Cellular immune mechanisms in chronic autoimmune thrombocytopenic purpura (ATP)
(1992) In Autoimmunity 13(4). p.9-311- Abstract
Chronic autoimmune thrombocytopenic purpura (ATP) is a common autoimmune-mediated bleeding disease in which autoantibodies are directed against platelets, resulting in their enhanced Fc-mediated destruction by macrophages in the spleen. While there has been extensive studies relating to the autoantibodies in this autoimmune disorder, relatively few have dealt with cell-mediated immunoregulation of the anti-platelet autoantibody response. Nonetheless, there is accumulating evidence that suggests the production of these anti-platelet autoantibodies is under the influence of several abnormal lymphocyte-mediated mechanisms, i.e. enhanced anti-platelet T helper cell activity with concomitant reduced T suppressor cell activity. This review... (More)
Chronic autoimmune thrombocytopenic purpura (ATP) is a common autoimmune-mediated bleeding disease in which autoantibodies are directed against platelets, resulting in their enhanced Fc-mediated destruction by macrophages in the spleen. While there has been extensive studies relating to the autoantibodies in this autoimmune disorder, relatively few have dealt with cell-mediated immunoregulation of the anti-platelet autoantibody response. Nonetheless, there is accumulating evidence that suggests the production of these anti-platelet autoantibodies is under the influence of several abnormal lymphocyte-mediated mechanisms, i.e. enhanced anti-platelet T helper cell activity with concomitant reduced T suppressor cell activity. This review focuses on these cellular events and presents a working model which attempts to explain their close interrelationships.
(Less)
- author
- Semple, J W LU and Freedman, J
- publishing date
- 1992
- type
- Contribution to journal
- publication status
- published
- keywords
- Autoantibodies/immunology, Autoimmune Diseases/immunology, B-Lymphocytes/immunology, Humans, Platelet Membrane Glycoproteins/immunology, Purpura, Thrombocytopenic, Idiopathic/immunology, T-Lymphocytes/immunology
- in
- Autoimmunity
- volume
- 13
- issue
- 4
- pages
- 9 - 311
- publisher
- Taylor & Francis
- external identifiers
-
- scopus:0026439098
- pmid:1472641
- ISSN
- 0891-6934
- DOI
- 10.3109/08916939209112340
- language
- English
- LU publication?
- no
- id
- 81263ceb-cc00-4519-8dc0-558b95a21822
- date added to LUP
- 2022-11-09 15:29:07
- date last changed
- 2024-01-03 09:02:53
@article{81263ceb-cc00-4519-8dc0-558b95a21822,
abstract = {{<p>Chronic autoimmune thrombocytopenic purpura (ATP) is a common autoimmune-mediated bleeding disease in which autoantibodies are directed against platelets, resulting in their enhanced Fc-mediated destruction by macrophages in the spleen. While there has been extensive studies relating to the autoantibodies in this autoimmune disorder, relatively few have dealt with cell-mediated immunoregulation of the anti-platelet autoantibody response. Nonetheless, there is accumulating evidence that suggests the production of these anti-platelet autoantibodies is under the influence of several abnormal lymphocyte-mediated mechanisms, i.e. enhanced anti-platelet T helper cell activity with concomitant reduced T suppressor cell activity. This review focuses on these cellular events and presents a working model which attempts to explain their close interrelationships.</p>}},
author = {{Semple, J W and Freedman, J}},
issn = {{0891-6934}},
keywords = {{Autoantibodies/immunology; Autoimmune Diseases/immunology; B-Lymphocytes/immunology; Humans; Platelet Membrane Glycoproteins/immunology; Purpura, Thrombocytopenic, Idiopathic/immunology; T-Lymphocytes/immunology}},
language = {{eng}},
number = {{4}},
pages = {{9--311}},
publisher = {{Taylor & Francis}},
series = {{Autoimmunity}},
title = {{Cellular immune mechanisms in chronic autoimmune thrombocytopenic purpura (ATP)}},
url = {{http://dx.doi.org/10.3109/08916939209112340}},
doi = {{10.3109/08916939209112340}},
volume = {{13}},
year = {{1992}},
}