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At least 919 records · Page 51Linked to original sources
PubMed1975

Donor HL-A incompatibility and lymphocytotoxic antibody response in human renal allotransplantation.

When 81 recipients of primary renal allografts were examined for the influence of donor HL-A incompatibilities (DIC) on the survival of allografts, an association was found between greater DIC and not only an increased loss of allografts in the 1st year, but also a decreased survival of transplants in the subsequent years. However, three allografts with no DIC were rejected, whereas nine others with three to four imcompatibilities have functioned well for 1-5 years. A surprisingly high proportion (52%) of 81 renal allograft recipients produced lymphocytotoxic antibodies which lack HL-A specificity but apparently detect a polymorphic antigenic system on normal human lymphocytes. Only three patients who rejected the allografts made detectable circulating antibodies specific to DIC. However, when patients received grafts with fewer DIC, there was a greater number of no antibody or low frequency antibody producers, whereas with a greater number of DIC there was an increased occurrence of high frequency antibody producers. These results suggest that HL-A as well as non-HL-A systems may play a significant role in the success of allotransplantation. Although the presence of non-HL-A antibodies was not always associated with allograft loss, further characterization of these antibodies may reveal a new genetic system(s).

Antibody Specificity↗
PubMed1981

Antibody response after alloimmunization with heart tissue in the rat. Characterization of the alloantibodies.

The autoantibody component of LEW anti-DA heart homogenate serum was removed by exhaustive absorption with LEW heart, and the remaining alloantibody component assayed on DA heart homogenate target using 125I antirat immunoglobulin binding assays. The alloantibodies could be divided into two components, one present on spleen and presumably directed at major histocompatibility complex (MHC) antigens and the other present on heart but absent from spleen, liver, and kidney, and therefore defining a heart-specific alloantigen. Localization studies on frozen sections showed the antigen to be localized to the membrane and T tubular system of the myocardial cells and also to the membrane of skeletal muscle cells. Backcross studies showed that the locus coding for this heart-specific antigen appeared not to be linked to the MHC, and that the MHC was the only locus of importance for acute rejection of heart grafts in the DA to LEW combination. Thus, it was concluded that the heart-specific alloantigen was not important for acute cardiac rejection at least in the DA to LEW rat strain combination. As regards antibodies to MHC antigens, there appeared to be substantially more of these in LEW anti-DA heart graft serum when compared to LEW anti-DA heart homogenate serum, and both anti-SD (RT1.Aa) and anti-Ia (RT1.Ba) antibodies could be demonstrated in the antiheart graft serum.

Animals↗
PubMed2000

Specific immunosuppression by postoperative infusion of allogeneic spleen cells: requirement of donor major histocompatibility complex expression and graft-versus-host reactivity.

BACKGROUND: Donor leukocytes may exert positive immunoregulatory effects on allograft acceptance. Most recent studies have focused on pretreatment protocols. In this study, the effect of postoperative infusion of donor leukocytes on graft survival and the phenotypic and functional requirements for infused cells were investigated in fully major histocompatibility complex (MHC)-mismatched rat heart transplant models. METHODS: LEW (RT1l) heart grafts were implanted heterotopically into abdomens of LEW.1W (RT1u), and different types of cells were infused postoperatively. Immunohistochemistry was used to evaluate histopathological changes of grafts. RESULTS: In the absence of any immunosuppressive agents, a single dose of viable donor spleen cells (SC), but not bone marrow cells, was able to prolong heart allograft survival to about 21 days, while they were rejected promptly at day 7 in controls. Infusion of T cell-depleted donor SC, irradiated donor SC or third-party (BN) SC showed no effect on graft survival. Compared with resting cells, neither in vitro nor in vivo prestimulation of infused donor SC improved graft survival. Clinical signs of graft-versus-host reaction were not observed in all above groups. Histology showed remarkable reduction in the severity of graft infiltrate and interleukin-2 receptor-positive cells in grafts of cell-treated animals. Postoperative infusion of SC of F1 generation between different strain combinations showed two requirements for infused cells to be effective: (1) expression of donor-type MHC antigens and (2) strong alloreactivity against the host MHC antigens. CONCLUSION: Postoperative infusion of viable donor SC can lead to allospecific down-regulation of alloreactivity by a graft-versus-host-associated effect.

Animals↗
PubMed2004

Critical evaluation of the amino acid triplet-epitope matching concept in cadaver kidney transplantation.

BACKGROUND: A computer-based approach for determining human leukocyte antigen (HLA) compatibility between kidney donors and recipients on the basis of differences of amino acid sequences as motifs for immunogenic epitopes was proposed by Duquesnoy et al. The HLAMatchmaker algorithm focuses on HLA class I polymorphisms of serologically defined antigens encoded by the HLA-A and -B loci. HLA phenotypic mismatches that represent only a few mismatches at the amino acid triplet level are held to be not or only mildly immunogenic. This approach was proposed as being especially suitable for the allocation of donor kidneys to highly sensitized patients. METHODS: We reexamined this attractive concept using the data of the Collaborative Transplant Study. Intra- and interlocus comparisons for HLA-A and -B were performed according to the original HLAMatchmaker algorithm. To exclude the influence of HLA-DR, only transplants with no HLA-DR mismatch were considered. Patients who had one HLA-A and one HLA-B antigen mismatch were separated into subgroups, depending on the number of triplet mismatches as calculated by the HLAMatchmaker software. Separate analyses were performed for first transplants, retransplants, and patients with a panel-reactive antibody activity of 50% or more. A total of 16,997 white patients matched for HLA-DR who received a cadaver kidney transplant between 1991 and 2001 formed the basis of this analysis. RESULTS: Application of the HLAMatchmaker method could not be shown to result in any statistically significant effect on graft survival. CONCLUSIONS: The HLAMatchmaker concept is theoretically attractive; however, it could not be shown to yield useful results in this analysis. Serologic HLA typing appears to provide an insufficient basis for applying epitope matching in clinical kidney transplantation.

Algorithms↗
PubMed1992

Effect of donor Langerhans cells on corneal graft rejection.

Unlike other cutaneous surfaces, the central portion of the corneal epithelium is typically devoid of Langerhans cells. The absence of Ia+ Langerhans cells in the central cornea is of more than casual interest and may explain the immunologic privilege that is characteristic of corneal allografts. The present communication summarizes previous studies that examined the role of corneal Langerhans cells in eliciting alloimmune responses and corneal graft rejection in rodents. Under normal circumstances, corneal allografts are poorly immunogenic when residing in the avascular ocular graft bed even though the graft displays large quantities of alloantigens. The afferent blockade of the immune response can be circumvented by donor-derived Langerhans cells that serve as potent immunogens for all categories of corneal allografts except grafts involving allodisparity only at class I major histocompatibility complex loci. Thus, the presence of donor-derived Langerhans cells exerts profound effects on the fate of corneal allografts.

Corneal Transplantation↗
PubMed2004

Haplotype associations of the MHC with psoriasis vulgaris in Chinese Hans.

Summary Haplotype associations of the major histocompatibility complex (MHC) with psoriasis vulgaris (PV) have been demonstrated in different racial or ethnic populations. The objective of this study was to demonstrate the different haplotype associations of the MHC in Chinese patients with psoriasis according to the type of onset and their sex. One hundred and thirty-eight patients with PV and 149 normal control subjects without psoriasis were typed for HLA-A, -B, -C, -DQA1, -DQB1 and -DRB1 by using the PCR with sequence-specific primers. The results showed: (i) HLA-A*26 (26.1% vs. 12.1%, Pc < 1 x 10(-5)), -B*27 (17.03% vs. 1.01%, Pc < 1 x 10(-7)), -Cw*0602 (15.58% vs. 5.03%, Pc < 1 x 10(-2)), -DQA1*0104 (19.93% vs. 9.40%, Pc < 1 x 10(-3)), -DQA1*0201 (22.40% vs. 10.74%, Pc < 1 x 10(-3)), -DQB1*0303 (18.12% vs. 9.73%, Pc < 1 x 10(-7)), and -DRB1*0701/02 (26.09% vs. 9.73%, Pc < 1 x 10(-7)) were significantly increased in PV patients, while HLA-B*57, -DQB1*0201 were slightly increased in PV patients. HLA-Cw*0304 (5.07% vs. 14.43%, Pc < 1 x 10(-3)), -DQA1*0501 (5.79% vs. 14.09%, Pc < 0.05) were found to be negatively associated with PV, but HLA-A*2 (2.54% vs. 6.38%, Pc < 0.5) was decreased in PV patients without statistical significance. (ii) HLA-A*26-B*27 [P < 0.0001, odds ratio (OR) = 48.38], -A*26-Cw*0602 (P < 0.0001, OR = 11.84), -B*27-Cw*0602 (P < 0.0001, OR = undefined), -DRB1*0701/02-B*27 (P < 0.0001, OR = 22.62), -DRB1*0701/02-DQA1*0104 (P < 0.0002, OR = 3.59), -DRB1*0701/02-DQB1*0303 (P < 0.0001, OR = 5.63), -DQA1*0201-DQB1*0303 (P < 0.0002, OR = 7.77), -A*26-B*27-Cw*0602 (P < 0.0004, OR = undefined), -A*26-DRB1*0701/02-DQA1*0201-DQB1*0303 (P < 0.01, OR = undefined) were identified as risk haplotypes for patients with PV in China. (iii) HLA-A*26 -B*27 (P < 0.0001, OR = 58.47), -DQA1*0201-DQB1*0303 (P < 0.0001, OR = 8.62), -DRB1*0701/02 -DQA1*0104 (P < 0.0002, OR = 4.13), -DRB1*0701/02-DQB1*0303 (P < 0.0001, OR = 6.68) and -A*26-DRB1*0701-DQA1*0201 -DQB1*0303 (P < 0.006, OR = undefined) were only significantly associated with type I psoriasis compared with controls, while others showed no differences in either type I or type II psoriasis. (iv) These associated haplotypes with PV were not different by sex, except that the frequency of DRB1*0701/02-DQB1*0303 (P < 0.0001, OR = 10.14) was higher in male patients with psoriasis. To summarize, this study demonstrated a differential association of HLA and identified some special risk haplotypes in Chinese patients with PV compared with other ethnic or racial populations.

Adolescent↗
PubMed1977

Human Ia-like antigens associated with HLA-d.

Antisera raised with HLA-A- and -B-compatible, HLA-D-disparate combinations were cytotoxic to B lymphocytes from the immunizing donor's HLA-D phenotype. Four antisera recognized structures closely associated with the HLA-D determinants Dw2, Dw3, Dw4, and LD 108. One antiserum had a broad reactivity pattern, including Dw3, Dw6, and some unknown specificity(ies). In population and family studies these B-lymphocyte antigens behaved as if they were governed by one genetic locus in the B-D region of the HLA complex. Furthermore, the antisera were cytotoxic to a minor concavalin-A-reactive T-cell subpopulation. The antisera had previously been shown to inhibit the stimulating cells in mixed lymphocyte culture and to be capable of inhibiting the Fc receptor in the EA rosette assay. We conclude that the antisera produced by this method recognize Ia-like antigens closely associated with the HLA-D determinants.

B-Lymphocytes↗
PubMed1975

Improved HL-A typing of cadaveric renal donors. I. Quantitation of HL-A gene dosage.

A quantitative microabsorption technique has been used to determine a gene dosage effect on HL-A. This allows homozygosity or heterozygosity of HL-A antigens to be determined prospectively in cadaver donors of renal allografts where less than four antigens were detected by standard lymphocytotoxicity. This in turn provides more precise matching of donor and recipient.

Cadaver↗
PubMed1976

Cell mediated lympholysis in man: an attempt to type with cytotoxic lymphocytes.

From approximately 3,000 CML combinations, originally established in order to evaluate the qualitative and quantitative influence of the serologically defined HLA-A, B, and C antigens on cellular, complement independent cytolysis, 12 combinations were selected yielding reproducible positive cytolysis on allogenic target cells, although no HLA-antigenic sharing could be demonstrated between stimulator and target lymphocytes. These 12 CytoToxic Lymphocytes (CTL's) have been tested in parallell as "CML typing combinations" against lymphocytes from a random population sample of 100 unrelated Danes. Based on a pairwise analysis 11 of these CTL's could be classified into two groups of significantly correlated CTL's. These two groups do not define monospecific traits of allelic genetic origin as judged by a mutually positive correlation and a poor fit to Hardy-Weinberg equilibrium. The traits defined by these groups may be either partially identical or governed by closely linked loci. The same groups were identified and the same conclusions reached after exclusion of those individuals in the population sample where HLA-A, B, C, or D antigens may be targets for destruction. Thus, this study gives direct evidence that known HLA antigens are not sole target determinants in CML or that cytotoxic lymphocytes recognize HLA molecules in a different way than lymphocytotoxic antibodies. The studies underline the immunogenetic complexity of CML although this reaction is most probably governed by genes in the HLA region. It is suggested that cytotoxic lymphocytes may recognize "backbone structures" of the HLA molecules.

Cytotoxicity Tests, Immunologic↗
PubMed1976

Second locus HL-A antigens and 4a or 4b.

A panel of over 100 individuals was tested against several 4a and 4b antisera. A 4a/4b type was assigned to each individual on the basis of overall reactions with each group of sera. It was felt that because 4a and 4b antisera rarely give identical reaction patterns the use of several sera in each group gave a better definition of the specificities. The relationship between each second locus HL-A specificity and 4a or 4b was assessed. Most of the "narrower" antigens showed complete inclusion within one group but there were some anomalies. Associations of these specificities were analysed further by absorption experiments. 4a and 4b antisera were able to define differences in some second locus specificities which were not picked up by the narrower antisera. It seems likely that 4a and 4b represent a separate public site on the HL-A gene product which is multifactorial. For a full description of the antigens all factors should be stated as there is not an invariant association between components.

Cytotoxicity Tests, Immunologic↗
PubMed1978

The genetic control of HLA-A and B antigens in somatic cell hybrids: requirement for beta2 microglobulin.

The lymphoblastoid cell line Daudi lacks both HLA-A and B antigens and beta2 microglobulin. Somatic cell hybrids derived from a fusion between this line and D98/AH--2 were shown to express four HLA antigens not detectable on either parent cell, A1, A10(Aw26), Bw16(Bw38, Bw17. The initial definition by direct cytotoxicity assay was confirmed by absorption of reactions against target T lymphocytes, thus avoiding problems due to contaminating Ia antibodies, and by blocking the reactions by pretreatment with a chicken anti-human beta2 microglobulin serum. That the new specificities were due to the Daudi HLA region was confirmed by the finding that interspecific hybrids between Daudi and A9L, containing a single human chromosome 6, expressed A10 and Bw17. This also defined the haplotypes of Daudi as A10(Aw26), Bw17 and A1, Bw16(Bw38). The re-expression of the Daudi HLA-A and B antigens in two independent sets of hybrids indicates that it does not carry a mutation in the HLA region. It has previously been reported that somatic cell hybrids with Daudi, which contain chromosome 15, do not express human beta2 microglobulin. These results suggest that the reason for the lack of HLA-A and B antigens on Daudi is a secondary effect due to the mutation(s) in the beta2 microglobulin gene.

Beta-Globulins↗