RESUMO
Most high-affinity phosphate transporter genes (OsPTs) in rice were highly induced in roots when phosphate was depleted. OsPT1, however, was highly expressed in primary roots and leaves regardless of external phosphate concentrations. This finding was confirmed histochemically using transgenic rice plants that express the GUS reporter gene under the control of the OsPT1 promoter, which exhibited high GUS activity even in the phosphate sufficient condition. Furthermore, transgenic rice plants overexpressing the OsPT1 gene accumulated almost twice as much phosphate in the shoots as did wild-type plants. As a result, transgenic plants had more tillers than did wild-type plants, which is a typical physiological indicator for phosphate status in rice.
Assuntos
Oryza/genética , Proteínas de Transporte de Fosfato/genética , Fosfatos/metabolismo , Sequência de Bases , Northern Blotting , Primers do DNA , Genes Reporter , Oryza/metabolismo , Proteínas de Transporte de Fosfato/metabolismo , Plantas Geneticamente Modificadas/genética , Plantas Geneticamente Modificadas/metabolismo , Regiões Promotoras GenéticasRESUMO
B7-H1 and B7-DC expressed on antigen-presenting cells inhibit the T-cell response via the PD-1 counter-receptor on T cells, and co-stimulate T-cell immunity under certain conditions via an unidentified co-stimulatory receptor. However, little is known about the functional consequence of T-cell-associated B7-H1 or B7-DC in the T-cell immune response. Therefore, we evaluated the physiological role of B7-H1 and B7-DC expressed on T cells in terms of cell proliferation and cytokine production by alloreactive T cells. We found that PD-1, B7-H1, and B7-DC were up-regulated in alloreactive CD4(+) and CD8(+) T cells in vitro and in vivo. In the alloreactive T-T model, blockade of the B7-H1:PD-1 or B7-DC:PD-1 pathways significantly increased the proliferation, and IFN-gamma and IL-2 production of alloreactive T cells, although it did not affect the production of other cytokines, including IL-4, IL-10, and IL-12. The data indicate that T-cell-associated B7-H1 and B7-DC negatively regulate the T-cell response via the T-T interaction.
Assuntos
Antígeno B7-1/imunologia , Citocinas/metabolismo , Glicoproteínas de Membrana/imunologia , Peptídeos/imunologia , Linfócitos T/imunologia , Animais , Antígenos de Diferenciação/biossíntese , Antígenos de Diferenciação/genética , Antígenos de Diferenciação/imunologia , Antígenos de Superfície/genética , Antígenos de Superfície/imunologia , Antígeno B7-1/biossíntese , Antígeno B7-1/genética , Antígeno B7-1/metabolismo , Antígeno B7-H1 , Proliferação de Células , Glicoproteínas de Membrana/metabolismo , Camundongos , Camundongos Endogâmicos BALB C , Camundongos Endogâmicos C57BL , Peptídeos/metabolismo , Proteína 2 Ligante de Morte Celular Programada 1RESUMO
The co-signaling molecule B7-H1 (CD274) functions as both a co-inhibitor through programmed death-1 (PD-1) receptor and a co-stimulator via an as-yet-unidentified receptor on T cells. We investigated the physiological role of endogenous B7-H1 in the pathogenesis of herpetic stromal keratitis (HSK) caused by herpes simplex virus type 1 (HSV-1). Following HSV-1 infection of the cornea of mice, B7-H1 expression was up-regulated in the CD11b+ macrophage population in the draining lymph nodes (dLN) and in the inflamed cornea. In addition, HSV-1 infection significantly increased PD-1 expression on CD4+ T cells in the dLN and inflamed cornea. The administration of antagonistic B7-H1 monoclonal antibody resulted in the proliferation of HSV-specific CD4+ T cells that secreted interferon (INF)-gamma, and inhibited the apoptosis of HSV-specific CD4+ T cells, which exaggerated HSK. These results strongly suggest that the B7-H1 may be involved in suppression of the development of HSK.