Platelet Alloimmunization after
Transfusion

Taaning, Ellen; Simonsen, Anne Catrine; Hjelms, E; Sveygaard, Arne; Morling, Niels

doi:10.1159/000462001

Cited by 11 publications

(3 citation statements)

References 10 publications

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“…All SCID mice were injected with 20 µl of anti‐asialo GM 1 antiserum (Wako Pure Chemical Industries, Dallas, TX, USA) 1 d before reconstitution and were exposed to 200 cGy of γ‐irradiation just before reconstitution to enhance cellular engraftment, as previously described ( Lazarus et al , 1997 ). Human PBLs (1 × 10 7 /mouse) were isolated and injected into the peritoneal cavity, as previously described ( Crow et al , 1999 ).…”

mentioning

confidence: 99%

“…Many patients who receive platelet transfusions become alloimmunized, rendering them refractory to subsequent platelet transfusions ( Friedman et al , 1996 ; Taaning et al , 1997 ; Novotny, 1999). It is thought that ‘contaminating’ human leucocyte antigen (HLA) class II‐bearing antigen‐presenting cells (APCs) augment the production of these alloantibodies ( Claas et al , 1981 ; Bordin et al , 1994 ) and various methods have been used to inactivate or remove these ‘contaminating’ cells, including the use of ultraviolet radiation ( Kao, 1982; Grijzenhout et al , 1994 ) and leucofiltration ( Freedman et al , 1994 ; TRAP Study Group, 1997); however, many multitransfused patients still become alloimmunized ( Freedman et al , 1994 ; TRAP Study Group, 1997).…”

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confidence: 99%

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Monoclonal antibody‐mediated inhibition of the human HLA alloimmune response to platelet transfusion is antigen specific and independent of Fcγ receptor‐mediated immune suppression

Crow¹,

Freedman²,

Hannach³

et al. 2000

Br J Haematol

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Summary. Presensitization of donor platelets with allospecific immunoglobulin (Ig)G results in a diminished immune response against subsequent transfusions of platelets. To understand better the mechanism of how alloantibody presensitization results in a decreased alloimmune response, we have used murine monoclonal antibodies directed to polymorphic and non-polymorphic regions of human leucocyte antigen (HLA) as well as platelet-specific molecules. Here, we demonstrated that presensitization with anti-human HLA class I antibodies, as well as b 2 -microglobulin-specific antibody, protected against alloantibody production to five subsequent untreated platelet challenges. Use of complement fixing, non-fixing or F(ab H ) 2 fragments of HLA-specific antibody also resulted in complete inhibition of alloantibody production. This protection was not seen when the platelets were presensitized with monoclonal antibodies to CD42a (GPIX), CD32 (low-affinity IgG/Fcg receptor) or murine IgG and was thus independent of B-cell FcgRII-mediated immune suppression. The inhibition observed was independent of HLA alloantigenic specificity as antibodies directed at the b 2 -microglobulin portion of HLA class I were as effective as antibodies against any of the HLA-a regions (either polymorphic or nonpolymorphic) of class I. This work demonstrates that monoclonal antibody-mediated suppression of the human HLA alloimmune response to platelet transfusion is antigen specific and is independent of FcgRII-mediated immune regulation, complement fixing or HLA alloantigenic specificity.

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confidence: 99%

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confidence: 99%

Monoclonal antibody‐mediated inhibition of the human HLA alloimmune response to platelet transfusion is antigen specific and independent of Fcγ receptor‐mediated immune suppression

Crow¹,

Freedman²,

Hannach³

et al. 2000

Br J Haematol

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“…We have identified, for the first time, anti-HLA antibodies in RA-ILD and RA patients; in other studies HLA cytotoxic antibodies were detected in transfused patients; a positive correlation between the transfused load and the frequency of alloimmunization against HLA antigens was also found [52]. With regard to anti-HLA Class II antibodies, patients who received a heart transplant developed IgG antibodies compared to control subjects [53].…”

Section: Discussionmentioning

confidence: 58%

Anti-HLA Class II Antibodies Correlate with C-Reactive Protein Levels in Patients with Rheumatoid Arthritis Associated with Interstitial Lung Disease

Ángel-Pablo

Buendía-Roldán

Mejía

et al. 2020

Cells

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The pathogenesis of Rheumatoid Arthritis (RA) is not fully understood, probably influenced by genetic and environmental factors. Interstitial Lung Disease (ILD) is an extra-articular manifestation of RA, which contributes significantly to morbidity and mortality. The identification of anti-HLA antibodies has been useful in the transplantation field; however, its contribution to autoimmune diseases as RA has not been fully studied. We aimed to determine the presence of anti-HLA antibodies in RA patients with and without ILD and its possible association with clinical and biochemical markers. One-hundred and forty-seven RA patients, of which 65 had ILD (RA-ILD group), were included. Sera samples for Anti-HLA Class II LABScreen panel-reactive antibodies (PRA) were analyzed. In both groups, women predominated, and lung function was worse in patients with ILD. The anti-CCP+ (UI/mL) was higher in the RA group in comparison to RA-ILD (p < 0.001). Expositional risk factors (tobacco smoking and biomass-burning smoke) were higher in RA-ILD patients. PRA+ was identified in ~25% RA-ILD patients, while ~29% in the RA group. The CRP levels have a positive correlation with the percentage of reactivity (%PRA, p = 0.02, r2 = 0.60) in the RA-ILD group. In conclusion, anti-HLA antibodies correlate with C-reactive protein levels in RA patients with ILD.

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Frequency of Platelet Crossmatch Positivity and Predictive Value for Poor Platelet Increment Among Paediatric Oncohaematology Patients in India

Kingsley

Chacko

Amal

et al. 2019

Indian J Hematol Blood Transfus

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Immune platelet destruction is a significant cause for platelet refractoriness. The platelet crossmatcha solid phase red cell adherence assay utilizes donor platelets and patient serum to assess compatibility and appears to be a feasible option in resource constrained settings. This study was done to evaluate the frequency of platelet crossmatch positivity among Paediatric Oncohaematology patients and also to assess whether a positive crossmatch is predictive of unsuccessful platelet transfusions in this group of patients. Paediatric Oncohaematology patients who received platelet transfusions between March 2013 and September 2013 were included in the study. The pretransfusion patient sample and a segment from the transfused donor unit were used for performing the platelet crossmatch. A blood sample was collected one hour after the transfusion to assess post-transfusion platelet count. Corrected count increment (CCI) was calculated using the standard formula. CCI B 7500/lL/m 2 /10 11 was considered evidence of an unsuccessful transfusion. Seventy-three platelet crossmatches were performed for 69 patients, of which 30 patient samples (41%) showed crossmatch positivity. 25 (89.2%) of 28 unsuccessful transfusions showed crossmatch positivity, and 40 (88.9%) of 45 successful transfusions showed negative crossmatches (p = 0.03).Crossmatch positivity among transfusion dependent Paediatric Oncohaematology patients was as high as 42%, when ABO matched platelet units were allocated without further testing. Our results indicate that this test may be a reliable tool to select compatible platelet units and an effective intervention in the management of patients at risk of immune platelet refractoriness.

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Platelet Alloimmunization after Transfusion

Cited by 11 publications

References 10 publications

Monoclonal antibody‐mediated inhibition of the human HLA alloimmune response to platelet transfusion is antigen specific and independent of Fcγ receptor‐mediated immune suppression

Monoclonal antibody‐mediated inhibition of the human HLA alloimmune response to platelet transfusion is antigen specific and independent of Fcγ receptor‐mediated immune suppression

Anti-HLA Class II Antibodies Correlate with C-Reactive Protein Levels in Patients with Rheumatoid Arthritis Associated with Interstitial Lung Disease

Frequency of Platelet Crossmatch Positivity and Predictive Value for Poor Platelet Increment Among Paediatric Oncohaematology Patients in India

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