Immune responsiveness against allogeneic platelet transfusions is determined by the recipient's major histocompatibility complex class II phenotype
(2004) In Transfusion 44(11). p.1572-1578- Abstract
BACKGROUND: Immunoglobulin G (IgG) anti-platelet (PLT) immunity has been shown to be initiated by indirect allorecognition where recipient T cells recognize donor PLT antigens presented by class II molecules encoded by the major histocompatibility complex (MHC) on recipient antigen-presenting cells. To understand how the recipient's MHC class II molecules may influence PLT alloimmunity, immune responsiveness against transfused PLTs was tested in different mouse strains. STUDY DESIGN AMD METHODS: Various inbred and mutant mouse strains were transfused with allogeneic PLTs and IgG donor antibodies were measured by flow cytometry. RESULTS: When recipient mice, expressing both MHC class II I-A and MHC class II I-E molecules, were transfused... (More)
BACKGROUND: Immunoglobulin G (IgG) anti-platelet (PLT) immunity has been shown to be initiated by indirect allorecognition where recipient T cells recognize donor PLT antigens presented by class II molecules encoded by the major histocompatibility complex (MHC) on recipient antigen-presenting cells. To understand how the recipient's MHC class II molecules may influence PLT alloimmunity, immune responsiveness against transfused PLTs was tested in different mouse strains. STUDY DESIGN AMD METHODS: Various inbred and mutant mouse strains were transfused with allogeneic PLTs and IgG donor antibodies were measured by flow cytometry. RESULTS: When recipient mice, expressing both MHC class II I-A and MHC class II I-E molecules, were transfused weekly with allogeneic PLTs, high titers of IgG donor antibodies were generated. In comparison, however, recipient mice expressing only MHC class II I-A molecules had significantly (p < 0.001) reduced IgG antibody responsiveness against PLT transfusions. The low IgG responder status against allogeneic PLT transfusions was rescued in transgenic mice expressing I-E molecules and in mice genetically deficient in either β2-microglobulin or CD8+ T cells. CONCLUSION: IgG immune responsiveness against allogeneic PLT transfusions is dependent on recipient expression of I-E MHC class II molecules, whereas I-A expression is linked with CD8-mediated suppression of PLT immunity. The data suggest that strategies to modify recipient MHC class II presentation of donor PLT antigens would be effective in eliminating PLT alloimmunity.
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- author
- Sayeh, Ebrahim ; Aslam, Rukshana ; Speck, Edwin R. ; Le-Tien, Hoang ; Lazarus, Alan H. ; Freedman, John and Semple, John W. LU
- publishing date
- 2004-11-01
- type
- Contribution to journal
- publication status
- published
- in
- Transfusion
- volume
- 44
- issue
- 11
- pages
- 1572 - 1578
- publisher
- Wiley-Blackwell
- external identifiers
-
- scopus:7244260718
- pmid:15504162
- ISSN
- 0041-1132
- DOI
- 10.1111/j.1537-2995.2004.04197.x
- language
- English
- LU publication?
- no
- id
- 7165ff23-8355-427a-974e-fc5464e90981
- date added to LUP
- 2019-12-03 10:21:26
- date last changed
- 2024-01-02 01:03:49
@article{7165ff23-8355-427a-974e-fc5464e90981, abstract = {{<p>BACKGROUND: Immunoglobulin G (IgG) anti-platelet (PLT) immunity has been shown to be initiated by indirect allorecognition where recipient T cells recognize donor PLT antigens presented by class II molecules encoded by the major histocompatibility complex (MHC) on recipient antigen-presenting cells. To understand how the recipient's MHC class II molecules may influence PLT alloimmunity, immune responsiveness against transfused PLTs was tested in different mouse strains. STUDY DESIGN AMD METHODS: Various inbred and mutant mouse strains were transfused with allogeneic PLTs and IgG donor antibodies were measured by flow cytometry. RESULTS: When recipient mice, expressing both MHC class II I-A and MHC class II I-E molecules, were transfused weekly with allogeneic PLTs, high titers of IgG donor antibodies were generated. In comparison, however, recipient mice expressing only MHC class II I-A molecules had significantly (p < 0.001) reduced IgG antibody responsiveness against PLT transfusions. The low IgG responder status against allogeneic PLT transfusions was rescued in transgenic mice expressing I-E molecules and in mice genetically deficient in either β<sub>2</sub>-microglobulin or CD8+ T cells. CONCLUSION: IgG immune responsiveness against allogeneic PLT transfusions is dependent on recipient expression of I-E MHC class II molecules, whereas I-A expression is linked with CD8-mediated suppression of PLT immunity. The data suggest that strategies to modify recipient MHC class II presentation of donor PLT antigens would be effective in eliminating PLT alloimmunity.</p>}}, author = {{Sayeh, Ebrahim and Aslam, Rukshana and Speck, Edwin R. and Le-Tien, Hoang and Lazarus, Alan H. and Freedman, John and Semple, John W.}}, issn = {{0041-1132}}, language = {{eng}}, month = {{11}}, number = {{11}}, pages = {{1572--1578}}, publisher = {{Wiley-Blackwell}}, series = {{Transfusion}}, title = {{Immune responsiveness against allogeneic platelet transfusions is determined by the recipient's major histocompatibility complex class II phenotype}}, url = {{http://dx.doi.org/10.1111/j.1537-2995.2004.04197.x}}, doi = {{10.1111/j.1537-2995.2004.04197.x}}, volume = {{44}}, year = {{2004}}, }