Literature DB >> 31355970

Red blood cell alloimmunization is associated with lower expression of FcγR1 on monocyte subsets in patients with sickle cell disease.

Raisa Balbuena-Merle1, Susanna A Curtis2, Lesley Devine1, David R Gibb1, Matthew S Karafin3,4, Chance John Luckey5, Christopher A Tormey1,6, Alexa J Siddon1,6,7, John D Roberts2, Jeanne E Hendrickson1,8.   

Abstract

BACKGROUND: Despite the clinical significance of red blood cell (RBC) alloantibodies, there are currently no laboratory tests available to predict which patients may be at risk of antibody formation after transfusion exposure. Given their phagocytic and inflammatory functions, we hypothesized that differences in circulating monocytes may play a role in alloimmunization. STUDY DESIGN AND METHODS: Forty-two adults with sickle cell disease (SCD) were recruited, with data extracted from the electronic medical record and peripheral blood analyzed by flow cytometry for total monocytes, monocyte subsets (CD14 high/CD16 low+ classical monocytes, CD14 high/CD16 high+ intermediate monocytes, and CD14 intermediate/CD16 high+ non-classical/inflammatory monocytes), and FcγR1 (CD64) expression. Thirteen "non-responder" patients (non-alloimmunized patients with documented RBC transfusion at the study institution) were compared to 20 alloimmunized "responder" patients, who had a total of 44 RBC alloantibodies identified.
RESULTS: There were no significant differences in the percentages of total monocytes, monocyte subsets, or measured cytokines between non-responders and responders. However, non-responders had higher CD64 expression on classical monocytes (MFI mean 3424 ± standard deviation 1141) compared to responders (MFI mean 2285 ± 1501), p = 0.029, and on intermediate monocytes (MFI mean 3720 ± 1191) compared to responders (MFI mean 2497 ± 1640), p = 0.033.
CONCLUSIONS: Monocytes and the inflammatory milieu increasingly are being appreciated to play a role in some complications of SCD. The differences in FcγR1 expression on monocyte subsets noted between responders and non-responders, which cannot be directly explained by the serum cytokines evaluated, warrant further investigation.
© 2019 AABB.

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Year:  2019        PMID: 31355970      PMCID: PMC7075520          DOI: 10.1111/trf.15463

Source DB:  PubMed          Journal:  Transfusion        ISSN: 0041-1132            Impact factor:   3.157


  49 in total

1.  Monocytosis is associated with hemolysis in sickle cell disease.

Authors:  Naritsara Wongtong; Susan Jones; Yu Deng; Jianwen Cai; Kenneth I Ataga
Journal:  Hematology       Date:  2015-04-15       Impact factor: 2.269

2.  Type I IFN Is Necessary and Sufficient for Inflammation-Induced Red Blood Cell Alloimmunization in Mice.

Authors:  David R Gibb; Jingchun Liu; Prabitha Natarajan; Manjula Santhanakrishnan; David J Madrid; Stephanie C Eisenbarth; James C Zimring; Akiko Iwasaki; Jeanne E Hendrickson
Journal:  J Immunol       Date:  2017-06-19       Impact factor: 5.422

3.  Alloimmunization in sickle cell anemia and transfusion of racially unmatched blood.

Authors:  E P Vichinsky; A Earles; R A Johnson; M S Hoag; A Williams; B Lubin
Journal:  N Engl J Med       Date:  1990-06-07       Impact factor: 91.245

4.  Tissue factor-positive monocytes in children with sickle cell disease: correlation with biomarkers of haemolysis.

Authors:  B N Yamaja Setty; Nigel S Key; A Koneti Rao; Suhita Gayen-Betal; Suba Krishnan; Carlton D Dampier; Marie J Stuart
Journal:  Br J Haematol       Date:  2012-02-24       Impact factor: 6.998

5.  B cells require Type 1 interferon to produce alloantibodies to transfused KEL-expressing red blood cells in mice.

Authors:  David R Gibb; Jingchun Liu; Manjula Santhanakrishnan; Prabitha Natarajan; David J Madrid; Seema Patel; Stephanie C Eisenbarth; Christopher A Tormey; Sean R Stowell; Akiko Iwasaki; Jeanne E Hendrickson
Journal:  Transfusion       Date:  2017-08-23       Impact factor: 3.157

6.  Prospective RBC phenotype matching in a stroke-prevention trial in sickle cell anemia: a multicenter transfusion trial.

Authors:  E P Vichinsky; N L Luban; E Wright; N Olivieri; C Driscoll; C H Pegelow; R J Adams
Journal:  Transfusion       Date:  2001-09       Impact factor: 3.157

7.  Increased expression of Fc gamma RI on isolated PMN from individuals of African descent.

Authors:  M M Moxey-Mims; M M Frank; E Y Lin; C Francis; T A Gaither
Journal:  Clin Immunol Immunopathol       Date:  1993-10

Review 8.  Red blood cell alloimmunization in sickle cell disease: pathophysiology, risk factors, and transfusion management.

Authors:  Karina Yazdanbakhsh; Russell E Ware; France Noizat-Pirenne
Journal:  Blood       Date:  2012-05-04       Impact factor: 22.113

9.  High prevalence of red blood cell alloimmunization in sickle cell disease despite transfusion from Rh-matched minority donors.

Authors:  Stella T Chou; Tannoa Jackson; Sunitha Vege; Kim Smith-Whitley; David F Friedman; Connie M Westhoff
Journal:  Blood       Date:  2013-05-30       Impact factor: 22.113

10.  A monocyte-TNF-endothelial activation axis in sickle transgenic mice: Therapeutic benefit from TNF blockade.

Authors:  Anna Solovey; Arif Somani; John D Belcher; Liming Milbauer; Lucile Vincent; Rafal Pawlinski; Karl A Nath; Robert J Kelm; Nigel Mackman; M Gerard O'Sullivan; Kalpna Gupta; Gregory M Vercellotti; Robert P Hebbel
Journal:  Am J Hematol       Date:  2017-07-29       Impact factor: 10.047

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  2 in total

1.  Red blood cell alloimmunization and sickle cell disease: a narrative review on antibody induction.

Authors:  Jeanne E Hendrickson
Journal:  Ann Blood       Date:  2020-12-30

2.  Type I interferon is induced by hemolysis and drives antibody-mediated erythrophagocytosis in sickle cell disease.

Authors:  Yunfeng Liu; Mouli Pal; Weili Bao; Patricia A Shi; Cheryl A Lobo; Xiuli An; Deepa Manwani; Hui Zhong; Karina Yazdanbakhsh
Journal:  Blood       Date:  2021-09-30       Impact factor: 25.476

  2 in total

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