Platelets inhibit in vitro response of lymphocytes to mitogens

Niu, Jingyi

doi:10.1016/j.imlet.2008.04.003

Cited by 6 publications

(5 citation statements)

References 34 publications

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“…Previous literature has reported that platelets dynamically influence the immune system through CD154 (CD40L) mediated interactions with CD40 on T and B lymphocytes [50]–[52]. Moreover, platelets enhance IL-10 expression by immature dendritic cells, which in turn promote the proliferation of naive T cells [42].…”

Section: Discussionmentioning

confidence: 99%

Coronary Artery Remodeling in a Model of Left Ventricular Pressure Overload Is Influenced by Platelets and Inflammatory Cells

et al. 2012

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Left ventricular hypertrophy (LVH) is usually accompanied by intensive interstitial and perivascular fibrosis, which may contribute to arrhythmogenic sudden cardiac death. The mechanisms underlying the development of cardiac fibrosis are incompletely understood. To investigate the role of perivascular inflammation in coronary artery remodeling and cardiac fibrosis during hypertrophic ventricular remodeling, we used a well-established mouse model of LVH (transverse aortic constriction [TAC]). Three days after pressure overload, macrophages and T lymphocytes accumulated around and along left coronary arteries in association with luminal platelet deposition. Consistent with these histological findings, cardiac expression of IL-10 was upregulated and in the systemic circulation, platelet white blood cell aggregates tended to be higher in TAC animals compared to sham controls. Since platelets can dynamically modulate perivascular inflammation, we investigated the impact of thrombocytopenia on the response to TAC. Immunodepletion of platelets decreased early perivascular T lymphocytes' accumulation and altered subsequent coronary artery remodeling. The contribution of lymphocytes were examined in Rag1−/− mice, which displayed significantly more intimal hyperplasia and perivascular fibrosis compared to wild-type mice following TAC. Collectively, our studies support a role of early perivascular accumulation of platelets and T lymphocytes in pressure overload-induced inflammation.

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Section: Discussionmentioning

confidence: 99%

Coronary Artery Remodeling in a Model of Left Ventricular Pressure Overload Is Influenced by Platelets and Inflammatory Cells

et al. 2012

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“…Before quantification of endotoxin contamination, the recombinant proteins were heat treated (100°C, 20 min). rAtHsp81.2, rNbHsp90.3, rLiHsp83 and rTgHsp28 presented LPS contamination between 1 and 5 ng/ml, a concentration well below what is needed for mitogen proliferation [51], [52]. However, when splenocytes were stimulated with the recombinant proteins, 2 µg/ml polymyxin B sulphate (PX; Sigma) was added to the culture to abolish any possibility of LPS induced proliferation.…”

Section: Methodsmentioning

confidence: 99%

Plant Hsp90 Proteins Interact with B-Cells and Stimulate Their Proliferation

et al. 2011

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BackgroundThe molecular chaperone heat shock protein 90 (Hsp90) plays an important role in folding stabilization and activation of client proteins. Besides, Hsp90 of mammals and mammalian pathogens displays immunostimulatory properties. Here, we investigated the role of plant-derived Hsp90s as B-cell mitogens by measuring their proliferative responses in vitro.MethodologyPlant cytosolic Hsp90 isoforms from Arabidopsis thaliana (AtHsp81.2) and Nicotiana benthamiana (NbHsp90.3) were expressed in E. coli. Over-expression of recombinant plant Hsp90s (rpHsp90s) was confirmed by SDS-PAGE and western blot using and anti-AtHsp81.2 polyclonal anti-body. Both recombinant proteins were purified by Ni-NTA affinity chromatography and their identity confirmed by MALDI-TOF-TOF. Recombinant AtHsp81.2 and NbHsp90.3 proteins induced prominent proliferative responses in spleen cells form BALB/c mice. Polymyxin-B, a potent inhibitor of lipopolysaccharide (LPS), did not eliminate the rpHsp90-induced proliferation. In addition, in vitro incubation of spleen cells with rpHsp90 led to the expansion of CD19-bearing populations, suggesting a direct effect of these proteins on B lymphocytes. This effect was confirmed by immunofluorescence analysis, where a direct binding of rpHsp90 to B- but not to T-cells was observed in cells from BALB/c and C3H/HeN mice. Finally, we examined the involvement of Toll Like Receptor 4 (TLR4) molecules in the rpHsp90s induction of B-cell proliferation. Spleen cells from C3H/HeJ mice, which carry a point mutation in the cytoplasmic region of TLR4, responded poorly to prAtHsp90. However, the interaction between rpHsp90 and B-cells from C3H/HeJ mice was not altered, suggesting that the mutation on TLR4 would be affecting the signal cascade but not the rpHsp90-TLR4 receptor interaction.ConclusionsOur results show for the first time that spleen cell proliferation can be stimulated by a non-pathogen-derived Hsp90. Furthermore, our data provide a new example of a non-pathogen-derived ligand for TLRs.

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“…Platelets have been demonstrated in vitro to decrease CD4 T‐cell proliferation in response to antigen stimulation, showing that platelets may also operate as an anti‐inflammatory agent by reducing the immune response. 12 , 14 There is a scarcity of data on the immunomodulatory effects of platelets or megakaryocytes in the genesis of ITP. Many studies have reported that only approximately 60% of ITP patients showed positive platelet antibody detection 15 , 16 with T helper 1/T helper 2 (Th1/Th2) cell subsets disequilibrium, 17 suggesting that T cell abnormality plays a vital role in the occurrence of ITP.…”

Section: Introductionmentioning

confidence: 99%

“…As a result, platelets play a role in the first (innate) host defense. Platelets have been demonstrated in vitro to decrease CD4 T‐cell proliferation in response to antigen stimulation, showing that platelets may also operate as an anti‐inflammatory agent by reducing the immune response 12,14 . There is a scarcity of data on the immunomodulatory effects of platelets or megakaryocytes in the genesis of ITP.…”

Section: Introductionmentioning

confidence: 99%

Role of IL‐10 and IL‐22 cytokines in patients with primary immune thrombocytopenia and their clinical significance

Liu

2022

Clinical Laboratory Analysis

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Background Immune thrombocytopenia purpura (ITP) is an autoimmune disease that leads to accelerated platelet clearance. The objective of this study was to examine the clinical role of cytokines in ITP patients and to correlate them with disease stages. Materials and Methods A total of 110 ITP patients were enrolled, including 55 with active ITP, 55 with remission ITP, and 55 with healthy controls. The enzyme‐linked immunosorbent assay technique was used to examine IL‐10 and IL‐22 serum levels in all subjects. Real‐time quantitative PCR was used to assess the mRNA expression of IL‐10 and IL‐22 in PBMC. The clinical significance of both cytokines was assessed using ROC analysis. Results IL‐10 serum levels in active ITP patients were significantly lower than in control and remission ITP subjects (p < 0.05). IL‐22 serum levels were elevated in active ITP patients compared to the control and remission group (p < 0.05). mRNA expressions of IL‐10 and IL‐22 in active ITP patients were also having a significant difference from than control and remission ITP group (p < 0.05). ROC analysis showed that IL‐10 and IL‐22 can differentiate the ITP patients from controls. A positive correlation between serum IL‐10 and PBMC IL‐10 with statistical significance was observed. Similarly, the serum IL‐22 and PBMC IL‐22 were correlated positively with statistical significance. Conclusion IL‐10 and IL‐22 seem to predict the clinical course of ITP, as a significant imbalance of these cytokines was detected in active ITP patients.

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Platelets inhibit in vitro response of lymphocytes to mitogens

Cited by 6 publications

References 34 publications

Coronary Artery Remodeling in a Model of Left Ventricular Pressure Overload Is Influenced by Platelets and Inflammatory Cells

Coronary Artery Remodeling in a Model of Left Ventricular Pressure Overload Is Influenced by Platelets and Inflammatory Cells

Plant Hsp90 Proteins Interact with B-Cells and Stimulate Their Proliferation

Role of IL‐10 and IL‐22 cytokines in patients with primary immune thrombocytopenia and their clinical significance

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