Journal
CELLULAR IMMUNOLOGY
Volume 351, Issue -, Pages -Publisher
ACADEMIC PRESS INC ELSEVIER SCIENCE
DOI: 10.1016/j.cellimm.2020.104096
Keywords
Immune thrombocytopenia; Platelet; Th1 cell; Th2 cell; Th17 cell; Th22 cell; Th9 cell; Treg; Tfh cell
Categories
Funding
- Ministry of Education, Science and Technological Development of the Republic of Serbia [41018]
- Medical Faculty of Nis, University of Nis, Serbia [30]
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Immune thrombocytopenia (ITP) is an autoimmune disorder characterized by low platelet counts due to enhanced platelet clearance and compromised production. Traditionally, ITP was regarded a B cell mediated disorder as anti-platelet antibodies are detected in most patients. The very nature of self-antigens, evident processes of isotype switching and the affinity maturation of anti-platelet antibodies indicate that B cells in order to mount anti-platelet immune response require assistance of auto-reactive CD4(+) T cells. For a long time, ITP pathogenesis has been exclusively reviewed through the prism of the disturbed balance between Th1 and Th2 subsets of CD4(+) T cells, however, more recently new subsets of these cells have been described including Th17, Th9, Th22, T follicular helper and regulatory T cells. In this paper, we review the current understanding of the role and immunological mechanisms by which CD4(+) T cells contribute to the pathogenesis of ITP.
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