scholarly journals Class I and class II anti-hla antibodies after implantation of cryopreserved allograft material in pediatric patients

2000 ◽  
Vol 119 (2) ◽  
pp. 324-330 ◽  
Author(s):  
John A. Hawkins ◽  
John P. Breinholt ◽  
Linda M. Lambert ◽  
Thomas C. Fuller ◽  
Tracie Profaizer ◽  
...  
Keyword(s):  
Pediatric Patients ◽  
Class Ii ◽  
Class I ◽  
Hla Antibodies

Prevalence and Significance of Pre-Formed Anti-HLA Antibodies in Hematopoietic Stem Cell Transplant Recipients.

Blood ◽  
2009 ◽  
Vol 114 (22) ◽  
pp. 1174-1174
Author(s):  
Darshan Gautam Gandhi ◽  
Jennifer Holter ◽  
Mohamad Khawandanah ◽  
Robert B. Epstein ◽  
Julie Stoner ◽  
...  
Keyword(s):  
Stem Cell ◽  
Hematopoietic Stem Cell ◽  
Graft Failure ◽  
Hla Antigens ◽  
Class Ii ◽  
Class I ◽  
Hla Antibodies ◽  
Hematopoietic Stem ◽  
Post Transplant ◽  
Antibody Levels

Abstract Abstract 1174 Poster Board I-196 Introduction: The presence of sensitization to HLA antigens has been an important consideration in solid organ transplantation. It is considered a standard process to check for donor-specific allogeneic (allo) antibodies (DSA) and monitor formation of such antibodies post-transplant which could predict early and late graft failure. Most of the current data regarding the importance of anti-HLA (human leukocyte antigen) antibodies is available from renal transplant where presence of HLA antibodies is clearly associated with an increased risk of early graft loss up to the magnitude of 21%. It is routine to perform desensitization to alleviate these antibodies in an effort to enhance their chances of engraftment. The role of and approach to prior sensitization in the hematopoietic stem cell transplantation (HSC) setting is far less clear. This is of unique importance as a wider range of donor cell sources and transplant applications are utilized to treat hematologic diseases. Many of our patients have had multiple transfusions in the past, been pregnant or have had prior HLA mismatched allograft, all of which predispose to development of anti-HLA antibodies. Here we analyze the prevalence of Class I and Class II antibodies as a primary goal and also see if they correlate with graft survival. Methods: 52 patients were followed between July 2008 and July 2009 with hematologic malignancies including leukemia's, lymphoma's, multiple myeloma and others. 37/52 underwent transplantation of which 14 were unrelated donor (URD), 5 cord blood (CB) and 8 sibling (sib) transplants. Donors with corresponding HLA were excluded. Post-transplantation with day 100 antibody testing was performed in eligible patients. Antibody determination was done by testing the patients' sera with a panel of fluorescent beads coated with single HLA antigens using a solid-phase Luminex™ platform. Cut-point of 1500 [mean fluorescence intensity (MFI) ≥ 1500 defined as positive] was used for performing statistical analyses. The prevalence of positive antibody levels was compared among the transplant groups using a Fisher's exact test. Level of expression of antibodies was evaluated with MFI <500 considered negative, 500-1500 weak, 1500-3000 intermediate and >3000 strong. High resolution HLA typing was performed. Results: Class I antibodies were positive in 24 out of 52 total (46%) with 95% CI: 32% to 61%.14/37 (38%) who underwent transplantation (95% CI: 22% to 55%), 12/27 (44%) undergoing allo transplant, CB (20%), sib (38%), and URD (57%) were positive. The prevalence did not differ significantly among the transplant groups (p=0.3). Class II antibodies were positive in 8 out of 52 total (15%) with 95% CI: 7% to 28%. 5/37 (14%) who underwent transplantation (95% CI: 5% to 29%), 4/27 (15%) undergoing allo transplant, Sib (0%), CB (20%) and URD (21%) were positive. The prevalence did not differ significantly among the transplant groups (p=0.6). In females, 18/28 (64%) were positive for Class I or Class II antibodies of which 5/6 (83%) underwent URD transplants. Persistent antibody levels were detected in 3 of 4 patients tested at day 100 post transplant. Conclusions: Based on this limited pilot study we conclude that there is a high prevalence of anti-HLA antibodies present in recipients at the time of HSC transplantation. However detection of such antibodies did not jeopardize engraftment from various donor sources when HLA donor specific reactions are excluded. Bray et al showed higher incidence of graft failure associated with DSA. Takanashi et al showed that in CB transplants, antibodies were not significant unless the corresponding HLA was present in the CB unit. Based on these studies, we excluded donors with corresponding HLA. All but one patient, in whom donor specific anti-HLA antibodies were identified, achieved sustained marrow engraftment. The long term implications of antibody evolution and specificity to sustained marrow engraftment, graft vs. host and graft vs. tumor effects remain to be clarified. A larger prospective study will need to be conducted to definitely evaluate these relationships including our own which is currently under way. Disclosures: No relevant conflicts of interest to declare.

Clinical Experience of Transfusion of Plasma from HLA Immunized Donors

Blood ◽  
2008 ◽  
Vol 112 (11) ◽  
pp. 4317-4317
Author(s):  
Fleur M Aung ◽  
Benjamin Lichtiger
Keyword(s):  
Whole Blood ◽  
Blood Donors ◽  
Hla Class I ◽  
Class Ii ◽  
Hla Class Ii ◽  
Biologically Active ◽  
Class I ◽  
Antibody Testing ◽  
Hla Antibodies ◽  
Male Donor

Abstract Transfusion-related acute lung injury (TRALI) is a serious complication of plasma-containing blood components. Studies have implicated HLA antibodies along with biologically active lipids in stored blood in the pathogenesis of TRALI. We reviewed the HLA Antibody testing of our whole blood donors during a three month period who were tested for HLA Class I and HLA Class II antibodies by the DONORSCREEN-HLA Class I and Class II ELISA from GTI Diagnostics @ Waukesha, WI. The testing for HLA Antibodies in our donors was implemented as both HLA Class I and HLA Class II antibodies have been implicated in TRALI. The goal was to quarantine the plasma from these donors in order to reduce the exposure to patients to plasma from HLA Immunized Donors. Of 4056 whole blood donors, there were twenty-two donors of which 21 female and one male who tested positive for either HLA Class I or HLA Class II antibodies whose plasma was transfused. Of the twenty two donors, twenty one were females and one was male. Of the twenty one females, fifteen tested positive for HLA Class I antibodies and seven tested positive for HLA Class II antibodies. The single male donor tested positive for HLA Class II antibodies. The cause of the HLA immunization of these donors was unknown (as to whether they were caused by multiparity or blood transfusions). The plasma from the HLA Immunized female donors were transfused to ten female patients and eleven male patients. The plasma from the male donor was transfused to a male patient. All of the plasma from the HLA immunized donors was pooled with other plasma products in pools ranging from three to eight. All of the plasma products were irradiated and transfused via Fenwal Sepacell Reduction Filter for Red cells and all of the patients were premedicated prior to transfusion. One male and one female patient received plasma on two occasions from two donors both of whom were positive for HLA Class I antibodies. The twenty two patients consisted of four with hematological malignancies, one with a lymphoid malignancy and seventeen with malignancies of solid organs. Three of the patients had received an autologous transplant and one had received an allogeneic unrelated transplant. None of the patients had received IVIG therapy. The transfusions reactions reported for the three months of this review was also reviewed. None of the patient that received the HLA immunized plasma products was reported to have suffered a transfusion reaction. Although we did not meet our goal of reserving 100% of our plasma products from HLA immunized donors as recovered plasma, we discovered that the plasma products that were transfused from the HLA immunized donors were not associated with transfusion reactions in our patient population. The reason for not meeting our goal was the test results for the HLA Class I and HLA Class II antibodies were received after the plasma products were released for transfusion, due to logistical limitations in the performance of the testing. Although the number is small, we feel that the results may be significant in light of the current thinking of accepting only male donors for plasma products.

scholarly journals Prevalence and Risk Factors of Antibodies to Class I and II Human Leukocyte Antigens in Haploidentical Allograft Candidates: A Prospective Study on 3805 Subjects

Blood ◽  
2021 ◽  
Vol 138 (Supplement 1) ◽  
pp. 2880-2880
Author(s):  
Ning Ma ◽  
Lan-Ping Xu ◽  
Xiaohui Zhang ◽  
Yu Wang ◽  
Huan Chen ◽  
...  
Keyword(s):  
Risk Factors ◽  
Lymphoblastic Leukemia ◽  
Class Ii ◽  
Class I ◽  
Hla Antibodies ◽  
Hematological Diseases ◽  
Factors Associated ◽  
Elder Patients ◽  
Hla Dq ◽  
Main Factors

Abstract The aim of this study is to investigate the prevalence and risk factors of anti-human leukocyte antigen (HLA) antibodies in haploidentical candidates. This study was completed at Peking University People's Hospital, Beijing China. We performed a prospective analysis of patients with hematological diseases concerning the prevalence and risk factors of anti-HLA antibodies. Patients were enrolled between July 2015 - December 2019. Serum was collected for PRAs test within 1 month before haploidentical transplantation. The risk factors, such as age, sex, total transfusion, red blood cell (RBC) transfusion, platelet (PLT) transfusion, pregnancy, disease duration and diagnosis were collected. Univariate and multivariate logistic regression analyses were performed to evaluate the risk factors of anti-HLA antibodies. Six hundred and eighty (17.9%) patients were positive for panel reactive antibodies (PRA)-class I, 360 (9.5%) for class II, 768 (20.2%) class I or II, and 272 (7.1%) positive for class I and II both. Multivariate analysis indicated that female was related to higher risk of having PRAs for class I (P = 0.011), class I or II (P = 0.009), anti-HLA-A (P = 0.015), anti-HLA-DP (P = 0.048) and also for having higher mean fluorescence intensity (MFI) (2000 or more) of PRAs in class I (P = 0.020) and class I or II (P = 0.005). Compared to patients with myelodysplastic syndrome (MDS), patients with acute myeloid leukemia (AML), acute lymphoblastic leukemia (ALL), aplastic anemia (AA) had a lower incidence for PRAs in class I, class II, class I or II, class I and II, anti-HLA-A. anti-HLA-B, anti-HLA-C, anti-HLA-DQ, anti-HLA-DR, anti-HLA-DP (Table 1). Prior pregnancy was a risk factor for PRAs (P &lt; 0.001), and no previous pregnancy group having lower MFI of PRAs in class I (P = 0.001) and class I or II (P = 0.004). PLT transfusion (more than 4 times) rleted with a higher prevalence of PRAs (P &lt; 0.001), and also had a higher MFI of PRAs in class II (P &lt; 0.001), class I and II (P &lt; 0.001). Patients with RBC transfusion (more than 3 times) had a higher prevalence of PRAs in class I (P = 0.001), class II (P = 0.029), class I or II (P &lt; 0.001), anti-HLA-A (P = 0.001), anti-HLA-B (P &lt; 0.001), anti-HLA-C (P = 0.007), anti-HLA-DQ (P &lt; 0.001) and anti-HLA-DR (P = 0.011). In addition, diseases duration (8 months or more) was also associated with higher MFI of PRAs in class I (P = 0.023) and class I or II (P = 0.004). Subgroup analysis showed that 11.7% of pediatric patients were positive for PRAs in class I; 19.2% of adults, 17.9% of elder patients; 12.4% of males; 26.1% of females; 21.0% of patients with AML; 10.5% of patients with acute lymphoblastic leukemia (ALL); 18.9% of patients with AA; 30.3% of patients with MDS; 16.6% of patients with other hematological diseases. The positive rate of class II PRAs in children was 4.3%; 11.1% for adults; 9.5% for elder patients; 5.5% for males; 15.4% for females; 11.4% for patients with AML; 5.2% for patients with ALL; 10.3% for patients with AA; 17.2% for patients with MDS; 6.6% of patients with other hematological diseases. Multivariate analysis showed that, in children, PLT transfusion and diagnosis were the two main risk factors of PRAs in class I and class II (P &lt; 0.001, P = 0.017). In adults, diagnosis (P = 0.003), transfusion (P &lt; 0.001) and pregnancy (P &lt; 0.001) were the three main factors associated with PRAs in class I and transfusion (P &lt; 0.001) and pregnancy (P &lt; 0.001) were the two main factors associated with PRAs in class II. In males, PLT transfusion (P &lt; 0.001) and diagnosis (P &lt; 0.001) were the two main factors associated with PRAs in class I and class II. In ALL subgroup, gender (P = 0.026, P = 0.048), pregnancy (P &lt; 0.001) and transfusion (P &lt; 0.001) were the three main factors associated with PRAs in class I and II. In AA subgroup, gender (P = 0.004) and PLT transfusion (P &lt; 0.001) were risk factors for class I PRAs, pregnancy (P = 0.008) and PLT transfusion (P = 0.003) were risk factors for class II PRAs. In elder patients, females, AML, MDS and other diseases subgroup, transfusion and pregnancy were the two main factors associated with PRAs in class I and class II. Our results indicated that female sex, diagnosis, pregnancy, transfusion, disease duration were independent risk factors of anti-HLA antibodies in haploidentical allograft candidates, which provided evidence for best haploidentical donor selection. The risk factors of anti-HLA antibodies were different among total patients and those of cases in different subgroups. Figure 1 Figure 1. Disclosures No relevant conflicts of interest to declare.

Alloimmunization To HLA Class I Antigens But Not H-Y Antigens Is Associated With Transfusion In Children With Sickle Cell Disease

Blood ◽  
2013 ◽  
Vol 122 (21) ◽  
pp. 39-39
Author(s):  
Robert S. Nickel ◽  
Jeanne E. Hendrickson ◽  
Leslie S. Kean ◽  
Marianne E. McPherson Yee ◽  
Robert A. Bray ◽  
...  
Keyword(s):  
Sickle Cell Disease ◽  
Sickle Cell ◽  
Graft Rejection ◽  
Hla Class I ◽  
Class Ii ◽  
Class I ◽  
Igg Antibodies ◽  
Cell Disease ◽  
Hla Antibodies ◽  
Rbc Transfusion

Abstract Introduction Patients with sickle cell disease (SCD) are at high risk for graft rejection after hematopoietic stem cell transplant (HSCT) especially when using reduced intensity conditioning (RIC). Alloimmunization from red blood cell (RBC) transfusions, critical to the management of SCD, may predispose these patients to HSCT rejection. Alloimmunization to major or minor histocompatibility antigens (mHA) may occur after RBC transfusion due to residual white blood cells or platelets present in RBC units even after leukoreduction. In mice, despite extensive leukoreduction, RBC transfusions caused alloimmunization and subsequent HSCT rejection after RIC. We conducted a cross-sectional study to determine if RBC transfusions are associated with alloantibody formation to human leukocyte antigens (HLA) and mHA, the target of the host versus graft rejection in HLA-identical transplantation. For mHA, we assessed immunity to H-Y antigens, mHA encoded on the Y chromosome. We have previously demonstrated the importance of H-Y antibodies in a variety of settings including chronic graft versus host disease (in male recipients of female grafts) and rejection of renal transplants (in female recipients of male grafts). Methods We enrolled 114 nulliparous pediatric SCD (SS or Sβ0) patients: 58 females on chronic transfusion, 32 males on chronic transfusion, and 24 females who had never been transfused. Serum was evaluated for HLA antibodies using the FlowPRA® (panel reactive antibody) screening test which detects IgG antibodies to the majority of HLA class I and II antigens. Serum was also tested for IgG antibodies against 5 H-Y antigens (DDX3Y [DBY], EIF1AY, RPS4Y1, UTY, ZFY) using protein microarray technology with each H-Y-seropositive threshold determined as a microarray mean fluorescence intensity (MFI) > the median MFI + 2.5 quartiles measured in 60 adult healthy males. Results Chronically transfused patients had a higher prevalence of HLA class I antibodies than never transfused patients (33.3% vs. 12.5%, p=0.074). This increased prevalence of HLA class I antibodies in the chronic transfusion group was significant when examining the number of patients who tested positive to more than 25% of the panel (17.8% vs. 0%, p=0.022). Few patients had detectable HLA class II antibodies with no significant differences between chronically transfused and non-transfused patients. Few SCD patients had detectable H-Y alloantibodies with no significant differences in chronically transfused females, chronically transfused males, and non-transfused females. Conclusions Leukocyte-reduced RBC transfusions appear to engender immunization to class I HLA but not class II HLA or H-Y antigens in pediatric SCD patients. Since hematopoietic progenitor cells express class I HLA, transfusion-related immunity to these antigens could pose a barrier to engraftment in HLA-disparate transplants. Since these antigens are also expressed on platelets, class I HLA antibodies in SCD could have important implications for platelet transfusion support during HSCT. While RBC transfusion does not appear to be an adequate stimulus for H-Y alloantibody formation, it is possible that exposure to mHA during transfusion could cause a cellular rather than a humoral immune response that may contribute to future HSCT graft rejection. Our result that few (6%) nulliparous female children with SCD had detectable H-Y alloantibodies is also a significant finding considering that 19-41% of healthy adult females had antibodies to at least one H-Y antigen in previous studies. Finally our finding that 25% of never transfused children with SCD had a positive HLA PRA is unexpected for an “unsensitized” group; its significance is being further investigated. Disclosures: No relevant conflicts of interest to declare.

scholarly journals Donor-specific antibodies development in renal living-donor receptors: Effect of a single cohort

2021 ◽  
Vol 35 ◽  
pp. 205873842110005
Author(s):  
Jorge Andrade-Sierra ◽  
Alfonso M Cueto-Manzano ◽  
Enrique Rojas-Campos ◽  
Ernesto Cardona-Muñoz ◽  
José I Cerrillos-Gutiérrez ◽  
...  
Keyword(s):  
T Cell ◽  
Living Donor ◽  
Class Ii ◽  
Class I ◽  
Steroid Withdrawal ◽  
Control Cohort ◽  
Hla Antibodies ◽  
Donor Specific Antibodies ◽  
The Relationship

Minimization in immunosuppression could contribute to the appearance the donor-specific HLA antibodies (DSA) and graft failure. The objective was to compare the incidence of DSA in renal transplantation (RT) in recipients with immunosuppression with and without steroids. A prospective cohort from March 1st, 2013 to March 1st, 2014 and follow-up (1 year), ended in March 2015, was performed in living donor renal transplant (LDRT) recipients with immunosuppression and early steroid withdrawal (ESW) and compared with a control cohort (CC) of patients with steroid-sustained immunosuppression. All patients were negative cross-matched and for DSA pre-transplant. The regression model was used to associate the development of DSA antibodies and acute rejection (AR) in subjects with immunosuppressive regimens with and without steroids. Seventy-seven patients were included (30 ESW and 47 CC). The positivity of DSA class I (13% vs 2%; P < 0.05) and class II (17% vs 4%, P = 0.06) antibodies were higher in ESW versus CC. The ESW tended to predict DSA class II (RR 5.7; CI (0.93–34.5, P = 0.06). T-cell mediated rejection presented in 80% of patients with DSA class I ( P = 0.07), and 86% with DSA II ( P = 0.03), and was associated with DSA class II, (RR 7.23; CI (1.2–44), P = 0.03). ESW could favor the positivity of DSA. A most strictly monitoring the DSA is necessary for the early stages of the transplant to clarify the relationship between T-cell mediated rejection and DSA.

Monitoring for HLA Antibodies in Cord Blood Transplantation.

Blood ◽  
2007 ◽  
Vol 110 (11) ◽  
pp. 2031-2031
Author(s):  
Jonathan A. Gutman ◽  
Susan K. McKinney ◽  
Sandra L. Warnock ◽  
Anajane Smith ◽  
Ann E. Woolfrey ◽  
...  
Keyword(s):  
Cord Blood ◽  
Graft Rejection ◽  
Cord Blood Transplantation ◽  
Hla Antigens ◽  
Class Ii ◽  
Class I ◽  
Antibody Specificity ◽  
Hla Antigen ◽  
Hla Antibodies ◽  
Blood Transplantation

Abstract Though graft rejection in hematopoietic cell transplantation (HCT) is presumed to be mediated primarily by host anti-donor T cells and natural killer cells, host antibodies which generate antibody dependent cellular cytotoxic reactions to donor antigens may also contribute. For patients undergoing HCT with a cord blood graft which is usually markedly mismatched to the recipient, alloimmunization is a potential significant issue. Cross-matching is not able to be performed secondary to limited cell numbers available from a cord blood graft. Delayed hematopoietic recovery and graft failure are known complications of cord blood transplantation (CBT), and though likely related primarily to small graft size and presence of primarily naïve immune cells in a cord blood graft, HLA antibodies may also contribute. At our center, we investigate recipient alloimmunity in all patients undergoing CBT to guide donor selection. Patients are first screened for the presence of antibodies against HLA antigens using an ELISA-based assay in which patient serum is tested against pools of purified class I and class II HLA antigens bound in wells of a plastic microtiter plate. Serum from patients noted to have evidence of HLA antibodies prompts further testing to identify the specific HLA antibodies using panels of color coded plastic microspheres each coated with a single purified class I or class II HLA antigen. To date, 4 of 29 patients screened have had evidence of HLA alloimmunization. Further investigation of antibody specificity in one patient undergoing double unit CBT demonstrated antibodies to HLA-Bw6, an epitope known to be present on one of the donor units. Because no other donors were available, the unit was used. Following a reduced intensity preparative regimen (RIT), the patient engrafted neutrophils on day 24 and platelets on day 42. However, the HLA-Bw6 positive unit was absent on all chimerism studies (beginning day 21 post transplantation). Three other patients with HLA alloimmunization did not have identifiable antibody specificity directed against mismatched HLA antigens, and engrafted neutrophils on days 25, 29, 25 and platelets on days 29, 41, and 102 respectively. To our knowledge, we are the first to report monitoring for alloimmunization in CBT and the first to describe the outcome of grafting a cord blood unit known to be HLA antibody incompatible with the patient. When patients undergo double unit CBT, cells from both units can generally be detected in the blood of the recipient during the first month, especially following RIT conditioning, but one unit eventually and consistently prevails (though predictive factors for the winning unit have not yet been satisfactorily described). In this case the compatible unit prevailed and there was no evidence at day 21 of cells from the antibody incompatible unit. Although we cannot attribute cause and effect to the anti-Bw6 alloantibody, it is interesting to note that all seven other patients transplanted on the same RIT protocol have demonstrated at least minimal bone marrow contributions to chimerism from both units at day 28. Hence, alloimmunization may be an important factor influencing graft rejection in CBT. CBT patients should likely be screened for HLA antibodies, and positive screenings warrant further investigation to avoid whenever possible donor/recipient mismatches against which the patient is sensitized. Ongoing monitoring will help clarify the clinical significance of this issue.

HLA Class I and HLA Class II Antibodies in Whole Blood Donors and a Lookback on Recipients of Their Blood Components.

Blood ◽  
2008 ◽  
Vol 112 (11) ◽  
pp. 3281-3281
Author(s):  
Fleur M Aung ◽  
Aida Narvios ◽  
Benjamin Lichtiger
Keyword(s):  
Whole Blood ◽  
Blood Donors ◽  
Hla Class I ◽  
Class Ii ◽  
Hla Class Ii ◽  
Class I ◽  
Blood Components ◽  
Hla Antibodies ◽  
Packed Rbcs ◽  
Transfusion Reactions

Abstract Introduction : Transfusion-related acute lung injury (TRALI) in recent years has become the leading cause of transfusion associated mortality. All transfusable blood components (and rarely IVIG) have been implicated in TRALI. However, plasma and single donor platelet products amount for the majority of cases. (Blood Products Advisory Committee 89th Meeting - April 27, 2007) Although the mechanism of pathogenesis is not fully known, 45 % to 60% of cases are reported to be associated with Neutrophil-Specific Antibodies (NSA) found in the donor. Less commonly, antibodies to HLA Class I and HLA Class II antigens have been implicated. Pregnancy is known to result in development of Leucocyte antibodies and HLA antibodies. (Transfusion1999; 39:103–6) For this reason, screening of blood donors for HLA antibodies and reduced use of female donors for the production of blood components containing large plasma volumes and the exclusion of multiparous women are options to prevent TRALI. (Vox Sang 2006; 91 (Suppl 3):227) Material and Methods : At our institution, a three month (May to July 2008) retrospective review was conducted on all whole blood donors screened by the ELISA test (DONORSCREEN-HLA Class I and Class II by GTI Diagnostics @ Waukesha, WI) performed on the Quick Biotest machine. The OD for the donors as well as the cut offs were reviewed for each run. A total number of 4056 whole blood donations collected at our blood center were tested for HLA Class I and HLA Class II antibodies by this method. The Whole Blood Donors met the criteria established by AABB and FDA standards. A look back was conducted on the final disposition of the components prepared from the donors that tested positive for either HLA Class I or HLA Class II antibodies or both HLA Class I and HLA Class II antibodies. We relied on existing reporting systems in place in our institution for reporting of transfusion reaction. Results : Of the 4056 whole blood donors there were tested, 231 (5.84%) donors of which 231 (97.47%) females and 6 (2.53%) males tested positive for HLA Class I antibodies and 198 (4.93%) donors tested positive for HLA Class II antibodies of which 186 (93.94%) were females and 14 (7.07%) were males. A total number of 52 (1.28%) donors tested positive for both HLA Class I and HLA Class II antibodies of which 51 (1.26%) were females and only 1 (0.02%) was male. From the HLA Class I positive donors, 217 packed RBCs, 176 platelets and 14 plasma components were transfused. From the HLA Class II positive donors, 183 packed RBCs, 153 platelets and 11 plasma components were transfused. All of the components were irradiated. The packed RBCs and plasma were transfused via Fenwal Sepacell Leukocyte Reduction Filters. The platelets were pooled and transfused via Fenwal Sepacell PLS-10A Leukocyte Reduction Y Administration Set. The platelets were issued for transfusion within two days of donation in most instances. The patients who received plasma from the HLA positive donors did not receive IVIG treatment. The plasma that was processed from these whole blood donors that tested positive for either HLA Class I or HLA Class II antibodies were pooled with other plasma products from other whole blood donors. There were no transfusion reactions attributable to TRALI that were reported in any of the patients that received packed RBCs, platelets or plasma from these donors. There were 48 transfusion reactions reported for the same period of time that this review was conducted. All of the reported transfusion reactions were also reviewed. There were no reported cases of transfusion reactions or clinical symptoms attributable to TRALI in any of the patients that received components processed from these donors or in the patients that had reported transfusion reactions. The patients at our institution may not reflect the general patient population of other institutions, as most of our patients are immunosuppressed. This retrospective review was conducted to correlate the reported transfusion reactions with components that were transfused from HLA immunized donors. The presence of antibodies to HLA Class I or HLA Class II may not reflect the incidence of TRALI in cancer patients.

Class I and II HLA antibodies in pediatric patients with thalassemia major

Transfusion ◽  
2015 ◽  
Vol 56 (4) ◽  
pp. 878-884 ◽  
Author(s):  
Marianne E. McPherson Yee ◽  
Ankoor Shah ◽  
Alan R. Anderson ◽  
Jeanne Boudreaux ◽  
Robert A. Bray ◽  
...  
Keyword(s):  
Pediatric Patients ◽  
Thalassemia Major ◽  
Class I ◽  
Hla Antibodies

Electron microscopy analysis of degenerating pancreatic ß cells in transgenic mice expressing the MHC Class I antigen Dd

1990 ◽  
Vol 48 (3) ◽  
pp. 548-549
Author(s):  
T. A. Stewart ◽  
D. Liggitt ◽  
S. Pitts ◽  
L. Martin ◽  
M. Siegel ◽  
...  
Keyword(s):  
Type I Diabetes ◽  
Disease Process ◽  
Class Ii ◽  
Class I ◽  
Type I ◽  
Aberrant Expression ◽  
Mhc Molecules ◽  
Endogenous Insulin ◽  
Class Ii Mhc ◽  
Ifn Γ

Insulin-dependant (Type I) diabetes mellitus (IDDM) is a metabolic disorder resulting from the lack of endogenous insulin secretion. The disease is thought to result from the autoimmune mediated destruction of the insulin producing ß cells within the islets of Langerhans. The disease process is probably triggered by environmental agents, e.g. virus or chemical toxins on a background of genetic susceptibility associated with particular alleles within the major histocompatiblity complex (MHC). The relation between IDDM and the MHC locus has been reinforced by the demonstration of both class I and class II MHC proteins on the surface of ß cells from newly diagnosed patients as well as mounting evidence that IDDM has an autoimmune pathogenesis. In 1984, a series of observations were used to advance a hypothesis, in which it was suggested that aberrant expression of class II MHC molecules, perhaps induced by gamma-interferon (IFN γ) could present self antigens and initiate an autoimmune disease. We have tested some aspects of this model and demonstrated that expression of IFN γ by pancreatic ß cells can initiate an inflammatory destruction of both the islets and pancreas and does lead to IDDM.

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