Document Detail

Understanding loss of donor white blood cell immunogenicity after pathogen reduction: mechanisms of action in ultraviolet illumination and riboflavin treatment.
MedLine Citation:
PMID:  19682337     Owner:  NLM     Status:  MEDLINE    
BACKGROUND: Donor white blood cells (WBCs) present in transfusion products can lead to immune sequelae such as production of HLA antibodies or graft-versus-host disease in susceptible transfusion recipients. Eliminating the immunogenicity of blood products may prove to be of clinical benefit, particularly in patients requiring multiple transfusions in whom allosensitization is common. This study examines a method of pathogen reduction based on ultraviolet light illumination in the presence of riboflavin. In addition to pathogens, WBCs treated with this system are affected and fail to stimulate proliferation of allogeneic peripheral blood mononuclear cells (PBMNCs) in vitro.
STUDY DESIGN AND METHODS: This study sought to determine the mechanisms regulating this loss of immunogenicity. Treated cells were examined for surface expression of a number of molecules involved in activation and adhesion, viability, cell-cell conjugation, and ability to stimulate immune responses in allogeneic PBMNCs.
RESULTS: Compared with untreated controls, ultraviolet (UV)-irradiated antigen-presenting cells showed slightly reduced surface expression of HLA Class II and costimulatory molecules and had more significant reductions in surface expression of a number of adhesion molecules. Furthermore, treated cells had a severe defect in cell-cell conjugation. The observed loss of immunogenicity was nearly complete, with UV-irradiated cells stimulating barely measurable interferon-gamma production and no detectable STAT-3, STAT-5, or CD3-epsilon phosphorylation in allospecific primed T cells.
CONCLUSION: These results suggest that defective cell-cell adhesion prevents UV-irradiated cells from inducing T-cell activation.
Rachael P Jackman; John W Heitman; Susanne Marschner; Raymond P Goodrich; Philip J Norris
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Publication Detail:
Type:  Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't     Date:  2009-08-04
Journal Detail:
Title:  Transfusion     Volume:  49     ISSN:  1537-2995     ISO Abbreviation:  Transfusion     Publication Date:  2009 Dec 
Date Detail:
Created Date:  2010-02-18     Completed Date:  2010-03-19     Revised Date:  2013-06-02    
Medline Journal Info:
Nlm Unique ID:  0417360     Medline TA:  Transfusion     Country:  United States    
Other Details:
Languages:  eng     Pagination:  2686-99     Citation Subset:  IM    
Department of Laboratory Medicine and Medicine, Blood Systems Research Institute, University of California, San Francisco, California, USA.
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MeSH Terms
Blood Preservation / methods*
Blood Transfusion*
Blood-Borne Pathogens / radiation effects
Cell Adhesion Molecules / immunology
Cell Death / radiation effects
Cell Division / drug effects
Cell Survival / radiation effects
Flow Cytometry
HLA Antigens / immunology
Isoantigens / immunology
Leukocytes* / drug effects,  immunology,  radiation effects
Lymphocyte Activation
Photosensitizing Agents / pharmacology*
Riboflavin / pharmacology*
Ultraviolet Rays*
Grant Support
Reg. No./Substance:
0/Cell Adhesion Molecules; 0/HLA Antigens; 0/Isoantigens; 0/Photosensitizing Agents; 83-88-5/Riboflavin

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine

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