Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P30536 (PBS)
 9,886 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We review our methods for definition and phenotypical characterisation of normal and activated rat monocytes. To obtain a comprehensive sample of all blood monocytes including cells from the marginal pool of the blood stream, we extensively perfuse the extrapulmonary circulation with cold PBS/EDTA. Normal rat monocytes are isolated from untreated specified pathogen-free male LEW rats. In vivo activated monocytes are investigated after three days of infusion of recombinant IFN-gamma or during acute renal allograft rejection. Rat monocytes are defined by reactivity with mAbs ED1 and ED9, detecting a lysosomal membrane antigen and a member of the signal-regulatory protein family, respectively, as well as by expression of CD11b. Concomitantly rat monocytes are characterized by the absence of CD5, the absence of the B cell form of CD45R, and the absence of reactivity with mAb RP-1. The majority of the monocytes from untreated LEW rats are CD4+, CD11a(high), CD18high, CD43high, CD62-L-, CD161-, and MHC class II-. Upon stimulation of the immune system in vivo, a second monocyte population increases in number. These cells have a larger diameter and an increased granularity. They are CD4-, CD11a(int), CD18int, CD43low, CD62-L+, CD161int, and MHC class II+. Although some reagents are not yet available (e.g. antibodies against rat CD14 and CD16), rat monocytes can be defined and their state of activation can be characterized. The functionally important population of monocytes, which have already marginated, is accessible by perfusion and relatively high monocyte numbers are isolated per rat. As specified pathogen-free rats are available and numerous experimental systems involving acute or chronic inflammation have been established in rats, differentially activated monocytes may be investigated. The rat is thus a suitable experimental animal for basic research on monocytes.
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PMID:Monocytes in the rat. 1087 93

Renal transplantation is the treatment of choice for end-stage renal failure. Although acute rejection is not a major issue anymore, chronic rejection, especially vascular rejection, is still a major factor that might lead to allograft dysfunction on the long term. The role of the local immune-regulating cytokine interleukin-10 (IL-10) in chronic renal allograft is unclear. Many clinical observations showed that local IL-10 level was negatively related to kidney allograft function. It is unknown this negative relationship was the result of immunostimulatory property or insufficient immunosuppression property of local IL-10. We performed ex vivo transduction before transplantation through artery of the renal allograft using adeno-associated viral vectors carrying IL-10 gene. Twelve weeks after transplantation, we found intrarenal IL-10 gene transduction significantly inhibited arterial neointimal proliferation, the number of occluded intrarenal artery, interstitial fibrosis, peritubular capillary congestion and glomerular inflammation in renal allografts compared to control allografts receiving PBS or vectors carrying YFP. IL-10 transduction increased serum IL-10 level at 4 weeks but not at 8 and 12 weeks. Renal IL-10 level increased while serum creatinine decreased significantly in IL-10 group at 12 weeks compared to PBS or YFP controls. Immunohistochemical staining showed unchanged total T cells (CD3) and B cells (CD45R/B220), decreased cytotoxic T cells (CD8), macrophages (CD68) and increased CD4+ and FoxP3+ cells in IL-10 group. In summary, intrarenal IL-10 inhibited the allograft rejection while modulated immune response.
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PMID:Transduction of interleukin-10 through renal artery attenuates vascular neointimal proliferation and infiltration of immune cells in rat renal allograft. 2731 47

Dendritic cells (DCs) are specialized antigen-presenting cells that play a pivotal role in the pathogenesis of periodontitis. The use of animal models to study the role of DCs in periodontitis has been limited by lack of a method for sustained depletion of DCs. Hence, the objectives of this study were to validate the zDC-DTR knockin mouse model of conventional DCs (cDCs) depletion, as well as to investigate whether this depletion could be sustained long enough to induce alveolar bone loss in this model. zDC-DTR mice were treated with different dose regimens of diphtheria toxin (DT) to determine survival rate. A loading DT dose of 20ng/bw, followed and maintained with doses of 10ng/bm every 3days for up to 4weeks demonstrated 80% survival. Animals were weighed weekly and peripheral blood was obtained to confirm normal neutrophil counts. Five animals per group were euthanized at baseline, 24h, 1 and 4weeks. Bone marrow (BM), spleen (SP) and gingival tissue (GT) were harvested, and cells were isolated, separated and stained for Pre-DCs precursors (CD45R-MHCII+CD11c+Flt3+CD172a+) in BM, cDCs (CD11c+MHCII+CD209+) in spleen, and DCs in GT (CD45R+MHCII+CD11c+ DC-SIGN/CD209+). Pre-DCs in BM were significantly depleted at 24h and depletion maintained for up to 4weeks, as compared to blank (PBS) controls. Circulating cDCs in spleen demonstrated a non-significant trend to deplete in 1week with high variability among mice. GT also showed a similar non-significant trend to deplete in 24h. The zDC-DTR model seems to be viable for evaluating the role of DCs immune homeostasis disruption and alveolar bone loss pathogenesis in response to long-term oral infection.
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PMID:Long-term sustainable dendritic cell-specific depletion murine model for periodontitis research. 2864 28