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Increased antiplatelet T helper lymphocyte reactivity in patients with autoimmune thrombocytopenia

Semple, J. W. LU and Freedman, J. (1991) In Blood 78(10). p.2619-2625
Abstract

Chronic autoimmune thrombocytopenic purpura (ATP) is a common hematologic disorder in which platelet-specific autoantibodies bind to platelets and enhance their destruction by the reticuloendothelial system. While there has been considerable investigation of the humoral immune abnormalities in ATP, little work has been performed on the cellular immunoregulatory aspects of this autoimmune disorder. We describe here that patients with ATP have lymphocytes that proliferate normally when stimulated by mitogens. However, when stimulated by normal control platelets in 7-day antigen-presenting cell cultures, peripheral blood mononuclear cells (PBMC) from patients with ATP proliferate at significantly higher levels (P < .001) and their... (More)

Chronic autoimmune thrombocytopenic purpura (ATP) is a common hematologic disorder in which platelet-specific autoantibodies bind to platelets and enhance their destruction by the reticuloendothelial system. While there has been considerable investigation of the humoral immune abnormalities in ATP, little work has been performed on the cellular immunoregulatory aspects of this autoimmune disorder. We describe here that patients with ATP have lymphocytes that proliferate normally when stimulated by mitogens. However, when stimulated by normal control platelets in 7-day antigen-presenting cell cultures, peripheral blood mononuclear cells (PBMC) from patients with ATP proliferate at significantly higher levels (P < .001) and their lymphocytes secrete significantly higher amounts of interleukin-2 (IL-2) (P < .001) than do lymphocytes from control subjects. Depletion studies with monoclonal anti-CD8 and complement did not reduce the proliferative capacity of the responding PBMC population, indicating that CD4+ T-helper cells may be responsible for the response. Phenotypic analysis of peripheral blood lymphocyte subsets from patients with ATP showed that there was a significant reduction in CD4+Leu8+ T suppressor-inducer cells (P < .001) and a concomitant increase in CD3+DR+ activated T cells (P < .001) and CD19+ B cells (P < .05). These data indicate that CD4+ T-helper cells from patients with ATP are stimulated by normal platelet antigen(s) to secrete IL-2 and may modulate the enhanced antiplatelet autoantibody response.

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author
and
publishing date
type
Contribution to journal
publication status
published
subject
in
Blood
volume
78
issue
10
pages
2619 - 2625
publisher
American Society of Hematology
external identifiers
  • scopus:0025876206
  • pmid:1840468
ISSN
0006-4971
DOI
10.1182/blood.V78.10.2619.2619
language
English
LU publication?
no
id
846888ca-056e-4146-a23c-e3901cc30fb9
date added to LUP
2019-12-03 10:36:02
date last changed
2025-07-26 09:55:32
@article{846888ca-056e-4146-a23c-e3901cc30fb9,
  abstract     = {{<p>Chronic autoimmune thrombocytopenic purpura (ATP) is a common hematologic disorder in which platelet-specific autoantibodies bind to platelets and enhance their destruction by the reticuloendothelial system. While there has been considerable investigation of the humoral immune abnormalities in ATP, little work has been performed on the cellular immunoregulatory aspects of this autoimmune disorder. We describe here that patients with ATP have lymphocytes that proliferate normally when stimulated by mitogens. However, when stimulated by normal control platelets in 7-day antigen-presenting cell cultures, peripheral blood mononuclear cells (PBMC) from patients with ATP proliferate at significantly higher levels (P &lt; .001) and their lymphocytes secrete significantly higher amounts of interleukin-2 (IL-2) (P &lt; .001) than do lymphocytes from control subjects. Depletion studies with monoclonal anti-CD8 and complement did not reduce the proliferative capacity of the responding PBMC population, indicating that CD4<sup>+</sup> T-helper cells may be responsible for the response. Phenotypic analysis of peripheral blood lymphocyte subsets from patients with ATP showed that there was a significant reduction in CD4<sup>+</sup>Leu8<sup>+</sup> T suppressor-inducer cells (P &lt; .001) and a concomitant increase in CD3<sup>+</sup>DR<sup>+</sup> activated T cells (P &lt; .001) and CD19<sup>+</sup> B cells (P &lt; .05). These data indicate that CD4<sup>+</sup> T-helper cells from patients with ATP are stimulated by normal platelet antigen(s) to secrete IL-2 and may modulate the enhanced antiplatelet autoantibody response.</p>}},
  author       = {{Semple, J. W. and Freedman, J.}},
  issn         = {{0006-4971}},
  language     = {{eng}},
  month        = {{01}},
  number       = {{10}},
  pages        = {{2619--2625}},
  publisher    = {{American Society of Hematology}},
  series       = {{Blood}},
  title        = {{Increased antiplatelet T helper lymphocyte reactivity in patients with autoimmune thrombocytopenia}},
  url          = {{http://dx.doi.org/10.1182/blood.V78.10.2619.2619}},
  doi          = {{10.1182/blood.V78.10.2619.2619}},
  volume       = {{78}},
  year         = {{1991}},
}