Purified protein derivative of tuberculin upregulates the expression of vascular endothelial growth factor in T lymphocytes <i>in vitro</i>

Matsuyama, Wataru; Hashiguchi, Teruto; Momi, Hiroaki; Kawabata, Masaharu; Nakagawa, Masanori; Arimura, Kimiyoshi; Osame, Mitsuhiro

doi:10.1046/j.1365-2567.2002.01395.x

Cited by 20 publications

(13 citation statements)

References 20 publications

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“…An acapsular strain appeared to be a better inducer than did an encapsulated strain. Finally, lymphocytes might contribute to VEGF secretion after antigen presentation via monocyte MHC class II, as was previously described for tuberculin-stimulated VEGF secretion by PBMCs [48]. From our results obtained with the MHC class II antibody, we determined that antigen presentation is responsible for the additive effect in VEGF release seen in PBMCs, compared with isolated monocytes and lymphocytes.…”

Section: Discussionmentioning

confidence: 64%

Intrathecal Production and Secretion of Vascular Endothelial Growth Factor during Cryptococcal Meningitis

et al. 2004

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Section: Discussionmentioning

confidence: 64%

Intrathecal Production and Secretion of Vascular Endothelial Growth Factor during Cryptococcal Meningitis

et al. 2004

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“…Since VEGF-A has been shown to be directly involved in mobilization of MSCs from the bone marrow (Pitchford et al, 2009) and CD4 pos T cells are able to produce VEGF-A upon activation (Matsuyama et al, 2002), we also determined the levels of VEGF-A in these supernatants. Even though detectable levels of VEGF-A could be measured, we did not observe increased VEGF-A levels in bone marrow samples derived from EAE mice when compared to controls, which could account for the mobilization of MSCs (Figure 3C).…”

Section: Resultsmentioning

confidence: 99%

“…Remarkably, systemic increase of IFN-y levels could not be measured in these mice suggesting that the action of IFN-y on MSCs is mediated when T cells and MSCs are in close proximity. In addition, upon activation, T cells are able to produce VEGF-A (Matsuyama et al, 2002). Whether VEGF-A production by activated T is under the influence of IFN-y and abrogated in CD70TG/IFN-y −/− is unknown but could explain the lack of mobilization in these mice, despite an active T cell compartment.…”

Section: Discussionmentioning

confidence: 99%

Mesenchymal stem cells are mobilized from the bone marrow during inflammation

Koning¹,

Kooij²,

Vries³

et al. 2013

Front. Immunol.

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Mesenchymal stem cells (MSCs) show great therapeutic potential for the treatment of various immune mediated diseases, including Multiple Sclerosis (MS). Systemic administration of MSCs during experimental allergic encephalomyelitis (EAE), an animal model for MS, was shown to reduce the infiltration of T cells, B cells, and macrophages into the CNS. Whether endogenous MSCs are mobilized and potentially modulate the severity of disease is not known. Here we show that during the acute phase of EAE, MSCs numbers in the bone marrow were severely reduced, which restored to control levels during the progressive phase of the disease. The number of bone marrow MSCs inversely correlated with the number of both CD4 and CD8 T cells present in the bone marrow indicating a link between activated T cells and MSC mobilization. Analysis of CD70-transgenic mice, which have a constitutively activated immune system and elevated number of activated T cells in the bone marrow, showed severely reduced number of bone marrow MSCs. Transfer of T cells that were activated through their CD27 receptor reduced the number of bone marrow MSCs dependent on IFN-y. These data provide a mechanism by which MSCs can be mobilized from the bone marrow in order to contribute to tissue repair at a distant location.

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“…A greater viral load may also lead to the exaggerated activation of both innate and adaptive immunity. In particular, T cells have been shown to produce VEGF, and VEGF has been reported to induce IFN-␥ production by T lymphocytes (30,32). Activation of dengue virus-reactive memory T cells that cross-recognize another dengue virus serotype may therefore contribute to the elevated VEGF and IFN-␥ levels observed in DHF patients.…”

Section: Discussionmentioning

confidence: 99%

Virus-Induced Decline in Soluble Vascular Endothelial Growth Receptor 2 Is Associated with Plasma Leakage in Dengue Hemorrhagic Fever

Srikiatkhachorn

Ajariyakhajorn

Endy

et al. 2007

J Virol

140

139

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Some individuals infected with dengue virus develop dengue hemorrhagic fever (DHF), a viral hemorrhagic disease characterized by a transient period of localized plasma leakage. To determine the importance of vascular endothelial growth factor A (VEGF-A) in this syndrome, we compared plasma levels of VEGF-A and the soluble forms of its receptors in patients with DHF to patients with dengue fever (DF), a milder form of dengue virus infection without plasma leakage. We observed a rise in the plasma levels of free, but not total VEGF-A in DHF patients at the time of plasma leakage. This was associated with a decline in the soluble form of VEGF receptor 2 (VEGFR2) and VEGF-soluble VEGFR2 complexes, but not the soluble form of VEGFR1. The severity of plasma leakage in patients inversely correlated with plasma levels of soluble VEGFR2. In vitro, dengue virus suppressed soluble VEGFR2 production by endothelial cells but up-regulated surface VEGFR2 expression and promoted response to VEGF stimulation. In vivo, plasma viral load correlated with the degree of decline in plasma soluble VEGFR2. These results suggest that VEGF regulates vascular permeability and its activity is controlled by binding to soluble VEGFR2. Dengue virus-induced changes in surface and soluble VEGFR2 expression may be an important mechanism of plasma leakage in DHF.

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Purified protein derivative of tuberculin upregulates the expression of vascular endothelial growth factor in T lymphocytes in vitro

Cited by 20 publications

References 20 publications

Intrathecal Production and Secretion of Vascular Endothelial Growth Factor during Cryptococcal Meningitis

Intrathecal Production and Secretion of Vascular Endothelial Growth Factor during Cryptococcal Meningitis

Mesenchymal stem cells are mobilized from the bone marrow during inflammation

Virus-Induced Decline in Soluble Vascular Endothelial Growth Receptor 2 Is Associated with Plasma Leakage in Dengue Hemorrhagic Fever

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