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Query: UMLS:C0432222 (SEM)
 47,337 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Endothelial cells serve an important role in augmenting immune responses through enhanced expression of MHC class II antigens. Immune-mediated vascular injury associated with rejection requires reendothelialization to restore vascular integrity. The origin of the reparative endothelial cells can be determined when ABO antigens expressed on these cells differ in the donor and recipient. To assess the frequency and significance of reendothelialization by recipient endothelial cells, we stained serial endomyocardial biopsies for ABO antigens in 34 (13%) compatible, nonidentical cardiac allograft recipients of 268 cardiac transplant procedures. In ten (30%) the allograft endothelial cells expressed the characteristics of the recipient (five partial and five complete) within 7.5 +/- 1.0 months (mean +/- SEM) after transplantation. Over 26.3 +/- 2.5 months follow-up no differences could be detected in pretransplant characteristics, allograft survival, survivor rejection morbidity, long-term allograft function, and presence of coronary vasculopathy between those whose endothelial cells expressed recipient blood group antigens and those who did not, which may merely be a reflection of the small sample size. This study indicates that recipient reendothelialization occurs frequently following cardiac transplantation and may result from immune-mediated vascular injury. The effect of recipient reendothelialization on allograft tolerance requires further investigation.
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PMID:Detection of allograft endothelial cells of recipient origin following ABO-compatible, nonidentical cardiac transplantation. 199 40

The effect of iC3b receptor (CR3)-mediated phagocytosis on the expression of CR (C3b receptor, CR3) and IgG FcR (FcRI, FcRII) has been investigated by using serum-opsonized zymosan as a multivalent ligand for CR3. Sixteen hours after a short (1-h) pretreatment of human monocyte monolayers with zymosan opsonized with human AB serum (250 micrograms/ml), CR3 expression (as assessed by flow cytometric analysis with mAb Mo1) was significantly reduced by 59 +/- 3% (mean +/- SEM, n = 15, p less than 0.001). Concomitant with CR3 down modulation, FcR binding activity (as assessed by binding of IgG-coated E) was also found to be decreased to 41 +/- 4% of control (n = 7, p less than 0.001). Reduced FcR function was paralleled by a decrease in the expression of FcRI (as assessed with mAb 32.2). This FcRI modulation was not caused by zymosan-bound IgG because zymosan opsonized with agammaglobulinemic serum equally down regulated CR3 and FcRI expression. Pretreatment with zymosan opsonized with human AB serum, however, did not change the expression of other IgG and C-binding sites such as FcRII (examined with mAb IV.3 and 2E1) and CR1 (assessed with mAb 57F) as well as of unrelated cell membrane structures (beta 2m, MHC class II). In contrast, co-modulation for FcR function and CR3 expression induced by polymeric IgG is accompanied by a decreased expression of FcRII. These data indicate that interaction of a specific receptor with its ligand not only changes the expression of the receptor triggered, but has also a modulating effect on other receptor systems on the same cell.
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PMID:Phagocytosis of serum-opsonized zymosan down-regulates the expression of CR3 and FcRI in the membrane of human monocytes. 297 75

Expression of major histocompatibility (MHC) class II molecules by enterocytes is known to be enhanced in coeliac disease and other disorders characterised by intestinal inflammation--an effect thought to be mediated via intestinal lymphocytes. To investigate if food peptides can exert direct effects on class II expression, the influence of gliadins, casein, and beta lactoglobulin on an intestinal epithelial cell line (HT-29) was examined in the absence of immune cells. Class II expression was determined by flow cytometry and immunofluorescence microscopy using antibodies against the beta chain of all products of the gene subregions DR, DQ, and DP. MHC expression was low in HT-29 cells but could be stimulated by interferon gamma. Tryptin digested gliadin had no effect on class II expression. In the presence of interferon gamma, however, it was able to amplify MHC class II expression to mean (SEM) 150 (4)%. Casein exerted a similar effect (160 (14)%), but undigested gliadin, tryptin digested casein, and beta lactoglobulin had no influence. The observations suggest that within the concert of cytokine mediated interactions between enterocytes and lymphocytes, some dietary peptides could upregulate the presentation of food antigens, leading to a more efficient stimulation of lymphocytes, which in the case of coeliac disease might result in damage to the enterocytes.
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PMID:Effect of gliadin and other food peptides on expression of MHC class II molecules by HT-29 cells. 773 62

Analysis of apoptosis in the human adrenal appears to be of eminent importance in the understanding of adrenal structure, zonation, and function. In this study we investigated the programmed cell death of normal adrenal tissues on the basis of apoptotic index by the nonradioactive in situ end labeling of DNA fragments, proliferating cell nuclear antigen, (PCNA), CD95 (cluster of differentiation), major histocompatibility complex class II immunohistochemistry, and ultrastructural analysis. The highest apoptotic index was detected in the outermost zones of the adrenal cortex, mainly in the zona glomerulosa. A labeling index of 50.46 +/- 5.22% (mean +/- SEM) for zona glomerulosa, 9.36 +/- 1.68% for zona fasciculata, 3.90 +/- 0.78% for zona reticularis, and 7.37 +/- 1.62% for the zona medullaris was found. Immunohistochemistry was used to distinguish between apoptotic and S phase cells. Positive anti-PCNA staining occurred in the inner cortical zones, whereas anti-CD95 signals appeared throughout the whole cortex, albeit at a much weaker level. MHC class II expression, which is known to be associated with programmed cell death, was demonstrated in the inner cortical zone. The data showed that mechanisms of cell death other than necrosis occur in the adrenal. In conclusion, we found a differential regulation of cell death for each zone of the adrenal cortex; the old theories of adrenal zonation (migrational vs. zonal or transformation theory) may, in fact, correlate with each other.
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PMID:Differential regulation of apoptosis in the normal human adrenal gland. 892 71

We have hypothesized that T cell cytokines participate in the pathogenesis of graft arterial disease (GAD). This study tested the consequences of IFN-gamma deficiency on arterial and parenchymal pathology in murine cardiac allografts. Hearts from C-H-2(bm12)KhEg (bm12, H-2(bm12)) were transplanted into C57/B6 (B6, H-2(b)), wild-type, or B6 IFN-gamma-deficient (GKO) recipients after immunosuppression by treatment with anti-CD4 and anti-CD8 mAbs. In wild-type recipients, myocardial rejection peaked at 4 wk, (grade 2. 1+/-0.3 out of 4, mean+/-SEM, n = 9), and by 8-12 wk evolved coronary arteriopathy. At 12 wk, the GAD score was 1.4+/-0.3, and the parenchymal rejection grade was 1.2+/-0.3 (n = 8). In GKO recipients of bm12 allografts, myocardial rejection persisted at 12 wk (grade 2.5+/-0.3, n = 6), but no GAD developed (score: 0.0+/-0.0, n = 6, P < 0.01 vs. wild-type). Mice treated with anti-IFN-gamma mAbs showed similar results. Isografts generally showed no arterial changes. In wild-type recipients, arterial and parenchymal cells showed increased MHC class II molecules, intercellular adhesion molecule-1, and vascular cell adhesion molecule-1 compared to normal or isografted hearts. The allografts in GKO recipients showed attenuated expression of these molecules (n = 6). Thus, development of GAD, but not parenchymal rejection, requires IFN-gamma. Reduced expression of MHC antigens and leukocyte adhesion molecules may contribute to the lack of coronary arteriopathy in hearts allografted into GKO mice.
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PMID:Interferon-gamma deficiency prevents coronary arteriosclerosis but not myocardial rejection in transplanted mouse hearts. 923 1

Major histocompatibility complex (MHC) class II antigens are expressed on adrenocortical cells of the zona reticularis and have been shown to be a marker of dignity. This suggests a correlation to the zellular differentiation of the adrenal cortex. Therefore, we immunohistochemically investigated the MHC class II expression in the context of the ontogenesis of the zonal and cellular differentiation in fetal, postnatal, childhood, and adult adrenals. Cell types and cell turnover were studied using specific immune markers (including expression of CD95/ Fas), in situ end labeling of apoptosis, and electron microscopy. We show that prenatal (fetal and definitive) steroid cells, as well as postnatal adrenals, reveal no expression of MHC class II. In childhood, these antigens first appear by the fourth year, in parallel with the differentiation of reticularis cells. The expression index in childhood was 7.43% +/- 2.78 (mean +/- SEM), in adult adrenals 18.63% +/- 3.14 (third decade), and 15.15% +/- 1.26 (fourth through sixth decade). In conclusion, MHC class II expression and the development of the functional maturation of the adult adrenal cortex occur simultaneously. The expression of MHC class II on steroid cells may thus be involved in potential immune-adrenal interactions.
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PMID:Relevance of major histocompatibility complex class II expression as a hallmark for the cellular differentiation in the human adrenal cortex. 928 58

During primary varicella-zoster virus (VZV) infection, it is presumed that virus is transmitted from mucosal sites to regional lymph nodes, where T cells become infected. The cell type responsible for VZV transport from the mucosa to the lymph nodes has not been defined. In this study, we assessed the susceptibility of human monocyte-derived dendritic cells to infection with VZV. Dendritic cells were inoculated with the VZV strain Schenke and assessed by flow cytometry for VZV and dendritic cell (CD1a) antigen expression. In five replicate experiments, 34.4% +/- 6.6% (mean +/- SEM) of CD1a(+) cells were also VZV antigen positive. Dendritic cells were also shown to be susceptible to VZV infection by the detection of immediate-early (IE62), early (ORF29), and late (gC) gene products in CD1a(+) dendritic cells. Infectious virus was recovered from infected dendritic cells, and cell-to-cell contact was required for transmission of virus to permissive fibroblasts. VZV-infected dendritic cells showed no significant decrease in cell viability or evidence of apoptosis and did not exhibit altered cell surface levels of major histocompatibility complex (MHC) class I, MHC class II, CD86, CD40, or CD1a. Significantly, when autologous T lymphocytes were incubated with VZV-infected dendritic cells, VZV antigens were readily detected in CD3(+) T lymphocytes and infectious virus was recovered from these cells. These data provide the first evidence that dendritic cells are permissive to VZV and that dendritic cell infection can lead to transmission of virus to T lymphocytes. These findings have implications for our understanding of how virus may be disseminated during primary VZV infection.
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PMID:Varicella-zoster virus infection of human dendritic cells and transmission to T cells: implications for virus dissemination in the host. 1139 Jun 20

Bacterial superantigens (SAgs) are enterotoxins that bind to MHC-II and TCR molecules, activating as much as 20% of the T cell population and promoting a cytokine storm which enhances susceptibility to endotoxic shock, causing immunosuppression, and hindering the immune response against bacterial infection. Since monocytes/macrophages are one of the first cells SAgs find in infected host and considering the effect these cells have on directing the immune response, here, we investigated the effect of four non-classical SAgs of the staphylococcal egc operon, namely, SEG, SEI, SEO, and SEM on monocytic-macrophagic cells, in the absence of T cells. We also analyzed the molecular targets on APCs which could mediate SAg effects. We found that egc SAgs depleted the pool of innate immune effector cells and induced an inefficient activation of monocytic-macrophagic cells, driving the immune response to an impaired proinflammatory profile, which could be mediated directly or indirectly by interactions with MHC class II. In addition, performing surface plasmon resonance assays, we demonstrated that non-classical SAgs bind the gp130 molecule, which is also present in the monocytic cell surface, among other cells.
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PMID:egc Superantigens Impair Monocytes/Macrophages Inducing Cell Death and Inefficient Activation. 3201 Jan 28