Platelets retain function and can be stored following disruption of human leucocyte antigens.
blood components
function
human leucocyte antigen
platelets
quality
refractoriness
Journal
Vox sanguinis
ISSN: 1423-0410
Titre abrégé: Vox Sang
Pays: England
ID NLM: 0413606
Informations de publication
Date de publication:
10 Apr 2024
10 Apr 2024
Historique:
revised:
15
02
2024
received:
05
11
2023
accepted:
25
03
2024
medline:
10
4
2024
pubmed:
10
4
2024
entrez:
10
4
2024
Statut:
aheadofprint
Résumé
Antibodies to human leucocyte antigen (HLA) Class-I antigens can lead to refractoriness to platelet transfusion. Although this can be overcome by transfusion of HLA-compatible platelets, they are not always available. Disruption of HLA antigens on platelets by acid treatment may be a suitable alternative when no other components are available. The aim of this study was to assess the effect of HLA disruption and subsequent storage of platelet components. Platelet components were treated with 0.9% saline or citric acid solution (pH 3.0), and then stored until expiry (Day 7). HLA and platelet glycoprotein expression, platelet viability, activation and sialylation were measured by flow cytometry. Release of soluble factors was measured by ELISA and metabolism by biochemistry analyser. Reactivity to patient anti-sera containing anti-HLA antibodies was measured using platelet immunofluorescence tests (PIFTs) and monoclonal antibody immobilization of platelet antigen (MAIPA) assays. Platelet function was measured using aggregometry and thromboelastography (TEG). Acid treatment reduced detection of HLA Class-I on platelets by 75%, with significant reductions in reactivity to patient anti-sera. Acid treatment reduced platelet content and viability, increased platelet activation and accelerated metabolism. Glycan cleavage was increased by acid treatment. Treatment reduced platelet activation following agonist stimulation by ADP and TRAP-6, but platelets remained functional, displaying increased aggregation response and reduced time to clot formation by TEG. Although HLA disruption had some detrimental effects, acid-treated platelets remained functional, retaining their capacity to respond to agonists and form clots, and with further development could be used to support refractory patients.
Sections du résumé
BACKGROUND AND OBJECTIVES
OBJECTIVE
Antibodies to human leucocyte antigen (HLA) Class-I antigens can lead to refractoriness to platelet transfusion. Although this can be overcome by transfusion of HLA-compatible platelets, they are not always available. Disruption of HLA antigens on platelets by acid treatment may be a suitable alternative when no other components are available. The aim of this study was to assess the effect of HLA disruption and subsequent storage of platelet components.
MATERIALS AND METHODS
METHODS
Platelet components were treated with 0.9% saline or citric acid solution (pH 3.0), and then stored until expiry (Day 7). HLA and platelet glycoprotein expression, platelet viability, activation and sialylation were measured by flow cytometry. Release of soluble factors was measured by ELISA and metabolism by biochemistry analyser. Reactivity to patient anti-sera containing anti-HLA antibodies was measured using platelet immunofluorescence tests (PIFTs) and monoclonal antibody immobilization of platelet antigen (MAIPA) assays. Platelet function was measured using aggregometry and thromboelastography (TEG).
RESULTS
RESULTS
Acid treatment reduced detection of HLA Class-I on platelets by 75%, with significant reductions in reactivity to patient anti-sera. Acid treatment reduced platelet content and viability, increased platelet activation and accelerated metabolism. Glycan cleavage was increased by acid treatment. Treatment reduced platelet activation following agonist stimulation by ADP and TRAP-6, but platelets remained functional, displaying increased aggregation response and reduced time to clot formation by TEG.
CONCLUSION
CONCLUSIONS
Although HLA disruption had some detrimental effects, acid-treated platelets remained functional, retaining their capacity to respond to agonists and form clots, and with further development could be used to support refractory patients.
Types de publication
Journal Article
Langues
eng
Sous-ensembles de citation
IM
Subventions
Organisme : Australian Governments
Informations de copyright
© 2024 Commonwealth of Australia. Vox Sanguinis published by John Wiley & Sons Ltd on behalf of International Society of Blood Transfusion.
Références
Legler TJ, Fischer I, Dittmann J, Simson G, Lynen R, Humpe A, et al. Frequency and causes of refractoriness in multiply transfused patients. Ann Hematol. 1997;74:185–189.
Seftel MD, Growe GH, Petraszko T, Benny WB, Le A, Lee CY, et al. Universal prestorage leukoreduction in Canada decreases platelet alloimmunization and refractoriness. Blood. 2004;103:333–339.
Doughty HA, Murphy MF, Metcalfe P, Rohatiner AZ, Lister TA, Waters AH. Relative importance of immune and non‐immune causes of platelet refractoriness. Vox Sang. 1994;66:200–205.
Schmidt AE, Refaai MA, Coppage M. HLA‐mediated platelet refractoriness. Am J Clin Pathol. 2019;151:353–363.
Datema G, Stein S, Eijsink C, Mulder A, Claas FHJ, Doxiadis IIN. HLA‐C expression on platelets: studies with an HLA‐Cw1‐specific human monoclonal antibody. Vox Sang. 2000;79:108–111.
Saito S, Ota S, Seshimo H, Yamazaki Y, Nomura S, Ito T, et al. Platelet transfusion refractoriness caused by a mismatch in HLA‐C antigens. Transfusion. 2002;42:302–308.
Brown CJ, Navarrete CV. Clinical relevance of the HLA system in blood transfusion. Vox Sang. 2011;101:93–105.
Marsh JC, Stanworth SJ, Pankhurst LA, Kallon D, Gilbertson AZ, Pigden C, et al. An epitope‐based approach of HLA‐matched platelets for transfusion: a noninferiority crossover randomized trial. Blood. 2021;137:310–322.
Salama OS, Aladl DA, El Ghannam DM, Elderiny WE. Evaluation of platelet cross‐matching in the management of patients refractory to platelet transfusions. Blood Transfus. 2014;12:187–194.
O'Connell B, Lee E, Rothko K, Hussein M, Schiffer C. Selection of histocompatible apheresis platelet donors by cross‐matching random donor platelet concentrates. Blood. 1992;79:527–531.
Moroff G, Garratty G, Heal J, Macpherson B, Stroncek D, Huang S, et al. Selection of platelets for refractory patients by HLA matching and prospective crossmatching. Transfusion. 1992;32:633–640.
Sugawara S, Abo T, Kumagai K. A simple method to eliminate the antigenicity of surface class I MHC molecules from the membrane of viable cells by acid treatment at pH 3. J Immunol Methods. 1987;100:83–90.
Kurata Y, Oshida M, Take H, Furubayashi T, Mizutani H, Tomiyama Y, et al. Acid treatment of platelets as a simple procedure for distinguishing platelet‐specific antibodies from anti‐HLA antibodies: comparison with chloroquine treatment. Vox Sang. 1990;59:106–111.
Novotny VM, Doxiadis IN, van Doorn R, Brand A. The kinetics of HLA class I elution and the relevance for the use of HLA‐eluted platelet transfusions. Br J Haematol. 1996;95:416–422.
Polakova K, Karpatova M, Russ G. Dissociation of beta 2‐microglobulin is responsible for selective reduction of HLA class I antigenicity following acid treatment of cells. Mol Immunol. 1993;30:1223–1230.
Murphy MF, Metcalfe P, Caples R, Waters AH. Function of acid‐treated platelets for transfusion. Br J Haematol. 1992;82:176–178.
Zou Y, Liu X, Liao S, Liu W, Lu Y, Tan X, et al. Acid treatment of platelets for removal of class I human leukocyte antigen (HLA) antigens. Sci Res Ess. 2011;6:4539–4544.
Hayashi T, Aminaka R, Fujimura Y, Koh Y, Sugaya S, Hayashi A, et al. A more efficient preparation system for HLA‐eliminated platelets. Vox Sang. 2020;115:159–166.
Mirlashari MR, Vetlesen A, Nissen‐Meyer LSH, Naper C, Tjønnfjord GE, Njerve IU, et al. HLA class I depletion by citric acid, and irradiation of apheresis platelets for transfusion of refractory patients. Transfusion. 2021;61:1222–1234.
Campbell K, Rishi K, Howkins G, Gilby D, Mushens R, Ghevaert C, et al. Modified rapid MAIPA protocol. Natl Inst Biol Stand Control. 2007;1–8.
Hartley PS, Savill J, Brown SB. The death of human platelets during incubation in citrated plasma involves shedding of CD42b and aggregation of dead platelets. Thromb Haemost. 2006;95:100–106.
Johnson L, Tan S, Wood B, Davis A, Marks DC. Refrigeration and cryopreservation of platelets differentially affect platelet metabolism and function: a comparison with conventional platelet storage conditions. Transfusion. 2016;56:1807–1818.
Johnson LN, Winter KM, Reid S, Hartkopf‐Theis T, Marks DC. Cryopreservation of buffy‐coat‐derived platelet concentrates in dimethyl sulfoxide and platelet additive solution. Cryobiology. 2011;62:100–106.
van der Wal DE, Davis AM, Mach M, Marks DC. The role of neuraminidase 1 and 2 in glycoprotein Ibalpha‐mediated integrin alphaIIbbeta3 activation. Haematologica. 2020;105:1081–1094.
Middelburg RA, Roest M, Ham J, Coccoris M, Zwaginga JJ, van der Meer PF. Flow cytometric assessment of agonist‐induced P‐selectin expression as a measure of platelet quality in stored platelet concentrates. Transfusion. 2013;53:1780–1787.
Meinke S, Sandgren P, Mortberg A, Karlstrom C, Kadri N, Wikman A, et al. Platelets made HLA deficient by acid treatment aggregate normally and escape destruction by complement and phagocytes in the presence of HLA antibodies. Transfusion. 2016;56:370–382. quiz 69.
Novotny VM, Huizinga TWJ, van Doorn R, Briet E, Brand A. HLA class I‐eluted platelets as an alternative to HLA‐matched platelets. Transfusion. 1996;36:438–444.
Mirlashari MR, Vetlesen A, Nissen‐Meyer LSH, Stensland ME, Singh SK, Nyman TA, et al. Proteomic study of apheresis platelets made HLA class I deficient for transfusion of refractory patients. Proteomics Clin Appl. 2021;15:e2100022.
Bertolini F, Porretti L, Corsini C, Rebulla P, Sirchia G. Platelet quality and reduction of HLA expression in acid‐treated platelet concentrates. Br J Haematol. 1993;83:525–527.
Mirlashari MR, Vetlesen A, Nissen‐Meyer LSH, Hetland G. Effects of storage on quality and function of acid‐treated platelets with reduced HLA class I surface expression. Transfus Med. 2023;33:329–336.
Shanwell A, Sallander S, Olsson I, Gulliksson H, Pedajas I, Lerner R. An alloimmunized, thrombocytopenic patient successfully transfused with acid‐treated, random‐donor platelets. Br J Haematol. 1991;79:462–465.
Novotny VM, Mast G, van Dijk F, Brand A, van Luyn MJA. HLA‐elution, different preparation techniques and platelet viability. Oslo, Norway: ISBT; 1998. p. 122.
Johnson L, Waters L, Green S, Wood B, Marks DC. Freezing expired platelets does not compromise in vitro quality: an opportunity to maximize inventory potential. Transfusion. 2020;60:454–459.
Li J, Van Der Wal DE, Zhu G, Xu M, Yougbare I, Ma L, et al. Desialylation is a mechanism of fc‐independent platelet clearance and a therapeutic target in immune thrombocytopenia. Nat Commun. 2015;6:7737.
Babic AM, Josefsson EC, Bergmeier W, Wagner DD, Kaufman RM, Silberstein LE, et al. In vitro function and phagocytosis of galactosylated platelet concentrates after long‐term refrigeration. Transfusion. 2007;47:442–451.
Ma R, Xie R, Yu C, Si Y, Wu X, Zhao L, et al. Phosphatidylserine‐mediated platelet clearance by endothelium decreases platelet aggregates and procoagulant activity in sepsis. Sci Rep. 2017;7:4978.
Sivakumaran M, Rajapakse R, Pavord S, Revill J, Clarke C. Treatment of alloimmunized, thrombocytopenic patient with acid‐treated random donor platelets. Br J Haematol. 1992;81:134–135.
Castro E, Muncunill J, Barea L, Gonzalez R, Fernandez‐Villalta MJ. Acid elution of platelets HLA‐class I antigens in the treatment of a refractory patient. Br J Haematol. 1998;100:245–246.
Novotny VM, Doxiadis I, Brand A. The reduction of HLA class I expression on platelets: a potential approach in the management of HLA‐alloimmunized refractory patients. Transfus Med Rev. 1999;13:95–105.
Johnson L, Lei P, Waters L, Padula MP, Marks DC. Identification of platelet subpopulations in cryopreserved platelet components using multi‐colour imaging flow cytometry. Sci Rep. 2023;13:1221.
Balitsky AK, Liu Y, Van der Meer PF, Heddle NM, Arnold DM. Exploring the components of bleeding outcomes in transfusion trials for patients with hematologic malignancy. Transfusion. 2021;61:286–293.