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Piemonti L.,San Raffaele Scientific Institute | Everly M.J.,Terasaki Foundation Laboratory | Maffi P.,San Raffaele Scientific Institute | Scavini M.,San Raffaele Scientific Institute | And 15 more authors.
Diabetes | Year: 2013

Long-term clinical outcome of islet transplantation is hampered by the rejection and recurrence of autoimmunity. Accurate monitoring may allow for early detection and treatment of these potentially compromising immune events. Islet transplant outcome was analyzed in 59 consecutive pancreatic islet recipients in whom baseline and de novo posttransplant autoantibodies (GAD antibody, insulinoma-associated protein 2 antigen, zinc transporter type 8 antigen) and donor-specific alloantibodies (DSA) were quantified. Thirty-nine recipients (66%) showed DSA or autoantibody increases (de novo expression or titer increase) after islet transplantation. Recipients who had a posttransplant antibody increase showed similar initial performance but significantly lower graft survival than patients without an increase (islet autoantibodies P < 0.001, DSA P < 0.001). Posttransplant DSA or autoantibody increases were associated with HLA-DR mismatches (P = 0.008), induction with antithymocyte globulin (P = 0.0001), and pretransplant panel reactive alloantibody >15% in either class I or class II (P = 0.024) as independent risk factors and with rapamycin as protective (P = 0.006) against antibody increases. DSA or autoantibody increases after islet transplantation are important prognostic markers, and their identification could potentially lead to improved islet cell transplant outcomes. © 2013 by the American Diabetes Association.


Frison S.,Organ and Tissue Transplantation Immunology | Longhi E.,Organ and Tissue Transplantation Immunology | Mantovani M.,Organ and Tissue Transplantation Immunology | Mantia M.,L.E.S.S. | And 4 more authors.
Human Immunology | Year: 2012

We describe here the sequences of 3 new HLA-DRB1 variants officially named DRB1*03:05:03, DRB1*11:10:02, and DRB1*14:86. These novel alleles have been detected in 3 Caucasoid individuals by sequence-based typing. The first and second alleles are the result of a silent mutation, which does not imply any amino acid change. The sequence of DRB1*14:86 exhibits a single nucleotide difference with the allele DRB1*14:01:01 at position 239. © 2012 American Society for Histocompatibility and Immunogenetics.


Zambelli M.,Ospedali Riuniti | Andorno E.,University of Genoa | De Carlis L.,Niguarda caGranda Hospital | Rossi G.,General Surgery and Liver Transplantation Unit | And 6 more authors.
American Journal of Transplantation | Year: 2012

Full-right-full-left split liver transplantation divides a donor liver into two grafts to be transplanted in adult-size patients. Major technical and organizational difficulties have limited its application to few single center series. We retrospectively analyzed the long-term results of the first multicenter series of this procedure with graft sharing. Between November 1998 and January 2005, 43 transplants were performed by five centers from 23 full-right-full-left in situ split liver procedures; 65% of the grafts were shared. A total of 31 (72%) patients had complications above grade II; 3 (6.9%) were retransplanted. Hospital mortality was 23% with sepsis as the main cause. Six patients died in the long term, two of them for a road accident. A total of 27 patients are alive after a median follow-up of 3200 days (2035-4256). Actuarial survival at 1 and 10 years were 72.1%, 62.6% and 65.1%, 57.9%, respectively for patients and grafts. These figures are similar to those reported for adult living donor liver transplantation by the European Registry over a similar period. Multicenter collaboration in sharing of these grafts is feasible and can help facing the organizational limits, thus increasing diffusion of full-right-full-left split liver transplantation. Full right and full left grafts from split liver procedures can be shared among different centers of the same area in the context of a collaborative activity, being safely and effectively transplanted in adult patients, thus optimizing the use of deceased donor livers. © Copyright 2012 The American Society of Transplantation and the American Society of Transplant Surgeons.


Longhi E.,Organ and Tissue Transplantation Immunology | Crivello P.,San Raffaele Scientific Institute | Mantovani M.,Organ and Tissue Transplantation Immunology | Frison S.,Organ and Tissue Transplantation Immunology | And 4 more authors.
International Journal of Immunogenetics | Year: 2014

Summary: Here we describe the molecular modelling of the new variant HLA-B*35:132. This allele shows one mismatch with B*35:01:01:01 in exon 3 at position 575 where a T is substituted by a C, which implies an amino acidic change from Leucine to Proline. This seems not to alter the molecular structure and not to compromise the HLA complex and T-cell receptor interaction. © 2014 John Wiley & Sons Ltd.


Lochmann E.,Hospital of Bolzano | Frison S.,Organ and Tissue Transplantation Immunology | Longhi E.,Organ and Tissue Transplantation Immunology | Moscetti A.,Camillo Forlanini Hospital | Vecchiato C.,Hospital of Bolzano
International Journal of Immunogenetics | Year: 2014

Summary: A novel allele, officially named B*18:80, was detected in a Caucasoid individual by polymerase chain reaction-sequence-specific primers and SBT. The new allele differs from B*18:01:01 at two nucleotidic positions in codon 24 at exon 2. © 2014 John Wiley & Sons Ltd.


Poli F.,Organ and Tissue Transplantation Immunology | Benazzi E.,Organ and Tissue Transplantation Immunology | Innocente A.,Organ and Tissue Transplantation Immunology | Nocco A.,Organ and Tissue Transplantation Immunology | And 4 more authors.
Human Immunology | Year: 2011

The development of solid-phase assays for antibody detection has aided in the frequent detection of human leukocyte antigen (HLA) antibodies in nonalloimmunized males. Some scientists have reported that these HLA antibodies are produced to pathogens or allergens and the reactivity with HLA coated beads is the result of cross-reactive epitopes. These antibodies may also be directed toward cryptic epitopes exposed on the denatured beads. In this report, we describe the case of a heart transplanted patient who exhibited anti-HLA-A*02:01 donor-specific antibodies detected with a bead-based assay (Luminex) and undetected with the complement-dependent cytotoxicity (CDC) test. Posttransplant monitoring, carried out with CDC and with Luminex on sera from this patient collected at the 2nd, 4th, 8th, and 12th posttransplant weeks and at 1 year confirmed the presence of anti-HLA-A*02:01 in all serum samples. Additional tests carried out with denatured and intact HLA molecules using single antigen beads demonstrated that the antibody was directed toward a cryptic epitope. One year after transplantation the patient is doing well. No sign of antibody-mediated rejection was observed throughout the follow-up. A comprehensive evaluation of the anamnesis and of antibodies is critical to avoid needless exclusion of organ donors. © 2011 American Society for Histocompatibility and Immunogenetics.


Mantovani M.,Organ and Tissue Transplantation Immunology | Crivello P.,Unit of Molecular and Functional Immunogenetics UMFI | Frison S.,Organ and Tissue Transplantation Immunology | Longhi E.,Organ and Tissue Transplantation Immunology | And 3 more authors.
Human Immunology | Year: 2012

We describe here the sequence and the molecular modeling of a new variant of HLA-A*32 allele officially named A*32:22. This novel allele has been detected in an Italian cord blood sample by sequence-based typing (SBT). The mutation (CAT →CGT), which has occurred at codon 151, at nucleotide position 524, implies an amino acidic change from Histidine to Arginine. Residue 151 is located on top of the molecule inside the region contacted by T cell receptor (TCR) and it is possibly involved in docking TCR. A positively charged residue is maintained on this position determining a slight change of electrostatic potential on the molecular surface. This suggests a limited functional relevance of the amino acid substitution encoded by A*32:22. © 2012 American Society for Histocompatibility and Immunogenetics.


Goh A.,Terasaki Foundation Laboratory | Scalamogna M.,Organ and Tissue Transplantation Immunology | De Feo T.,Organ and Tissue Transplantation Immunology | Poli F.,Organ and Tissue Transplantation Immunology | Terasaki P.I.,Terasaki Foundation Laboratory
Liver Transplantation | Year: 2010

Although human leukocyte antigen (HLA) crossmatching is often thought to be unnecessary for liver transplants (LTs), we provide evidence that for retransplants, it is essential. Sera from 139 retransplant patients who had received livers from deceased donors were retrospectively analyzed with single antigen beads on a Luminex platform for HLA antibodies. Each patient received at least 2 transplants and was followed up for at least 6 months from the second LT, which was deemed to have failed if the patient had a third LT or died. Second LT survival was calculated from the date of the second LT to the date of the third LT or death. Our study cohort consisted of 118 adult patients (≥18 years old) as well as 21 pediatric patients (<18 years old). Class I HLA antibodies were associated with significantly poorer regraft survival in adults [survival differences of 21.3% (P = 0.046), 22.1% (P = 0.042), and 23.7% (P = 0.033) at 1, 3, and 5 years, respectively]; however, the presence of these antibodies was not associated with significant survival differences in the pediatric population. A univariate analysis of the effect of class I antibodies on second LT survival in adults showed a hazard ratio of 2.0 (95% confidence interval = 1.0-3.8, P = 0.028). Graft survival in patients with and without HLA antibodies or class II antibodies was similar. Because class I antibodies have a deleterious effect on liver regraft survival, crossmatch testing should be performed before liver retransplantation. © 2010 AASLD.


Frison S.,Organ and Tissue Transplantation Immunology | Longhi E.,Organ and Tissue Transplantation Immunology | Mantovani M.,Organ and Tissue Transplantation Immunology | Malagoli A.,Servizio di Immunologia Clinica e Allergologia | And 3 more authors.
International Journal of Immunogenetics | Year: 2013

Summary: Two novel human leucocyte antigen (HLA) class I alleles have been identified in two Italian individuals. HLA-B*27:07:02 is identical to HLA-B*27:07:01 except for a nucleotide substitution at position 846 (A->G) resulting in a silent mutation. HLA-B*35:206 differs from the most similar allele, HLA-B*35:08:01, because of a single base mutation at position 149 (G->C) causing an aminoacidic change at codon 26 from Gly to Ala. © 2012 John Wiley & Sons Ltd.


PubMed | Organ and Tissue Transplantation Immunology
Type: Journal Article | Journal: International journal of immunogenetics | Year: 2013

Two novel human leucocyte antigen (HLA) class I alleles have been identified in two Italian individuals. HLA-B*27:07:02 is identical to HLA-B*27:07:01 except for a nucleotide substitution at position 846 (A->G) resulting in a silent mutation. HLA-B*35:206 differs from the most similar allele, HLA-B*35:08:01, because of a single base mutation at position 149 (G->C) causing an aminoacidic change at codon 26 from Gly to Ala.

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