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PubMed1993

Micelle-bound conformational preferences of a peptide derived from a murine major histocompatibility complex class I molecule.

Models of the micelle-bound conformation of a 17-residue major histocompatibility complex-derived peptide, [Ala85]Dk(69-85), have been determined by NMR spectroscopy and simulated annealing calculations. This peptide is a truncated, substituted version of Dk(61-85), which is a fragment of the murine major histocompatibility complex class I molecule H-2Dk. Dk(61-85) has been shown to adopt an ordered conformation required for augmentation of insulin-stimulated glucose uptake (Stagsted, J., Baase, W. A., Goldstein, A., and Olsson, L. (1991) J. Biol. Chem. 266, 12844-12847). [Ala85]Dk(69-85) retains full biological activity. Thirty-eight converged NMR structures of [Ala85]Dk(69-85) bound to dodecyl phosphocholine micelles have been generated. The NMR-derived models display a propensity for a type-I beta-bend involving residues 73-76 and an amphipathic helical region involving residues 77-84. CD spectra yield a helical content (8% at 20-25 degrees C) consistent with transient, partial helix formation. The relative orientation of the beta-bend region with respect to the helical region is not well defined by the NMR data. This may reflect true heterogeneity of the micelle-bound conformation. The NMR structures were compared with a model of [Ala85]Dk(69-85) derived from the x-ray coordinates of the human major histocompatibility complex class I allele HLA-Aw68 (Garrett, T. P. J., Saper, M. A., Bjorkmann, P. J., Strominger, T. L., and Wiley, D. C. (1989) Nature 342, 692-696). Structural features that are important for the bioactivity of [Ala85]Dk(69-85) are discussed with reference to reported structure-activity relationships (Stagsted, J., Mapelli, C., Myers, C., Matthews, B. W., Anfinsen, C. B., Goldstein, A., and Olsson, L. (1993) Proc. Natl. Acad. Sci. U.S.A., in press). A general description of the structural properties of the putative receptor site(s) that are likely to be required for binding [Ala85]Dk(69-85) is given.

Amino Acid Sequence↗

PubMed1996

The role of major and minor histocompatibility antigens in orthotopic corneal transplantation in mice.

The mouse model of orthotopic corneal transplantation was used to evaluate the clinical course of corneal graft rejection process. Corneal grafts were placed into eyes of naive, unmodified recipients or recipients presensitized with skin graft two weeks before corneal transplantation. Two strain combinations were used, one with genetic disparity at both major and minor histocompatibility antigens and the other with the difference only at multiple minor histocompatibility antigens. A panel of syngeneic graft recipients served as controls. In naive recipients, rejection reaction was recorded in more than 90% of recipients mostly during the third week after grafting and 40-50% of corneas displayed irreversible failure in both strain combinations. Both MHC compatible and incompatible corneal grafts in all presensitized recipients were irreversibly rejected by a second-set allograft reaction. The results thus show an important role of multiple minor histocompatibility antigens in corneal allotransplantation in mice. In addition, the prompt reaction in presensitized recipients is evidence for expression of allotransplantation immunity in the eye, which has been for a long time considered as a privileged site sequestered from systemic immunity.

Animals↗

PubMed1994

Genetics of histocompatibility.

Molecular studies of the major histocompatibility complex region, its genes, and its products are progressing in a number of different directions, and this progress is becoming of increasing interest not only to immunologists but also to geneticists and clinicians. Here I select only certain aspects of this field, stressing the biological importance of a few recent developments. This review concentrates on two topics of clinical importance and where important recent progress is reported: the "revolution" of HLA genotyping for histocompatibility matching in transplantation and the elucidation of a genetic disease of gene regulation, primary major histocompatibility complex class II deficiency (or bare lymphocyte syndrome).

Animals↗

PubMed1975

Interlamellar corneal grafts in rats. Effect of histocompatibility.

A technique of interlamellar keratoplasty was employed to evaluate the influence of difference in histocompatibility on the results of corneal transplantation in highly inbred rats. The degree of corneal clarity and vascularity and the incidence of rejection of relatively conpatible ("weak") and incompatible ("strong") allografts were recorded blindly in recipients with normal and vascularized corneas and in recipients sensitized with donor tissue either before or after corneal grafting. In contrast to the well-known effects of histocompatibility on skin and organ allografts, there was no substantial effect whatsoever of histocompatibility on either the severity of corneal allograft reactions orthe incidence of rejection. Consequently, the results of this experimental investigation suggest that tissue typing may have little or no value in clinical keratoplasty.

Animals↗

PubMed1975

Histocompatibility antigens acting as helper determinants for tumor-associated antigens of murine lymphosarcoma.

The mechanism of effectiveness of allogeneic versus syngeneic immunization in mounting a humoral specific immune response against tumor-associated antigens of murine urethan-induced thymic lymphosarcomas was studied. C57BL mice immunized with untreated or blocked C3Hf lymphoma cells yielded sera with complement-dependent cytotoxicity for C57BL lymphosarcomas, whereas they did not respond to repeated injections of blocked syngeneic lymphoma cells, indicating a helper activity of alien alloantigens in the reflex of tumor antigens. Thymectomized, lethally-irradiated and T, but not B-reconstituted mice produced active sera, suggesting a T-dependent response. The anti-tumor activity of the serum ran parallel with the anti-histocompatibility one. The tumor-associated and the alien histocompatibility determinants had to be present on the same cell membrane. In addition, active sera were obtained when immunizing syngeneic lymphoma cell inocula were followed by allogeneic normal immunocompetent cells. It is suggested that either a helper mechanism with B and T cells cooperating in recognizing haptenic tumor-associated and carrier histocompatibility antigens or a graft-versus-host reaction determining an abnormal induction of the immune system is needed in order to detect the weak tumor-associated antigens of urethan-induced lymphomas.

Animals↗

PubMed1976

Relationship between the enhanced expression of histocompatibility antigens on interferon-treated L 1210 cells and their position in the cell cycle.

We have determined the cell cycle position of individual mouse leukemia L 1210 cells by cytophotometric and autoradiographic techniques and simultaneously determined the amount of histocompatibility antigens expressed on the surface of individual cells by quantitative immunofluorescence. Interferon treatment of L 1210 cells was accompanied by an enhanced expression of histocompatibility surface antigens. The distribution of interferon-treated cells in the various phases of the cell cycle was similar to that for control cells and the enhanced expression of histocompatibility antigens was observed on interferon-treated cells in all phases of the cell cycle. We conclude, therefore, that this enhancement is not due to a preferential concentration of these cells in any one particular phase of the cell cycle.

Animals↗

PubMed1993

Immunization against tumor and minor histocompatibility antigens by eluted cellular peptides loaded on antigen processing defective cells.

Material eluted from RMA lymphoma or B6 spleen cells under acid conditions was fractionated by reverse phase high-performance liquid chromatography, and tested for ability to restore the sensitivity to cytotoxic T lymphocytes of the processing/presentation defective mutant line RMA-S. This allowed identification of three fractions (termed M1, M2 and M3) carrying B6 antigens recognized by cytotoxic T lymphocytes (CTL) elicited across the minor histocompatibility barrier A.BY anti-B6 (both H-2b) and one fraction (termed T1) carrying a tumor antigen recognized by B6 anti-RMA CTL. By parallel runs of material from cell lysates over major histocompatibility complex class I affinity columns, the M2 and M3 antigens were defined as Kb restricted, and M1 and T1 as Db restricted. Isolated fractions loaded onto RMA-S cells could be used to prime anti-minor histocompatibility antigen and tumor CTL in vivo. They could also be used for in vitro restimulation of spleen cells from mice that had been primed either by antigen-loaded RMA-S, or by wild-type RMA tumor cells and B6 splenocytes. The CTL generated by these methods were specific for the loading antigen, and they also recognized the antigen on the "physiological" target, i.e. RMA or B6 lymphoblasts. This system based on RMA-S as an immunization and target antigen reporter cell may be used for dissection of complex CTL responses, e.g. in studies of clonal composition and epitope dominance, or for studies of tumors that are poor stimulators of immunity.

Animals↗

PubMedDate not supplied

In situ distribution of major histocompatibility complex products and viral antigens in chronic hepatitis B virus infection: evidence that HBc-containing hepatocytes may express HLA-DR antigens.

Using a double-staining immunohistochemical procedure, the topographical relationship between viral antigens on the one hand and the expression of major histocompatibility complex products by hepatocytes on the other hand was analyzed in a series of 19 liver biopsies from patients with chronic hepatitis B virus infection. In areas of piecemeal necrosis, periportal hepatocytes demonstrated Class I major histocompatibility complex products or HLA-A, B and C antigens, but did not show a preferential expression of either HBcAg or HBsAg. The cellular infiltrate of piecemeal necrosis consisted of helper/inducer and suppressor/cytotoxic T-lymphocytes, and was admixed in four cases with branching dendritic processes of sinusoidal lining cells which strongly expressed Class II major histocompatibility complex products or HLA-DR antigens. The latter surrounded small groups of periportal hepatocytes. In areas of spotty necrosis, the hepatocytes expressed HLA-A, B and C antigens in all cases, and were admixed with variable numbers of suppressor/cytotoxic T-lymphocytes. In 14 cases, the clustered hepatocytes in areas of spotty necrosis expressed HLA-DR antigens, associated in 11 of the cases with immunoreactive HBcAg in the nuclei of some of the HLA-DR-positive hepatocytes. Immunoelectron microscopy, performed in one such case, demonstrated the presence of HLA-DR antigen in a discontinuous pattern at the plasma membrane of some hepatocytes, together with the presence of core particles in the nucleus of HLA-DR-positive hepatocytes. Our findings further contribute to the growing evidence that HBcAg represents the major target antigen for T-cell attack in areas of spotty necrosis.(ABSTRACT TRUNCATED AT 250 WORDS)

Antigens, Viral↗

PubMedDate not supplied

Expression of class I and class II major histocompatibility complex antigens on human hepatocytes.

We analyzed whether normal human hepatocytes, which normally do not display Class II major histocompatibility complex antigens, can be induced to express them in vitro, and whether this induction has an in vivo counterpart in chronic liver diseases. While both alpha- and gamma-interferon induced expression of Class I antigens, only gamma-interferon induced expression of Class II antigens on hepatocytes in vitro. Recombinant interleukin 2 had no effect on major histocompatibility complex antigen expression. Both Class I and Class II antigens could be detected by indirect immunofluorescence on hepatocytes from patients with various forms of chronic liver disease, regardless of etiology. These findings suggest that gamma-interferon produced by T lymphocytes that infiltrate the liver during the course of chronic hepatitis induces Class II major histocompatibility complex antigen expression and may endow the hepatocytes with the capacity to perform accessory (antigen-presenting) cell functions.

Antibodies, Monoclonal↗

PubMed1992

Administration of interleukin-2 induces major histocompatibility complex class II expression on the biliary epithelial cells, possibly through endogenous interferon-gamma production.

In various organ-specific autoimmune diseases, aberrant expression of major histocompatibility complex class II antigens on each target epithelial cell has been reported. Some researchers have attempted to link this phenomenon to the antigen-presenting capacity and the induction of autoimmunity, whereas others think it might serve as a peripheral mechanism for the induction and the maintenance of self-tolerance in autoreactive T cells. In this study, we showed that intraperitoneal administration of interleukin-2 (1.2 x 10(6) IU/kg) to 4-wk-old male BALB/c mice for 35 consecutive days induced lymphocyte infiltration around bile ducts in the liver and major histocompatibility complex class II expression on biliary epithelial cells, which was immunoelectron microscopically confined to the luminal cell surface. Immunohistochemically, lymphocytes accumulating around bile ducts were mainly T cells, positive for CD3, L3T4 and H-2 class II molecules, and a few of them were positive for Lyt-2 and negative for immunoglobulin. Half of the infiltrates were positive for asialo GM1, and one-third was positive for interferon-gamma. Interferon-gamma-positive, L3T4-positive cells were detected in mirror sections. However, neither the destruction of biliary epithelial cells nor the presence of granulomas was observed. Autoantibodies were serologically undetectable. The existence of interferon-gamma-positive cells in the lesion and the fact that intravenous administration of anti-interferon-gamma twice a week completely inhibited the lymphocyte infiltration and the major histocompatibility complex class II expression on biliary epithelial cells suggested that these changes were induced through endogenous interferon-gamma production.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed2006

Cyto- and histocompatibility of multilayered DNA-coatings on titanium.

DNA-containing biomaterial coatings offer potential beneficial effects for both soft and hard tissue implants because of the structural properties of DNA. In the current study, the aim was to assess the in vitro cyto- and in vivo histocompatibility of multilayered DNA-coatings generated using the electrostatic self-assembly technique, with poly-D-lysine or poly(allylamine hydrochloride) as the cationic counterparts of anionic DNA. Multilayered DNA-coatings were fabricated on titanium substrates. Noncoated titanium substrates served as controls. In vitro experiments with rat primary dermal fibroblasts (RDF) assessing their viability were performed using a Live/Dead assay and an MTT-based assay. The presence of multilayered DNA-coatings did not affect RDF cell viability. On the other hand, an increased proliferation was demonstrated on both types of multilayered DNA-coatings. An in vivo rat model was used to study the soft tissue histocompatibility of subcutaneously inserted implants during implantation periods of 4 and 12 weeks. Light microscopic analysis revealed that all implants were surrounded by a fibrous capsule containing alpha-smooth muscle actin, and that the presence of a multilayered DNA-coating did not induce any adverse effects in terms of inflammation and wound healing. Histomorphometrically, no significant differences in capsule quality or thickness were observed dependent on multilayered DNA-coating or implantation period. The cyto- and histocompatibility of multilayered DNA-coatings demonstrated in this study allows their use and functionalization with appropriate compounds to modulate cell and tissue responses in dental and medical implantology.

Animals↗

PubMed1989

Transfected rat islet tumour cells express mouse major histocompatibility complex class I antigens functionally. Applicable as "pseudo-syngeneic" targets in the multiple low-dose streptozotocin diabetes model.

Rat insulinoma cells clone 5AH-B, were transfected by electroporation with the gene encoding the mouse major histocompatibility complex class I antigen H-2Kb, whereupon stable transfectants were selected and analysed. Data from flow cytometric analyses using three different H-2Kb specific monoclonal antibodies and functional assays using H-2Kb specific alloimmune cytotoxic T cells revealed that the encoded H-2 antigen was expressed in a functional manner. Similar experiments employing the monoclonal antibody OX-18, which recognizes rat major histocompatibility class I molecules, and xenoimmune cytotoxic T cells specific for the endogenously expressed RT1g antigen showed that functional expression of the RT1g antigen was maintained. However, a down-regulation of the expression was observed in H-2Kb positive transfectants, whereas normal expression was retained in Kb negative transfectants. The function of the native promoters of both the endogenous and the transfected class I genes was found to be preserved in the transfectants as assessed by the response to stimulation with interferon-tau. The present study was unable to confirm the reports of RIN specific lysis by T cells from multiple low dose streptozotocin diabetic mice. Even in the presence of the syngeneic restriction element no lysis was observed. We conclude, that rat insulinoma cells clone 5AH-B, are able to integrate a foreign class I antigen gene and express the encoded product functionally. The data also suggest the possibility of creating major histocompatibility antigen positive rat insulinoma cells which are RT1g negative. Such transfectants will be of great potential value for the dissection of cell mediated B cell destructive processes.

Adenoma, Islet Cell↗

PubMed1979

The influence of the major histocompatibility complex (H-2) on experimental diabetes in mice.

Mice with different histocompatibility loci on an identical background genome (congenic resistant lines of mice) were used to study the possible influence of the histocompatibility complex on experimental diabetes. The major histocompatibility complex (H-2) was not found to influence the diabetogenic effect of encephalomyocarditis (EMC) virus. In contrast the glucose intolerance following heterologous and homologous immunization with pancreatic antigens appeared H-2 influenced. Antibodies against cell surface components on viable B-cells were present in serum from mice with glucose intolerance induced by homologous immunization. The results suggest that the susceptibility to experimental autoimmune diabetes in mice is influenced by the H-2 complex.

Animals↗

PubMed2003

Presentation assessment of minor histocompatibility antigens by predictive proteasomal cleavage analysis.

Minor histocompatibility peptides (mHps) derived from polymorphic segments of endogenous proteins are thought to be targets for graft-versus-host and graft-versus-leukemia reactions after HLA-identical stem cell transplantation. A great majority of antigenic peptides is generated by fragmentation of proteins in the course of proteasomal processing. An algorithm was recently developed to predict cleavage sites during proteasomal processing. We tested the accuracy of the algorithm to predict mHps using 18 amino acid (AA) sequences of minor histocompatibility antigens (mHags) encoded by autosomal genes representing single nucleotide polymorphisms or by Y-chromosomal genes. The algorithm correctly predicted the C-termini of 11 of 13 experimentally confirmed mHps: 1) Correct prediction of C- and N-termini, e.g., for HA-1(H); 2) Correct prediction of C- and N-termini while anticipating intra-epitope cleavage sites, e.g., for SMCY-A*0201; 3) Correct prediction of C-termini and N-terminal extensions, e.g., for HA-8(R/V); and 4) Correct prediction of C-termini and N-terminal extensions while anticipating intra-epitope cleavage sites, e.g., for UTY-B8. Analysis of experimentally unconfirmed allelic counterparts of four autosomal mHags showed that AA substitutions either led to the insertion of an epitope-destroying cleavage site (e.g., in HA-1(R)) or abolished the correct C-terminus (e.g., in HA-2(M)). The proteasomal processing algorithm provides reliable data on the generation of mHps and forecasts their presence or absence. Combined with MHC class I ligand prediction, it can be a useful tool for the prediction of generation and presentation of new CTL epitopes derived from minor histocompatibility antigens.

Algorithms↗

PubMed1989

Comparative mapping of the human major histocompatibility complex in different racial groups by pulsed field gel electrophoresis.

The molecular map of the human major histocompatibility complex was examined in multiple examples of various Caucasoid and Japanese major histocompatibility complex supratypes using pulsed field gel electrophoresis. Extensive differences in restriction fragment lengths were observed. However, each supratype showed specific genomic characteristics including deletions, duplications, or insertions supporting the hypothesis that these supratypes are markers of conserved ancestral haplotypes. Some of the gene arrangements are consistent with the deletions or duplications previously described or suggested by conventional DNA techniques and protein typing, while others have not been recognized previously. Characterization of the gene organization within disease-associated ancestral haplotypes will provide new insights into the functional role and evolution of the major histocompatibility complex.

Asian People↗

PubMed2004

Evolution of responding CD4+ and CD8+ T-cell repertoires during the development of graft-versus-host disease directed to minor histocompatibility antigens.

Graft-versus-host disease (GVHD) can be induced in lethally irradiated mice after allogeneic bone marrow transplantation between major histocompatibility complex-matched strains expressing multiple minor histocompatibility antigen differences. In the B6 --> BALB.B irradiation model, both CD4(+) and CD8(+) donor T cells have the capacity to mediate lethal GVHD. Previously, CDR3-size spectratyping was used to analyze these T-cell responses at a single early time point (day 5) after transplantation and revealed clonal or oligoclonal expansions of the V beta 2, 4, and 6 to 14 families for the CD4(+) response and of the V beta 4, 6, 8 to 11, and 14 families for the B6 CD8(+) response. Appropriate positive selection of these T-cell receptor V beta-skewed CD4(+) and CD8(+) T-cell subsets and their subsequent transfer into lethally irradiated BALB.B recipients resulted in fatal GVHD induction. In contrast, BALB.B mice transplanted with nonskewed V beta CD4(+) T cells survived, with minimal symptoms of GVHD. This study was undertaken to investigate the evolution of the donor/antihost minor histocompatibility antigen T-cell repertoire responses throughout the course of GVHD development. The results indicated that a number of V beta families were consistently involved throughout the course of GVHD, whereas some V beta families exhibited skewed expansions only in either the early or late stages of disease. In addition, sequence analysis of relevant representative skewed CDR3 bands from the CD4(+) V beta 11(+) and the CD8(+) V beta 14(+) families, both of which exhibited strong consistent responses, demonstrated increased use of the J beta 2.5 and J beta 2.4 segments, respectively, thus identifying the T-cell receptor specificities involved.

Animals↗

PubMed2005

Effector cells derived from host CD8 memory T cells mediate rapid resistance against minor histocompatibility antigen-mismatched allogeneic marrow grafts without participation of perforin, Fas ligand, and the simultaneous inhibition of 3 tumor necrosis factor family effector pathways.

Reduced-intensity conditioning regimens for transplant recipients have heightened awareness of immunologic resistance to allogeneic bone marrow transplants (BMT). Although T cell-mediated cytotoxicity has been assumed to play a role in the resistance against donor allogeneic hematopoietic stem and progenitor cell grafts, several studies have reported relatively unimpaired resistance by recipients who lack perforin, Fas ligand (FasL), and other cytotoxic mediators. This study compared the early kinetics of T cell-mediated resistance in B6 (H2b) cytotoxically normal versus deficient recipients after transplantation with major histocompatibility complex-matched, minor histocompatibility antigen (MiHA)-mismatched allogeneic marrow grafts. Wild-type B6 or cytotoxic double-deficient perforin-/-/gld+/+ (B6-cdd) mice were sensitized against major histocompatibility complex-matched BALB.B or C3H.SW (H2b) MiHA and transplanted with a high dose (1 x 10(7)) of T cell-depleted bone marrow. CD8 T memory cells were shown to be present in recipients before BMT, and anti-CD8 monoclonal antibody infusion abolished resistance, thus demonstrating that CD8 T cells are the host effector population. Donor-committed and high proliferative potential progenitor numbers were markedly diminished by 48 hours after transplantation in both wild-type B6 and B6-cdd anti-donor MiHA-sensitized recipients. These observations indicate that the resistance pathway used in the cytotoxic deficient mice was both potent and rapidly induced--consistent with a CD8 memory T-cell response. To examine the role of Tumor necrosis factor-like weak inducer of apoptosis (TWEAK)- and TL1A-mediated cytotoxicity in this strong resistance, newly generated monoclonal antibodies specific for these ligands were administered to B6-cdd recipients sensitized to donor antigens. Recipients of syngeneic B6-gfp bone marrow exhibited significant donor colony-forming unit numbers after BMT. In contrast, low or absent colony-forming unit levels were detected in allogeneic recipients, including those that lacked perforin and FasL and that received anti-TWEAK, anti-tumor necrosis factor-related apoptosis-inducing ligand, and anti-TL1A monoclonal antibodies. These findings extend previous observations by demonstrating the existence of a rapidly effected resistance pathway mediated by memory CD8 effector T cells independent of the 2 major pathways of cytotoxicity. Together with previous findings, these results support the notion that effector cells derived from memory CD8 T-cell populations can mediate strong resistance against donor allogeneic MiHA-disparate hematopoietic engraftment by using a mechanism that is independent of the contribution of perforin, FasL, and the known death ligand receptor pathways.

Animals↗

PubMed2006

Immune tolerance to self-major histocompatibility complex class II antigens after bone marrow transplantation: role of regulatory T cells.

The immune system undergoes rapid reconstitution after autologous or syngeneic bone marrow transplantation with the re-establishment of tolerance to self-antigens. Administration of drugs such as cyclosporine that inhibit thymic-dependent clonal deletion disrupts the reconstitution of the immune system. In the absence of a peripheral regulatory T cells eliminated by the preparative regimen, systemic autoimmunity with pathology similar to graft-versus-host disease often develops. Moreover, the resolution of autoaggression is dependent on the reconstitution of CD4+ regulatory T cells. This study examined the specificity and function of this regulatory population assessed ex vivo that plays a critical role in down-regulating the autoreactive T lymphocyte response in cyclosporine-induced syngeneic graft-versus-host disease. The results suggest that both the antigen-specific regulatory and pathogenic effector T cells recognize a common peptide antigen framework (CLIP, a peptide derived from the invariant chain) presented by major histocompatibility complex class II molecules. Analysis of the CD4+ T-cell compartment revealed two subsets of CLIP-reactive T cells that differentially require the N- and C-terminal flanking domain of this peptide. Regulatory function is associated with the cells that require the C-terminal flanking domain. This population expresses the Foxp3 nuclear transcription factor and plays a critical role in re-establishing tolerance to self-major histocompatibility complex class II antigens. In addition to suppressing the production of type 1 cytokines, these regulatory T cells can direct the apoptotic death of the pathogenic autoreactive lymphocytes. This study also suggests that the development of functional regulatory activity is an active response initiated by the presence of autoreactive lymphocytes that can present the target antigen (major histocompatibility complex class II CLIP) to the regulatory T cells. Moreover, this process can be mimicked by peptide antigen in the absence of the pathogenic effector lymphocytes leading to the development of functional regulatory T-cell activity.

Adoptive Transfer↗