T cell and cytokine abnormalities in patients with autoimmune thrombocytopenic purpura
(2003) In Transfusion and Apheresis Science 28(3). p.42-237- Abstract
Autoimmune thrombocytopenic purpura (AITP) is a bleeding disorder in which autoantibodies are directed against an individual's own platelets, leading to enhanced clearance through Fc receptor (R)-mediated phagocytosis by macrophages residing in the reticuloendothelial system, particularly in the spleen. Although the immunopathogenesis of the disease is autoantibody-mediated, there is now substantial evidence that suggest that the antiplatelet autoantibodies are under the control of T helper (Th) cells and the cytokines that they produce. This review will summarize the recent literature regarding abnormal Th cell reactivities and cytokine secretion in AITP. Reviews of the earlier literature regarding cell mediated immunity in chronic... (More)
Autoimmune thrombocytopenic purpura (AITP) is a bleeding disorder in which autoantibodies are directed against an individual's own platelets, leading to enhanced clearance through Fc receptor (R)-mediated phagocytosis by macrophages residing in the reticuloendothelial system, particularly in the spleen. Although the immunopathogenesis of the disease is autoantibody-mediated, there is now substantial evidence that suggest that the antiplatelet autoantibodies are under the control of T helper (Th) cells and the cytokines that they produce. This review will summarize the recent literature regarding abnormal Th cell reactivities and cytokine secretion in AITP. Reviews of the earlier literature regarding cell mediated immunity in chronic AITP have been published [; ]. Understanding the immune mechanisms controlling cell-mediated mechanisms is vital for developing antigen specific immunotherapies to treat the disease.
(Less)
- author
- Semple, John W LU
- publishing date
- 2003-06
- type
- Contribution to journal
- publication status
- published
- subject
- keywords
- Autoimmunity, Cytokines/immunology, Humans, Immunity, Cellular, Purpura, Thrombocytopenic, Idiopathic/etiology, T-Lymphocytes, Helper-Inducer/immunology
- in
- Transfusion and Apheresis Science
- volume
- 28
- issue
- 3
- pages
- 6 pages
- publisher
- Elsevier
- external identifiers
-
- scopus:0037410054
- pmid:12725949
- ISSN
- 1473-0502
- DOI
- 10.1016/S1473-0502(03)00041-7
- language
- English
- LU publication?
- no
- id
- a71b31dc-2cfc-4a4b-ac5f-813de9ba8b80
- date added to LUP
- 2022-11-09 15:26:30
- date last changed
- 2024-01-14 12:46:51
@article{a71b31dc-2cfc-4a4b-ac5f-813de9ba8b80,
abstract = {{<p>Autoimmune thrombocytopenic purpura (AITP) is a bleeding disorder in which autoantibodies are directed against an individual's own platelets, leading to enhanced clearance through Fc receptor (R)-mediated phagocytosis by macrophages residing in the reticuloendothelial system, particularly in the spleen. Although the immunopathogenesis of the disease is autoantibody-mediated, there is now substantial evidence that suggest that the antiplatelet autoantibodies are under the control of T helper (Th) cells and the cytokines that they produce. This review will summarize the recent literature regarding abnormal Th cell reactivities and cytokine secretion in AITP. Reviews of the earlier literature regarding cell mediated immunity in chronic AITP have been published [; ]. Understanding the immune mechanisms controlling cell-mediated mechanisms is vital for developing antigen specific immunotherapies to treat the disease.</p>}},
author = {{Semple, John W}},
issn = {{1473-0502}},
keywords = {{Autoimmunity; Cytokines/immunology; Humans; Immunity, Cellular; Purpura, Thrombocytopenic, Idiopathic/etiology; T-Lymphocytes, Helper-Inducer/immunology}},
language = {{eng}},
number = {{3}},
pages = {{42--237}},
publisher = {{Elsevier}},
series = {{Transfusion and Apheresis Science}},
title = {{T cell and cytokine abnormalities in patients with autoimmune thrombocytopenic purpura}},
url = {{http://dx.doi.org/10.1016/S1473-0502(03)00041-7}},
doi = {{10.1016/S1473-0502(03)00041-7}},
volume = {{28}},
year = {{2003}},
}