cells into neonatal CBA mice rendered them tolerant to skin grafts of (CBA X A)F1 origin. Limiting dilution analysis revealed a very low frequency of tolerogen-inducible cytotoxic T lymphocyte precursors (CTL-P) in spleens of tolerant mice. Two in vitro procedures allowed, however, the induction of tolerogen-specific CTL-P of high frequencies in tolerant mice: (a) the "by-pass" activation of spleen cells from tolerant mice by concanavalin A under short-term bulk culture conditions followed by culture of limiting numbers of activated responder cells, and (b) absorption of spleen cells from tolerant mice on monolayers of tolerogen-activated T cells from normal syngeneic mice. Furthermore, spleen cells from tolerant mice, recently challenged with a tolerogen-bearing skin graft, specifically suppressed the activation of tolerogen-reactive splenic CTL-P from normal CBA mice under limiting dilution conditions. These data confirm the presence of tolerogen-specific CTL-P of high frequency in tolerant mice and suggest their functional inactivation through a suppressive mechanism.

Animals↗
PubMed1998

Rejection of wild-type and genetically engineered major histocompatibility complex-deficient glial cell xenografts in the central nervous system results in bystander demyelination and Wallerian degeneration.

Mixed glial cell cultures prepared from neonatal wild type and mutant male mice lacking either major histocompatibility complex class I, class II or both class I and II molecules (major histocompatibility complex class I(o/o)II(o/o)), and from syngeneic male rats were transplanted into female rat spinal cord white matter. Graft survival was monitored using DNA probes specific to the Y chromosome. Survival of major histocompatibility complex class-deficient grafts was not prolonged compared to wild-type grafts and in most cases grafts could not be detected at 28 days post-transplantation, at which time syngeneic grafts were still present. However, rejection of xenografts resulted in significant bystander damage to host tissue. In recipients of wild-type and major histocompatibility complex class I(o/o) xenografts the predominant pathology was demyelination. Demyelination was also observed in recipients of major histocompatibility complex class II(o/o) and major histocompatibility complex class I(o/o)II(o/o) xenografts, however in addition there was marked collagen deposition and meningeal cell invasion. Significantly more axons had undergone Wallerian degeneration in recipients of major histocompatibility complex class II(o/o) and major histocompatibility complex class I(o/o)II(o/o) xenografts than recipients of wild-type and major histocompatibility complex class I(o/o) xenografts. These findings were interpreted as evidence of a more destructive immune response associated with rejection of grafts lacking major histocompatibility complex class II molecules. It was proposed that the difference in the severity of bystander damage may be related to the previously demonstrated ability of xenogeneic major histocompatibility complex class II molecules to activate host T cells directly, whereas xenografts lacking major histocompatibility complex class II molecules were capable of activating host T cells only by the indirect pathway.

Animals↗
PubMed1990

Induction of minor histocompatibility antigen-specific T-helper but not T-cytotoxic response is dependent on the source of antigen-presenting cell.

We studied the accessory cell requirements for triggering in vivo primed human major histocompatibility complex class I- and class II-restricted T cells specific for minor histocompatibility antigens. We compared the antigen-presenting capacities of peripheral blood lymphocytes (PBLs) and Epstein-Barr virus-transformed lymphoblastoid cell lines (EBV-LCLs), both derived from the same donor, to induce minor histocompatibility antigen-specific cytotoxic and proliferative T cells. PBLs and EBV-LCLs were equally effective as antigen-presenting cells to trigger cytotoxic-T-cell responses specific for minor histocompatibility antigens, some of which were reactive with B cells only. In contrast, a clear difference was found between the capacities of the two antigen-presenting cell types to induce minor histocompatibility antigen-specific T-helper-cell responses. PBLs as antigen-presenting cells could induce T-helper-cell lines reactive against minor histocompatibility antigens presented on PBLs, on EBV-LCLs, or on both cell types as stimulator cells. Unexpectedly, however, EBV-LCLs as antigen-presenting cells in all instances failed to induce T-helper-cell responses specific for minor histocompatibility antigens presented on PBLs or on both PBLs and EBV-LCLs as stimulator cells and could only trigger T-helper cells directed against B-cell-specific minor histocompatibility antigens. Our findings indicate a dichotomy in the capacity of EBV-LCLs to present minor histocompatibility antigens in the induction versus the effector phse of the in vitro T-helper-cell response. Furthermore, the results show different in vitro accessory cell requirements for major histocompatibility complex class I- and class II-restricted T-cell responses specific for human minor histocompatibility antigens.

Adolescent↗
PubMedDate not supplied

Minor histocompatibility antigens: allo target molecules for tumor-specific immunotherapy.

Minor histocompatibility antigens have to be considered as key molecules in the stem cell-based immunotherapy of malignancies. Allogeneic stem cell transplantation (SCT) is a well-established and effective therapy for advanced hematologic malignancies. The apparent powerful graft-versus-leukemia effect of SCT led clinicians to apply SCT for the treatment of metastatic solid tumors. The SCT-based graft-versus-tumor reaction in the allogeneic human leukocyte antigen-matched SCT setting is mediated by allo-immune effectorcells directed against tumor-related target antigens. The target molecules involved in the allo-immune graft-versus-tumor reaction are tumor-specific antigens, tumor-associated antigens, and tissue- and cell-specific minor histocompatibility antigens. The power of the minor histocompatibility antigens in the human leukocyte antigen-identical, stem cell-based immunotherapy for malignancies is their "allo-ness." As opposed to tumor-associated self antigens, the complexes of MHC and allo-target peptide are likely to be more immunogeneic than the major histocompatibility complex and self-target peptide complexes. Moreover, minor histocompatibility allo-antigens are not subject to self tolerance. Earlier minor histocompatibility antigens were seen as alien entities, disturbing the success of the so ideally matched organ and SCT donor-recipient combinations. To date, minor histocompatibility antigens can be set in the favorable light of useful tools for immunotherapy for cancer. The first clinical application of the hematopoietic minor histocompatibility antigens HA-1 and HA-2 is currently being explored in a stem cell-based setting for hematologic malignancies. Because HA-1 is also expressed on carcinoma cells, a stem cell-based vaccination trial for patients with metastatic breast or renal cancer is about to start as well. The immunotherapeutic potential of minor histocompatibility antigens demands serious searches for new minor histocompatibility antigens and analyses of their phenotype frequency, tissue distribution, and functional membrane expression. The minor histocompatibility antigens meeting the prerequisites for specific immunotherapy for malignancies, such as membrane expression and tissue and/or cell specificity, may offer the curative tools for stem cell-based immunotherapy for various hematologic and nonhematologic malignancies.

Antigens, Neoplasm↗
PubMed2005

Isolation and characterization of a protochordate histocompatibility locus.

Histocompatibility--the ability of an organism to distinguish its own cells and tissue from those of another--is a universal phenomenon in the Metazoa. In vertebrates, histocompatibility is a function of the immune system controlled by a highly polymorphic major histocompatibility complex (MHC), which encodes proteins that target foreign molecules for immune cell recognition. The association of the MHC and immune function suggests an evolutionary relationship between metazoan histocompatibility and the origins of vertebrate immunity. However, the MHC of vertebrates is the only functionally characterized histocompatibility system; the mechanisms underlying this process in non-vertebrates are unknown. A primitive chordate, the ascidian Botryllus schlosseri, also undergoes a histocompatibility reaction controlled by a highly polymorphic locus. Here we describe the isolation of a candidate gene encoding an immunoglobulin superfamily member that, by itself, predicts the outcome of histocompatibility reactions. This is the first non-vertebrate histocompatibility gene described, and may provide insights into the evolution of vertebrate adaptive immunity.

Animals↗
PubMed2025

Major histocompatibility complex class IIB disassortative mate choice in a genetically monogamous seabird.

Among species reproducing sexually, mating strategies represent a major component of individual fitness. The major histocompatibility complex (MHC) is an extremely diverse set of genes responsible for immunological recognition and defence against pathogens. Although dissimilarity between mates at the major histocompatibility complex has been proposed to drive mate choice through increased offspring pathogen resistance, evidence is mixed. In addition, explorations of the role of the major histocompatibility complex in other mating strategies, such as divorce, are rare. We investigated whether dissimilarity at the major histocompatibility complex class IIB is associated with mate choice and divorce probability in the genetically monogamous black-legged kittiwake (Rissa tridactyla). We found that first-time male breeders, as well as divorced males, were paired with females more dissimilar at the major histocompatibility complex class IIB than expected under random mating. We did not find evidence for mate choice based on major histocompatibility complex class IIB dissimilarity when considering females. In addition, in the studied population, divorce probability was very low compared with other populations and did not significantly vary with the dissimilarity of the pair at the major histocompatibility complex class IIB. Our results pave the way to a better understanding of the complex role of major histocompatibility complex dissimilarity in mating decisions of species displaying mutual choice and biparental care.

Animals↗
PubMed1994

Upregulation and induction of major histocompatibility complex class I and II antigens on microglial cells in early postnatal rat brain following intraperitoneal injections of recombinant interferon-gamma.

Interferon-gamma when given intraperitoneally by single daily injection into one-day-old rats upregulated the expression of major histocompatibility complex class I antigen on ramified microglial cells in cerebral cortex and induced the expression of major histocompatibility complex class II antigen both on amoeboid and ramified microglial cells present in corpus callosum and cerebral cortex, respectively. In rats receiving single daily injections of interferon-gamma over a period of three consecutive days and killed at the age of seven days, the endothelium exhibited a moderate to weak immunoreaction for major histocompatibility complex class I antigen as detected with the monoclonal antibody OX-18. The immunoreactivity of major histocompatibility complex class I antigen on amoeboid microglial cells was comparable to that of control rats. On the other hand, it was remarkably enhanced on ramified microglial cells and was further intensified with four or six injections of interferon-gamma. In the latter, the endothelial cells also showed a stronger immunoreactivity with OX-18. In rats given three successive injections of interferon-gamma and killed at the age of seven days, 7.5% of amoeboid microglial cells in corpus callosum were induced to exhibit major histocompatibility complex class II antigen as detected with OX-6. An upsurge of the amoeboid microglial cells with major histocompatibility complex class II antigen amounting to about 40% was observed following four and six injections of interferon-gamma. A minimum of four successive injections of interferon-gamma were needed to elicit the expression of major histocompatibility complex class II antigen on ramified microglial cells in cerebral cortex.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1987

Endogenous retroviruses lead to the expression of a histocompatibility antigen detectable by skin graft rejection.

Mov mouse strains differ from their respective, coisogenic partner strains by the embryonic, germ-line introduction of Moloney murine leukemia virus genomes. The possibility that retroviral insertions into the mouse genome resulted in gain or loss mutations at non-H-2 histocompatibility loci was investigated by reciprocal skin grafting between Mov mice and mice from coisogenic, background strains. Two B6-derived and eight 129-derived Mov strains were analyzed. B6 mice rejected skin from the viremic Mov-3 and Mov-14 strains, indicating that these mice had new histocompatibility antigens. No rejections were observed with reciprocal skin grafts exchanged between mice of the 129 background strain and 129-derived Mov strains, one of which (Mov-9) is viremic. To investigate the potential viral origin of the new histocompatibility antigen in Mov-14, lymphocytes from B6 mice primed in vivo with Mov-14 cells or skin were restimulated in vitro with Mov-14 spleen cells and with two retroviral-induced B6 lymphomas, MBL-2 and RBL-5. All three cell types stimulated cytotoxic lymphocytes that lysed Mov-14 Con A lymphoblasts, MBL-2 and RBL-5. The same cytotoxic lymphocytes lysed only lymphoblasts from the viremic Mov-9 strain when tested on cells from 129 and 129 Mov mice. Thus the insertion and expression of exogenous Moloney murine leukemia virus results in the appearance of a new histocompatibility antigen as defined by its stimulation of skin-graft rejection and cytotoxic effector T-cell generation. The non-H-2 histocompatibility antigen identified in this study has been designated H-43 and is encoded by genes mapping to different loci in different Mov strains. These observations suggest that at least a subgroup of non-H-2 histocompatibility antigens is encoded by endogenous retroviruses; the implications of these results for understanding the origin and the identity of non-H-2 histocompatibility antigens are discussed.

Animals↗
PubMed1989

The chicken major histocompatibility complex in disease resistance and poultry breeding.

Numerous studies confirm that genes in the chicken major histocompatibility complex exert major genetic control over host resistance to autoimmune, viral, bacterial, and parasitic diseases. Examples of major histocompatibility complex associations with traits of growth and reproduction in the chicken are also available. Thus, the major effects of the major histocompatibility complex on the economically important traits of disease resistance, growth, and reproduction make the major histocompatibility complex a valuable subject for intensive analysis in agricultural species. This paper examines, as a model for integration of genetics and immunology, the research on the chicken major histocompatibility complex, which confirmed its role in genetic control of disease resistance, focusing on Marek's disease, a virally induced cancer. Current knowledge of associations of the chicken major histocompatibility complex with specific disease resistance, immune response, and other economic traits are selectively reviewed. Use of major histocompatibility complex typing in the poultry industry, including speculation about future applications, is presented.

Animals↗
PubMed1977

Histocompatibility requirements for cellular cooperation in the chicken: generation of germinal centers.

Cyclophosphamide-treated newly hatched chicks were transplanted with histocompatible, semiallogeneic and allogeneic combinations of B (bursa) and T (thymus) cells from newly hatched donors. At the age of 5 weeks the birds were studied for an anti-SRBC response and for the generation of germinal centers in the spleen. The results of these experiments are summarized as follows. i) Allogeneic bursal stem cells have the capacity to restore the bursal structures of CY-treated recipients, but not the germinal center or anti-SRBC formation. ii) When allogeneic B cells are combined with T cells histocompatible or semiallogeneic with them, a restoration of the germinal center formation is achieved, but not to the same level as observed in normal birds or in CY-treated birds transplanted with histocompatible or semiallogeneic B cells. iii) Allogeneic B cells, even when complemented with T cells histocompatible with them, fail to restore the antibody production against SRBC; this is achieved only after transplantation of B cells histocompatible or semiallogeneic with the recipient. These findings indicate that germinal center formation is dependent on cooperation of histocompatible or semiallogeneic B and T cells, and furthermore, that an additional factor provided by the host is involved. Studies with transplantation of histocompatible and histoincompatible 'empty' splenic stromata revealed that the additional factor is not related to the splenic stroma.

Animals↗