Clinical features and major histocompatibility complex genes as potential susceptibility factors in pediatric immune thrombocytopenia

Ho, Wan‐Ling; Lu, Meng-Yao; Hu, Fu‐Chang; Lee, Chin-Cheng; Huang, Li‐Min; Jou, Shiann-Tarng; Lin, Dong‐Tsamn; Lin, Kai‐Hsin

doi:10.1016/j.jfma.2011.06.025

Cited by 4 publications

(2 citation statements)

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“…Polymorphisms in genes encoding specific cyto- or chemokines, such as interleukin (IL)-1, IL-2, IL-4, IL-6, IL-10, IL-17, TNF-α, TGF-β, and IFN-γ, have been associated with ITP ( 33 – 37 ). Several studies have also investigated whether specific HLA class I or II alleles are elevated in patients with ITP ( 38 – 45 ); current findings suggest that polymorphic sites within the HLA locus are not linked to ITP as studies have reported both significant and nonsignificant findings ( 37 – 44 ). The variation in studies could potentially be explained by small sample size, ethnic variability, or differences in diagnosis, yet does not allow to reach a consensus.…”

Section: Introductionmentioning

confidence: 87%

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Emerging Concepts in Immune Thrombocytopenia

et al. 2018

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Immune thrombocytopenia (ITP) is an autoimmune disease defined by low platelet counts which presents with an increased bleeding risk. Several genetic risk factors (e.g., polymorphisms in immunity-related genes) predispose to ITP. Autoantibodies and cytotoxic CD8+ T cells (Tc) mediate the anti-platelet response leading to thrombocytopenia. Both effector arms enhance platelet clearance through phagocytosis by splenic macrophages or dendritic cells and by induction of apoptosis. Meanwhile, platelet production is inhibited by CD8+ Tc targeting megakaryocytes in the bone marrow. CD4+ T helper cells are important for B cell differentiation into autoantibody secreting plasma cells. Regulatory Tc are essential to secure immune tolerance, and reduced levels have been implicated in the development of ITP. Both Fcγ-receptor-dependent and -independent pathways are involved in the etiology of ITP. In this review, we present a simplified model for the pathogenesis of ITP, in which exposure of platelet surface antigens and a loss of tolerance are required for development of chronic anti-platelet responses. We also suggest that infections may comprise an important trigger for the development of auto-immunity against platelets in ITP. Post-translational modification of autoantigens has been firmly implicated in the development of autoimmune disorders like rheumatoid arthritis and type 1 diabetes. Based on these findings, we propose that post-translational modifications of platelet antigens may also contribute to the pathogenesis of ITP.

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Section: Introductionmentioning

confidence: 87%

“…As of yet, the target peptides expressed on MHC class I recognized by platelet specific CD8 + Tc have not been identified. Interestingly, no clear HLA association is found in ITP patients ( 38 – 45 ), as opposed to other autoimmune diseases. In H. pylori -mediated ITP, HLA associations were also unclear ( 114 , 164 ).…”

Section: Etiologymentioning

confidence: 93%