2013
DOI: 10.1016/j.thromres.2013.04.025
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Involvement of levels of Toll like receptor-4 in monocytes, CD4+ T-lymphocyte subsets, and cytokines in patients with immune thrombocytopenic purpura

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Cited by 31 publications
(17 citation statements)
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“…% than those with other genotypes. This reflects a state of TH1 polarization in childhood ITP as previously shown . This bias even returning to a dominant TH1 response was demonstrated in relapsed patients after corticosteroid treatment .…”
Section: Discussionsupporting
confidence: 80%
“…% than those with other genotypes. This reflects a state of TH1 polarization in childhood ITP as previously shown . This bias even returning to a dominant TH1 response was demonstrated in relapsed patients after corticosteroid treatment .…”
Section: Discussionsupporting
confidence: 80%
“…Previous study demonstrated that IL-23 can be induced by Toll-like receptor (TLR) agonists and interactions with T cells (CD40/CD40L interaction) [ 24 ]. Liu et al found that TLR4 was abnormal expression in ITP patients and demonstrated that TLR4 in combination with FcγRII could cause DCs to express cytokines IL-23 then promote effector Th17 cell responses [ 25 ]. These may suggest that the elevated of IL-23 may cause by abnormal TLR, but the exact mechanism need further study.…”
Section: Discussionmentioning
confidence: 99%
“…Indeed, ITP is considered a Th1/Th17 type of disease . Investigators have shown that ITP is associated with an increase in Th1‐ and Th17‐cell cytokine profiles, including IL‐2, IL‐16, IL‐17, and IFN‐γ . Also, because it has previously been reported that there are strain‐specific differences in responses to IVIG in mouse models, we evaluated cytokine profiles in two different mouse strains, BALB/c and C57BL/6J (B6), commonly used for these experimental studies.…”
Section: Discussionmentioning
confidence: 99%
“…In human ITP, patients have extravascular‐mediated destruction of autoantibody‐sensitized platelets (PLTs) as well as impaired production of PLTs . This condition is associated with an inflammatory state that is manifest by increased Th17 and Th1 cells and increased production of proinflammatory cytokines including interleukin (IL)‐1α, IL‐2, IL‐6, IL‐16, IL‐17, IL‐23, and interferon (IFN)‐γ 17‐26. The majority of published mouse models of human ITP use passive administration of a rat monoclonal PLT antibody to initiate and maximize the thrombocytopenia.…”
mentioning
confidence: 99%