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)

The property of adherence to nylon wool was used to separate and characterize pig blood lymphocyte subpopulations. Thymus-dependent null cells proved the least adherent lymphocytes, and B cells, bearing surface Ig or Fc receptor, the most adherent. sIg+ lymphocytes detected by immunofluorescence and by 51Cr release cytotoxicity showed similar frequency and adherence properties. Lymphocytes rosetting with SRBC in PBS or in dextran had similar adherence patterns and showed both non-adherent and adherent components. Lymphocytes bearing major histocompatibility complex (MHC) Ia-like antigens shown by eosin exclusion or 51Cr release cytotoxicity were enriched in the adherent fraction, but also occurred in significant numbers in the non-adherent fraction. Non-adherent Ia+ cells were predominantly sIg- and probably T cells, whereas the adherent Ia+ group included the sIg+ cells and some sIg- cells.
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PMID:Characterization of pig lymphocyte subpopulations by adherence to nylon wool. 37 27

Circulating immune complexes are considered to have a profound effect on host defense mechanisms against invading pathogens and to modulate cellular interactions required for an appropriate course of the immune response. In this study we have investigated the influence of polymeric IgG (used as a model system for immune complexes) on accessory functions of human monocytes. We show that a short (1 hr) incubation of human monocytes in the presence of polymeric IgG (16 hr prior to antigen pulsing) led to a significant decrease of these cells' antigen-presenting capacity while accessory functions in alloantigen- or mitogen-driven proliferation systems remained unimpaired. The polymeric IgG-induced impairment of antigen presentation, which was assessed by diminished proliferation of antigen-reactive T cells following stimulation by antigen-pulsed polymeric IgG-treated or Dulbecco's phosphate-buffered saline (PBS-D)-treated control monocytes, could not be attributed to the generation of suppressor mechanisms (no release of soluble suppressor factors, no induction of suppressive monocytes). The release of interleukin-1 by polymeric IgG-treated monocytes and PBS-D-treated monocytes was comparable and polymeric IgG did not down modulate major histocompatibility complex (MHC) class II molecules already expressed in the monocyte plasma membrane. Profound changes in the monocyte plasma membrane occurring subsequent to polymeric IgG treatment possibly accompanied by altered kinetics of MHC class II reexpression are likely to contribute to the observed decrease of antigen presentation.
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PMID:Effect of polymeric IgG on human accessory cell function. 293 62

We tested whether the in vivo infusion of recombinant, soluble CTLA4 fused with Ig heavy chains, as a surrogate ligand used to block CD28/CTLA4 T-cell costimulation, could prevent efficient T-cell activation and thereby reduce graft-versus-host disease (GVHD). Lethally irradiated B10.BR recipients of major histocompatibility complex disparate C57BL/6 donor grafts received intraperitoneal injections of human CTLA4-Ig (hCTLA4-Ig) or murine CTLA4-Ig (mCTLA4-Ig) in various doses and schedules beginning on day -1 or day 0 of bone marrow transplantation (BMT). In all five experiments, recipients of CTLA4-Ig had a significantly higher actuarial survival rate compared to mice injected with an irrelevant antibody control (L6) or saline alone. Survival rates in recipients of hL6 or PBS were 0% at 29 to 45 days post-BMT. In recipients of CTLA4-Ig, survival rates were as high as 63% mice surviving 3 months post-BMT. However, protection was somewhat variable and recipients of CTLA4-Ig were not GVHD-free by body weight, clinical appearance, and histopathologic examination. There were no significant differences in the survival rates in comparing injection dose, injection duration, or species of CTLA4-Ig (hCTLA4-Ig v mCTLA4-Ig). Splenic and peripheral blood flow cytometry studies of long-term hCTLA4-Ig-injected survivors showed a significant peripheral B-cell and CD4+ T-cell lymphopenia, consistent with GVHD. A kinetic study of splenic reconstitution was performed in mice that received hCTLA4-Ig and showed that mature splenic localized CD8+ T-cell repopulation was not significantly different in recipients of hCTLA4-Ig compared with hL6, despite the significant increase in actuarial survival rate in that experiment. These data suggest that the beneficial effect of hCTLA4-Ig on survival is not mediated by interfering with mature donor-derived T-cell repopulation post-BMT. Neither hCTLA4-Ig nor mCTLA4-Ig interfered with hematopoietic recovery post-BMT. We conclude that CTLA4-Ig (most likely in combination with other agents) may represent an important new modality for GVHD prevention.
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PMID:In vivo blockade of CD28/CTLA4: B7/BB1 interaction with CTLA4-Ig reduces lethal murine graft-versus-host disease across the major histocompatibility complex barrier in mice. 751 23

An improved method of removing rat corneal endothelial sheets for study of endothelial pathology is described. The method was validated by examining morphological changes and changes in expression of major histocompatibility complex (MHC) and intercellular adhesion molecule (ICAM)-1 on endothelium undergoing immunological rejection. PVG strain rats received LEW strain corneal transplants or corneal isografts. Just prior to and during graft rejection, animals were killed, together with a group of untreated animals. The corneal stroma was injected with dispase or PBS, the cornea was carefully removed, fixed in acetone and the endothelium was gently peeled off and flattened on to a glass slide. Morphological changes, together with MHC class I, class II and ICAM-1 expression were visualised by immuno-histochemical staining and quantified by image analysis. Near complete endothelial sheets were obtained by this method. Because of the thin cell layer, there was minimal background staining, permitting rejection-associated changes to be clearly seen. MHC class I expression on normal endothelium was low and not significantly increased on endothelial cells of allografts at the time of rejection compared with controls (P = 0.1). MHC class II and ICAM-1 were induced de novo, expression being significantly higher on allografts than on isografts (P = 0.004 for MHC class II and P = 0.01 for ICAM-1). MHC class I and II and ICAM-1 were expressed on many infiltrating cells. Thus, this preparation method permits clear identification of the distribution and morphology of infiltrating cells and other mediators of the immune response in the entire donor endothelium. It confirms that MHC class I expression is low during rejection, while MHC class II and ICAM-I are induced de novo and strongly expressed.
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PMID:An improved method for examining the corneal endothelium during graft rejection in the rat. 999 Mar 27

We previously found that an extracellular polysaccharide, AC-1, produced by Acetobacter polysaccharogenes composed of (1,4)-beta-D-glucan with branches of glucosyl residues showed a strong activity to induce production of interleukin (IL)-12 p40 and tumor necrosis factor-alpha by macrophage cell lines in vitro via Toll-like receptor-4 signaling. In the present study, we examined the effects of oral administration of AC-1 on protection against 2 types of murine B16 melanoma lines, major histocompatibility complex (MHC) class I-negative B16L and MHC class I gene-transfected B16K(b) cells. Mice were inoculated subcutaneously with B16L or B16K(b) cells on day 0 and administrated intragastrically with AC-1 or PBS once every 5 days from 1 day before tumor inoculation. The tumor growth was severely retarded in AC-1-treated mice after subcutaneous inoculation with B16L or B16K(b) cells. The AC-1-treated mice showed augmented natural killer (NK) cell activity against B16L cells, and in vivo depletion of NK cells by antiasialoGM1 antibody (Ab) treatment abrogated the antitumor activity in AC-1-treated mice. On the other hand, AC-1-treated mice inoculated with B16K(b) cells developed a significantly higher level of cytotoxic T-lymphocyte response against B16K(b) cells, and in vivo depletion of CD8(+) T cells by anti-CD8 mAb treatment abrogated the antitumor activity. Thus, AC-1 augmented antitumor activity against different tumors via augmentation of different antitumor mechanisms. These results suggest a possible prophylactic application of AC-1 for human neoplasms irrespective of expression levels of their MHC class I molecules.
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PMID:Soluble branched (1,4)-beta-D-glucans from Acetobacter species enhance antitumor activities against MHC class I-negative and -positive malignant melanoma through augmented NK activity and cytotoxic T-cell response. 1572 92

We evaluated the usefulness of fusion vaccine prepared from IL-2-gene-transduced splenic dendritic cells (DCs) and fibrosarcoma tumor cells (QRsP) in treating of lung metastasis. The IL-2 or LacZ gene was transferred into spleen-derived DCs using an adenoviral vector. Irradiated QRsP tumor cells were fused with IL-2 gene transduced DCs (fusion/IL-2) or LacZ gene transduced DCs (fusion/LacZ) by polyethyleneglycol. These fusion cells expressed major histocompatibility complex (MHC) class I and MHC class II, CD86, CD11c and CD8alpha. IFN-gamma and cytotoxic T lymphocyte (CTL) activity of splenic lymphocytes in mice vaccinated with fusion cells increased significantly as compared with those of DC or tumor cells vaccinated mice. CTL levels in fusion/IL-2-vaccinated mice were higher than that in fusion/LacZ-vaccinated mice. The number of lung metastasis in the fusion/IL-2 or fusion/LacZ-vaccineatd mice was significantly lower than that in mice vaccinated with DCs, tumor or PBS. The introduction of the IL-2 gene into fusion cells produced more potent therapeutic effects. Our results suggest that the fusion cells prepared from IL-2 gene transduced spleen derived DCs and tumor cells have the ability to induce therapeutic effect against lung metastasis.
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PMID:[Fusion vaccine therapy by IL-2-gene-transduced dendritic cells and tumor cells]. 1631 76

The vomeronasal organ (VNO) has evolved to link an animal's behavior to its environment in a highly species-specific fashion. In mice, it is thought to be the primary sensory system responsible for the detection of pheromones. Pheromones regulate a variety of responses including mate recognition in the context of selective pregnancy failure. MHC (major histocompatibility complex) class I peptides have been identified as compounds that elicit the pregnancy block effect via the VNO. However, the transduction cascade of these molecules is unknown and it is not known if the production of these compounds are androgen dependent. By using male urine and MHC peptides, we show that female mice treated with MHC peptides (in urine or PBS) and urine from castrated males or juvenile mice of different haplotypes respond to the Bruce Effect paradigm in a manner equivalent to female mice exposed to whole urine. In addition to providing new evidence that urine from castrated or juvenile males and MHC peptides can induce pregnancy block, we show correlation of the effect with an increase in inositol 1,4,5-trisphosphate.
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PMID:Pregnancy block by MHC class I peptides is mediated via the production of inositol 1,4,5-trisphosphate in the mouse vomeronasal organ. 1740 Nov 23

The aim of the present study was to assess genes expressed in maternal uterine tissue and pre-implantation embryos which are presumably involved in maternal recognition and establishment of canine pregnancy. For this purpose, 10 pregnant bitches were ovariohysterectomized between days 10 and 12 after mating. Four non-pregnant bitches served as controls. Early pregnancy was verified by flushing the uterine horns with PBS solution. The collected embryos (n = 60) were stored deep-frozen (-80 degrees C). Uterine tissue was excised, snaps frozen in liquid nitrogen and homogenized using TRI Reagent. All embryos from one litter were thawed together and also homogenized in TRI Reagent. RT-PCR was performed to prove mRNA expression of progesterone receptor, key enzymes of the prostaglandin synthesis pathway, selected growth factors, cytokines, immune cell receptors, major histocompatibility complex (MHC) and matrix-metalloproteinases (MMP). Only pregnant uteri revealed the presence of mRNA for interferon (IFN)-gamma, IL-4 and CD-8, which resembles the milieu in humans and other mammalians. Similarly, in day 10 embryos, mRNA for transforming growth factor-beta, insulin-like growth factor-1,-2, hepatocyte growth factor, leukaemia inhibitor factor, tumour necrosis factor-alpha, interleukin-1beta,-6,-8, cyclooxygenase-2, CD4(+) cells, and MMP-2 and -9 were detected, but not MHC-I or -II. We therefore suppose that the canine embryo, like its human counterpart, actively initiates measures to prevent attacks from the maternal immune system to prepare its own adhesion, nidation, growth and further development.
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PMID:Expression of genes in the canine pre-implantation uterus and embryo: implications for an active role of the embryo before and during invasion. 1839 90

Host antidonor effector T cells represent a major barrier to the successful engraftment of allogeneic donor hematopoietic progenitor and stem cells. Here, administration of a complex of IL-2 and anti-IL 2 antibodies (IAC) significantly enhanced donor chimerism early as well as long-term engraftment following reduced-intensity conditioning (RIC) and allogeneic major histocompatibility complex (MHC)-matched hematopoietic cell transplantion (HCT). Timing of administration of this complex was crucial: administration of IAC post-HCT more efficiently facilitated marrow engraftment than pre-HCT treatment. Donor chimerism persisted to >6 months post-HCT. Importantly, this approach clearly suppressed the emergence of host antidonor CD8 T cells 2 to 3 weeks post-HCT as assessed by tetramer staining. Following in vivo reactivation of IAC-treated and control recipients at >5 months post-HCT with donor antigen, only PBS-treated control marrow allograft recipients responded with tetramer-binding CD8 cells. In total, the present findings support the notion that the transient activation and expansion of host Tregs in situ post-HCT can be explored as a new approach to regulate host alloreactivity posttransplant. Interestingly, direct stimulation of recipient Treg cells in RIC recipients obviated a requirement for exogenous Treg cell transfusion in this model and may represent a viable alternative to, and/or complement the adaptive transfer of Treg populations in clinical HCT.
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PMID:In situ activation and expansion of host tregs: a new approach to enhance donor chimerism and stable engraftment in major histocompatibility complex-matched allogeneic hematopoietic cell transplantation. 1953 9

FVE is a documented immunomodulatory protein purified from Enoki mushroom (Flammulina velutipes) and known as an activator for human T lymphocytes. This present study was aimed to investigate the anti-tumor effect and the related mechanisms of oral administration of FVE using a murine hepatoma model. Oral administration of FVE (10mg/kg) significantly increased the life span and inhibited the tumor size of BNL 1MEA.7R.1 (BNL) hepatoma-bearing mice. Tumor-bearing mice receiving oral FVE treatment had the highest tumoricidal capacity of peritoneal macrophages and tumor-specific splenocytes against BNL hepatoma cells. In addition, in vivo neutralization of interferon-gamma (IFN-gamma) demonstrated a significant decrease of FVE-induced anti-tumor effect (P<0.05). The expression levels of major histocompatibility complex (MHC) class I and II molecules and costimulatory molecule CD80 on peripheral blood mononuclear cells obtained from the FVE-treated mice were upregulated as compared with those of the PBS-treated mice. Furthermore, immunohistochemical staining showed a strong inhibition of tumor growth and angiogenesis in hepatoma tissues after oral administration of FVE. Taken together, oral administration of FVE displayed anti-tumor activity through activating both innate and adaptive immunity of the host to prime a cytotoxic immune response and IFN-gamma played a key role in the anti-tumor efficacy of FVE.
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PMID:Oral administration of an Enoki mushroom protein FVE activates innate and adaptive immunity and induces anti-tumor activity against murine hepatocellular carcinoma. 1990 27


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