MHC Class I–Associated Peptides Identified From Normal Platelets and From Individuals With Idiopathic Thrombocytopenic Purpura

Hopkins, Leann M.; Davis, John M.; Buchli, Rico; VanGundy, Rodney S.; Schwartz, Kenneth A.; Gerlach, John

doi:10.1016/j.humimm.2005.06.004

Cited by 12 publications

(8 citation statements)

References 57 publications

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“…Specific signals were normalized to GAPDH and the average signal intensity was determined for each proteasomal subunit. Relative expression of the different donors is displayed for each protein related to the mean (donors are representative for >20 donors) [69][70][71][72][73] Activated platelets form aggregates with T cells, which most likely establish immunological synapses between these two cell types. 74 Although platelets mainly express denatured MHC class I heavy chains on their surface, which are adsorbed from plasma and cannot stimulate cytotoxic T lymphocytes (CTL)-mediated cytotoxicity, 75 especially young platelets express intact MHC class I.…”

Section: Pl Atele Ts and Their Rele Van Ce A S Immune And Immunomodmentioning

confidence: 99%

“…Increasing evidence supports the presence of a fully active MHC class I signaling system in platelets. This is based on the observation that almost all components of the APP machinery are present in platelets, albeit at different expression levels (Figures and and Table ), and by recently published data demonstrating (a) a regulatory function of platelet β2‐microglobulin on monocyte differentiation, (b) a protection of tumor cells from NK cell surveillance by transfer of platelet MHCs to tumor cells, and (c) by the presentation of MHC class I complexes loaded with peptides on platelets of normal as well as individuals with immune thrombocytopenia (ITP) …”

Section: Platelets and Their Relevance As Immune And Immunomodulatorymentioning

confidence: 99%

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Structure and function of the ubiquitin‐proteasome system in platelets

Colberg

Cammann

Greinacher

et al. 2020

Journal of Thrombosis and Haemostasis

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Platelets are small anucleate blood cells with a life span of 7 to 10 days. They are main regulators of hemostasis. Balanced platelet activity is crucial to prevent bleeding or occlusive thrombus formation. Growing evidence supports that platelets also participate in immune reactions, and interaction between platelets and leukocytes contributes to both thrombosis and inflammation. The ubiquitin‐proteasome system (UPS) plays a key role in maintaining cellular protein homeostasis by its ability to degrade non‐functional self‐, foreign, or short‐lived regulatory proteins. Platelets express standard and immunoproteasomes. Inhibition of the proteasome impairs platelet production and platelet function. Platelets also express major histocompatibility complex (MHC) class I molecules. Peptide fragments released by proteasomes can bind to MHC class I, which makes it also likely that platelets can activate epitope specific cytotoxic T lymphocytes (CTLs). In this review, we focus on current knowledge on the significance of the proteasome for the functions of platelets as critical regulators of hemostasis as well as modulators of the immune response.

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Section: Pl Atele Ts and Their Rele Van Ce A S Immune And Immunomodmentioning

confidence: 99%

Section: Platelets and Their Relevance As Immune And Immunomodulatorymentioning

confidence: 99%

Structure and function of the ubiquitin‐proteasome system in platelets

Colberg

Cammann

Greinacher

et al. 2020

Journal of Thrombosis and Haemostasis

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“…Earlier reports showed that peptides from platelet GP1b could be presented on platelet MHC-I in patients with ITP [ 153 ]. In a subsequent report, it was shown that platelets could functionally present ovalbumin (OVA) and malarial peptides to activate CD8+ T-cells [ 151 ].…”

Section: Introductionmentioning

confidence: 99%

The Immune Nature of Platelets Revisited

Maouia

Rebetz

Kapur

et al. 2020

Transfusion Medicine Reviews

142

136

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Platelets are the primary cellular mediators of hemostasis and this function firmly acquaints them with a variety of inflammatory processes. For example, platelets can act as circulating sentinels by expressing Toll-like receptors (TLR) that bind pathogens and this allows platelets to effectively kill them or present them to cells of the immune system. Furthermore, activated platelets secrete and express many pro- and anti-inflammatory molecules that attract and capture circulating leukocytes and direct them to inflamed tissues. In addition, platelets can directly influence adaptive immune responses via secretion of, for example, CD40 and CD40L molecules. Platelets are also the source of most of the microvesicles in the circulation and these miniscule elements further enhance the platelet’s ability to communicate with the immune system. More recently, it has been demonstrated that platelets and their parent cells, the MK, can also uptake, process and present both foreign and self-antigens to CD8+ T-cells conferring on them the ability to directly alter adaptive immune responses. This review will highlight several of the non-hemostatic attributes of platelets that clearly and rightfully place them as integral players in immune reactions.

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“…Major histocompatibility complex (MHC) class I human leukocyte antigen (HLA)-B7 -associated peptides identified as glycoprotein Ib have been detected on the platelet membrane in healthy individuals and ITP patients [ 11 ]. However, there is no clear evidence of an association between ITP and specific MHC class I or II polymorphism [ 11 , 17 , 18 ].…”

Section: Introductionmentioning

confidence: 99%

Association between <i>Helicobacter pylori</i> infection and platelet count in mice

et al. 2018

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Strong evidence for an association between idiopathic thrombocytopenic purpura (ITP) and Helicobacter pylori (HP) infection has been reported in humans. Chronic ITP is known to be improved by the eradication of HP. The purpose of this study was to reproduce these events by the experimental infection of several strains of mice with HP. BALB/c, C57BL/6, and DBA/2 mice were untreated or orally inoculated with HP. Two months later, platelet counts were compared in samples from HP-infected and noninfected mice. Platelet counts (mean ± SD, × 104 cells/µl) in blood samples from HP-infected BALB/c, C57BL/6, and DBA/2 mice were 102.28 ± 14.71, 99.65 ± 17.00, and 111.57 ± 16.20, respectively; the respective counts from noninfected mice were 121.80 ± 13.30, 104.35 ± 18.20, and 107.84 ± 14.33. A significant difference in platelet counts between HP-infected and noninfected mice was observed in BALB/c mice (P≤0.01) but was not observed in DBA/2 mice, even though the histocompatibility (H)-2 type of the DBA/2 was the same as that of BALB/c mice. According to ELISA results, the optical density value for the anti-HP antibody in HP-infected BALB/c mice was not correlated with the number of platelets (P>0.50). These results suggest that the decrease in platelet count caused by HP infection is not related to antibody titer and histocompatibility-2 type. Experimental infection of BALB/c mice with HP can reproduce the relationship between HP and ITP and serves as a good model to investigate the mechanistic basis for the effectiveness of HP eradication therapy for ITP treatment.

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MHC Class I–Associated Peptides Identified From Normal Platelets and From Individuals With Idiopathic Thrombocytopenic Purpura

Cited by 12 publications

References 57 publications

Structure and function of the ubiquitin‐proteasome system in platelets

Structure and function of the ubiquitin‐proteasome system in platelets

The Immune Nature of Platelets Revisited

Association between <i>Helicobacter pylori</i> infection and platelet count in mice

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