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PubMed1985

Successful renal transplantation of patients sensitized following deliberate unrelated blood transfusions.

One of the most powerful influences on cadaveric renal graft survival is the enhancing effect of blood transfusions from unrelated individuals (1, 2). However, the optimum number of transfusions required to achieve this effect remains controversial. Enhanced graft survival following only one or two transfusions has been observed (3), although graft survival has also been found to be better for multitransfused recipients (4). Extrapolating from their studies on mice, Wood et al. (5) suggested that only a very small volume of blood may induce the transfusion effect in humans. As the number of transfusions increases so does the risk of sensitizing the patient to produce lymphocytotoxic antibodies that may impair the chances of the patient receiving a crossmatch-negative kidney graft (6, 7). Thus the problem is to minimize the chance of sensitization while still maintaining the beneficial effect of blood transfusion.

Adolescent↗
PubMed1996

No advantage of flow cytometry crossmatch over complement-dependent cytotoxicity in immunologically well-documented renal allograft recipients.

The effect of flow cytometry crossmatches on clinical outcome was studied retrospectively in two groups of immunologically well-documented patients who had received transplants with a negative complement-dependent cytotoxicity crossmatch. The first group consisted of 114 consecutive renal allograft recipients, and the second group consisted of 76 immunologically at-risk recipients. Flow cytometry crossmatches were performed with current and historic sera. In group 1, positive flow cytometry (FC) crossmatches were shown in 15/114 (13%) recipients. Rejection occurred in 8/15 (53%) FC-positive versus 41/99 (41%) FC-negative recipients. The 1-year graft survival rate was 80% for FC-positive patients and 87% for FC-negative patients. Sixty-seven patients were nonsensitized patients; 4 of them had a positive FC crossmatch but no rejection episodes, graft loss, or patient loss. Of 47 retransplanted and/or sensitized recipients, 11 had a positive FC crossmatch. Rejection treatment was needed in 8/11 (73%) FC-positive patients compared with 19/36 (53%) FC-negative patients. Their 1-year graft survival rates were 73% and 81%. None of these differences reached statistical significance. Group 2 consisted of 76 at-risk recipients; 37 were retransplant patients and 39 were sensitized first-transplant patients. Twenty-one (28%) patients showed a positive FC crossmatch. Rejection episodes did not differ between the FC-positive (48%) and FC-negative patients (46%). There was no difference in 1-year graft survival rate (76% vs. 80%) or in 1-year patient survival rate (100% vs. 95%). We conclude that FC crossmatches in our patient group are not superior to the classical complement-dependent cytotoxicity crossmatches with regard to clinical outcome. On the contrary, transplantation with a mandatory negative FC crossmatch would have excluded 28% of the recipients from transplantation, who in fact are doing well.

Adult↗
PubMed1997

New strategies for early diagnosis of heart allograft rejection.

BACKGROUND: Allograft rejection is mediated by T cells that recognize allogeneic major histocompatibility complex (MHC) molecules via the direct and indirect pathway. The direct pathway involves T cells that react against MHC/peptide complexes expressed on the surface of donor antigen-presenting cells (APCs). In contrast, T cells involved in the indirect pathway recognize peptides derived from processing and presentation of allogeneic MHC molecules by self (recipient) APCs. To explore the relative contribution of these two pathways to rejection, we have evaluated the response of peripheral blood T cells from 50 heart transplant recipients against donor APCs (direct recognition) and against self APCs pulsed with synthetic peptides corresponding to the hypervariable region of the mismatched HLA-DR antigens of the donor (indirect recognition). METHODS: T cell reactivity against donor APCs was quantitated by measuring the expression of CD69 on allostimulated CD3+ LDA1+ cells. Reactivity to synthetic allopeptides was determined in limited dilution assays. RESULTS: Serial studies of the kinetics of direct and indirect recognition showed that both pathways contribute to early acute rejection episodes. Primary rejection was accompanied invariably by indirect recognition of a dominant allopeptide. Intermolecular spreading of T cell epitopes was observed during recurrent rejections. Enhanced recognition of donor alloantigens via the direct pathway was found predominantly during early rejection episodes. A single form of allorecognition was shown to occur in some rejection episodes. CONCLUSIONS: Monitoring of the direct and indirect pathway of allorecognition provides a reliable method for prediction and differential diagnosis of acute rejection of heart allografts.

Antigen-Presenting Cells↗
PubMed1999

Influence of the additional injection of host-type bone marrow on the immune tolerance of minor antigen-mismatched chimeras: possible involvement of double-negative (natural killer) T cells.

BACKGROUND: It has previously been demonstrated that adding T cell-depleted (TCD) host bone marrow (BM) to an MHC-mismatched BM inoculum allows for induction of long-term stable chimeras without graft-versus-host disease (GVHD) even when non-TCD allogeneic BM was used. AIMS: The present study was undertaken to investigate immune tolerance mechanisms in minor antigen-mismatched allogeneic BM chimeras when host-type BM was added to the BM inoculum. METHODS: C3H (H2k, Thy 1.2, Mls 2a) recipients were conditioned with 9.5 gray (Gy) of total body irradiation. To exclude any interference with possible subclinical GVHD, 5x10(6) TCD AKR (H2k, Thy 1.1, Mls 1a) BM cells were injected with (syn + allo) or without (allo) 5x 10(6) TCD C3H BM cells. Chimerism, clonal deletion, and T lymphocyte subsets were scored using FACS and anti-mouse Thy, Vbeta6, Vbeta3, CD3, CD4, or CD8 monoclonal antibodies. The stability of tolerance was studied by investigating mixed lymphocyte reaction and cytotoxic T cell induction in chimeras after immunization with host, donor, or third-party (BALB/c) splenocytes. Breaking of chimerism was attempted by injecting nontolerant 40x10(6) host-type splenocytes 2 months after BM transplantation. Cytokines and Valpha14 mRNA were assayed using real time quantitative reverse transcriptase-polymerase chain reaction at 4 and 48 hr, respectively, after injection of nontolerant host-type splenocytes. RESULTS: Both groups of mice became long-term stable mixed chimeras without any clinical sign of GVHD. Neither group was able to produce antihost nor antidonor cytotoxic T cells, even after immunization. The addition of syngeneic BM to the allogeneic inoculum reduced the overall level of allogeneic chimerism (from approximately 70% or approximately 85% in peripheral blood lymphocytes and spleen, respectively, in allo chimeras versus approximately 35% and approximately 60% in syn + allo chimeras). Moreover, it resulted in complete clonal deletion of both host-reactive (Vbeta3) and donor-reactive (Vbeta6) lymphocytes in syn + allo chimeras in contrast to in allo chimeras, in which only donor-reactive lymphocytes were completely deleted. After nontolerant C3H splenocyte injection, high levels of interleukin 2 mRNA were produced and chimerism decreased in syn + allo chimeras. In contrast, in allo chimeras, this maneuver was followed by the production of higher levels of interleukin 4 and interferon-gamma, and of Valpha14 mRNA, as well as by the proliferation of CD3+CD4-CD8- (double-negative) T cells and by an increase of donor chimerism. CONCLUSION: The addition of host-type BM to the allogeneic inoculum has an influence on the level of chimerism, the extent of clonal deletion, and the reaction of chimeras after the injection of nontolerant host-type splenocytes. In the latter phenomenon, cytokine production and proliferation of Valpha14+ CD3+CD4-CD8- (double-negative, natural killer T) lymphocytes may be involved.

Animals↗
PubMed2006

A sensitive and rapid alternative to HLA typing as a genetic screening test for abacavir hypersensitivity syndrome.

BACKGROUND: Abacavir hypersensitivity reaction (ABC HSR) is a potentially life-threatening adverse reaction that affects approximately 8% of patients that initiate this antiretroviral drug. Independent groups have shown a strong predictive association between ABC HSR and HLA-B*5701, indicating that exclusion of HLA-B*5701 positive individuals from abacavir treatment would largely prevent ABC HSR. However, the limited availability and relatively high cost of human leukocyte antigen (HLA) typing represent barriers to the widespread implementation of this pharmacogenetic approach to abacavir prescribing. To facilitate routine screening, we have developed a rapid flow cytometry method for HLA-B57 phenotyping using commercially available B17 monoclonal antibodies. METHODS: Whole blood samples from 84 human immunodeficiency virus (HIV) patients were examined by standard flow cytometry methods, using a two-colour B17-specific immunofluorescence assay in the CD45 lymphocyte population. RESULTS: All eight HLA-B57 individuals examined tested positive, while HLA-B57/58 negative individuals (n=74) tested negative for this flow cytometry test. Two non-HLA-B57 individuals showed weak cross-reactivity. CONCLUSION: In our predominantly Caucasian population, B17/CD45 dual staining was sufficient to identify individuals carrying B17 cell surface antigens. This approach, utilizing flow cytometry methods that are widely available in HIV laboratories, therefore offers a sensitive, rapid and cost-effective screening assay prior to abacavir prescription. Following risk stratification with this assay, it would be anticipated that identification of HLA-B*5701 using molecular HLA typing methods would be required in <10% of the screened population.

Alleles↗
PubMed1975

Agglutinability of cattle red cells. 3. Conglutination.

Addition of both complement and conglutinin was necessary to conglutinate the cattle red cells (CRC) when they were sensitized by different blood typing reagents. Although the degree of conglutinability of the CRC was influenced by the particular blood factor-reagent combination the average conglutinability (i.e. average titre scores) of CRC from different MZ pairs varied from 1.9 to 16.2. The titres of complement varied from zero to 1:32, while the titres of conglutinin ranged from 1:8 to 1:1024 in the different sera from MZ cattle twins. The variance due to differences in the titre scores between MZ pairs was 82.2% for conglutinin and 68.3% for complement. There was no evident association between the titres of conglutinin and complement.

Adsorption↗
PubMed1975

HL-A phenotyping in an Indonesian population.

The frequencies of 30 HL-A antigens were studied in an Indonesian population of 95 individuals from the city of Jakarta. The antigens HL-A9, or more precisely W24, and HL-A11 (first series) and W15 (second series) occurred with high frequencies, whereas HL-A8, W14 and W22 were completely absent. These results are consistent with previous reports of HL-A typing in South East Asian populations.

Complement Fixation Tests↗
PubMed1977

Serological identification of five HLA-D associated (Ia-like) determinants.

Five antisera raised within HLA-A and -B compatible, HLA-D disparate combinations were reactive in a modified NIH microcytotoxicity test with B lymphocytes, but not with T lymphocytes from the immunizing donor, as well as with B lymphocytes from most or all donors sharing his immunizing HLA-D phenotype. Four antisera recognized structures closely associated with the HLA-D determinants Dw2, Dw3, Dw4 and LD 108. One serum 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. We conclude that the antisera produced by this method recognize Ia-like antigens identical to or very closely associated with the HLA-D determinants.

B-Lymphocytes↗
PubMed1979

The comparison between normal and Epstein-Barr virus-transformed homozygous typing cells and their use for MLC, PLT and serological detection of human Ia-type alloantigens.

Normal human lymphocytes isolated from freshly drawn blood were repeatedly stimulated (up to five times) in mixed lymphocyte cultures (MLC) with five different Epstein-Barr virus (EBV)-transformed homozygous typing cells (HTC-LCL). Each time, the same WDW-specificity was used for the restimulation. The first and the second stimulations resulted in an 2.4- to 3.1-fold increase of the original responder cell number. But after the third, fourth and fifth stimulation decreasing amounts of specifically primed lymphocytes were recovered. Primed lymphocyte typing (PLT) showed significant differences in the intensity of the stimulation depending on whether homozygous typing cells (HTC) or HTC-LCL were used as stimulators. Except for one cell type, the PLT-response was significantly stronger with HTC-LCL than with HTC. The time needed to reach the maximal PLT-response got shorter and shorter the more often the cells were reprimed by the same stimulator cell. Further differences between HTC and HTC-LCL were observed in the complement-dependent cytotoxicity assay: HTC-LCL were more sensitive towards rabbit complement and they showed an enhanced binding of anti-Ia-alloantibodies but HTC reacted more specifically with the antibodies.

B-Lymphocytes↗
PubMed1985

HLA typing of Epstein-Barr virus transformed lymphoblastoid cell lines (LCL).

The application of standard tissue typing techniques to cells other than peripheral blood lymphocytes has been accompanied by the problem of extra reactions. This applies as well to Epstein-Barr virus transformed lymphoblastoid cell lines (LCL) as to leukemic cells and human spleen cells. These extra reactions are attributable to additional antibodies in the typing sera which are not apparent under standard conditions with PBLs. Two types are described: Type 1 extras, which becomes apparent after longer incubation times and are attributed to weak antibodies and type 2 extras which are apparent after shorter incubation times and are attributed to subpopulation specific or differentiation antigens. Technical modifications are proposed by which these extras can be circumvented. They include: Only start typing when cells have been cultured for 2 to 3 days. Remove dead cells by spinning over standard ficoll-hypaque or 11% triosil. Use shorter incubation times. Avoid using sera that give too many type 2 extras. In this way phenotypes can be accurately identified on LCL's obtained from kidney transplant donors and recipients. When LCL's were compared with their matching PBL, HLA phenotypes were concordant in 87% of cases for HLA-A, 90% for HLA-B, 81% for HLA-C and 70% for HLA-DR.

Cell Line↗
PubMed1996

Sequenase sequence profiles used for HLA-DPB1 sequencing-based typing.

Sequencing-based HLA typing (SBT) is a PCR based high resolution HLA typing method in which polymorphic regions of the gene are sequenced and directly used for typing. Currently, for class II SBT, alleles are identified by comparison of the exon 2 sequence with their corresponding allele sequence library. Routine SBT requires reliable identification of heterozygosity, and automated assignment of the alleles. In sequencing strategies different enzymes can be used for primer extension. The most characteristic difference between sequences obtained by two protocols using Sequenaseregistered, or Taq-cycle sequencing, respectively, is a difference in incorporation of nucleotides in the primer extension leading to different sequence profiles. In Taq-cycling sequencing variable nucleotide incorporation results in irregular, but reproducible peak patterns, whereas Sequenase incorporates nucleotides in nearly equal amounts, resulting in more even peak patterns. In a previously published multi-center study we evaluated HLA-DPB1 SBT using Taq-cycle sequencing, and showed that typing can reliably be performed, considering the specific sequence profiles. In this study the applicability of Sequenase for HLA-DPB1 SBT was tested. A panel of samples were typed by SBT at five test sites which participate in the Sequencing Based Typing component of the 12th International Histocompatibility Workshop. The panel represents the existing polymorphism at all known polymorphic positions of exon 2, both in homozygous and heterozygous combinations. The assignment of homozygosity and heterozygosity was validated by Multi-Sequence Analysis, performing cluster analysis of chromatographic data of all sequences at each position. Sequence characteristics were examined and considered for appropriate assignment. Data reveals that Sequenase sequencing can also reliably be used for HLA-DPB1 typing.

Bacteriophage T7↗
PubMed1975

Differences in the immunogenicity of the HL-A antigens.

Comparing the expected and observed HL-A antibody forming in condition of fetomaternal immunization in 184 pregnant women, some differences in the immunogenic strength of HL-A antigens were investigated. The HL-A antigens were graded in three groups in accordance with their coefficient of immunogenicity as follows: in first group, with a coefficient more than 50 are HL-A2, HL-A7, HL-A5, W22, HL-A13, W27 and W10; in second group, with a coefficient from 25 to 50 are HL-A1, W24, HL-A11, W5, W14 and HL-A12; and in the third group, with a coefficient less than 25 are HL-A3, W25 and HL-A8. The data about the other HL-A antigens are not significant.

Antibody Formation↗