scholarly journals Splenic Immunoglobulin Variable Region Genes Encoding Red Blood Cell Binding Fab Fragments in Autoimmune Hemolytic Anemia

Hematology ◽  
1999 ◽  
Vol 4 (2) ◽  
pp. 165-178 ◽  
Author(s):  
A. K. Stewart ◽  
H. Gupta ◽  
D. Cappe ◽  
D. R. Sutherland
Blood ◽  
2002 ◽  
Vol 100 (13) ◽  
pp. 4529-4536 ◽  
Author(s):  
Andrew M. Hall ◽  
Frank J. Ward ◽  
Mark A. Vickers ◽  
Lisa-Marie Stott ◽  
Stanislaw J. Urbaniak ◽  
...  

Regulatory T cells have been shown to control animal models of immune-mediated pathology by inhibitory cytokine production, but little is known about such cells in human disease. Here we characterize regulatory T-cell responses specific for a human red blood cell autoantigen in patients with warm-type autoimmune hemolytic anemia. Peripheral blood mononuclear cells from patients with autoimmune hemolytic anemia were found either to proliferate and produce interferon-γ or to secrete the regulatory cytokine interleukin 10 when stimulated in vitro with a major red blood cell autoantigen, the RhD protein. Flow cytometric analysis confirmed that the majority of the responding cells were of the CD4+phenotype. Serial results from individual patients demonstrated that this bias toward proliferative or interleukin-10 responses was unstable over time and could reverse in subsequent samples. Epitope mapping studies identified peptides from the sequence of the autoantigen that preferentially induced interleukin-10 production, rather than proliferation, and demonstrated that many contain naturally processed epitopes. Responses to such peptides suppressed T-cell proliferation against the RhD protein, an inhibition that was mediated largely by interleukin 10 and dependent on cytotonic T lymphocyte–associated antigen (CTLA-4) costimulation. Antigenic peptides with the ability to stimulate specific regulatory cells may represent a new class of therapeutic agents for immune-mediated disease.


Transfusion ◽  
2020 ◽  
Vol 60 (8) ◽  
pp. 1856-1866
Author(s):  
Evgenia M. Bloch ◽  
Haley A. Branch ◽  
Darinka Sakac ◽  
Regina M. Leger ◽  
Donald R. Branch

1991 ◽  
Vol 53 (1) ◽  
pp. 19-21
Author(s):  
Shuichi TSUCHIDA ◽  
Reiko USUI ◽  
Ryouichi USUI ◽  
Umetaro MURAMATSU ◽  
Hiroyasu EJIMA ◽  
...  

1986 ◽  
Vol 30 (4) ◽  
pp. 247-250
Author(s):  
Eiji Kajii ◽  
Yuhji Yamaguchi ◽  
Juichi Ueki ◽  
Yasusada Miura ◽  
Haruhiro Yoshida ◽  
...  

2009 ◽  
Vol 84 (2) ◽  
pp. 98-101 ◽  
Author(s):  
Toyomi Kamesaki ◽  
Takashi Oyamada ◽  
Mitsuhiro Omine ◽  
Keiya Ozawa ◽  
Eiji Kajii

1999 ◽  
Vol 11 (6) ◽  
pp. 995-1000 ◽  
Author(s):  
Toshio Sakiyama ◽  
Koichi Ikuta ◽  
Sazuku Nisitani ◽  
Kiyoshi Takatsu ◽  
Tasuku Honjo

2015 ◽  
Vol 139 (11) ◽  
pp. 1455-1458 ◽  
Author(s):  
Erin Quist ◽  
Scott Koepsell

Autoimmune hemolytic anemia is a rare disorder caused by autoreactive red blood cell (RBC) antibodies that destroy RBCs. Although autoimmune hemolytic anemia is rare, RBC autoantibodies are encountered frequently and can complicate transfusion workups, impede RBC alloantibody identification, delay distribution of compatible units, have variable clinical significance that ranges from benign to life-threatening, and may signal an underlying disease or disorder. In this review, we discuss the common presenting features of RBC autoantibodies, laboratory findings, ancillary studies that help the pathologist investigate the clinical significance of autoantibodies, and how to provide appropriate patient care and consultation for clinical colleagues. Pathologists must be mindful of, and knowledgeable about, this entity because it not only allows for direct clinical management but also can afford an opportunity to preemptively treat an otherwise silent malignancy or disorder.


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