排序方式: 共有29条查询结果,搜索用时 15 毫秒
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Gille C Spring B Bernhard W Gebhard C Basile D Lauber K Poets CF Orlikowsky TW 《Journal of lipid research》2007,48(2):307-317
Blood monocyte-derived macrophages invading the alveolus encounter pulmonary surfactant, a phospholipoprotein complex that changes composition during lung development. We tested the hypothesis that characteristic phosphatidylcholine (PC) components differentially influence macrophage phenotype and function, as determined by phagocytosis of green fluorescent protein-labeled Escherichia coli and alphaCD3-induced T cell proliferation. Human macrophages were exposed to surfactant (Curosurf(R)), to two of its characteristic phosphadidylcholine (PC) components (dipalmitoyl-PC and palmitoylmyristoyl-PC), and to a ubiquituous PC (palmitoyloleoyl-PC) as control. Interaction of Curosurf and PC species with macrophages was assessed using Lissaminetrade mark-dihexadecanoyl-phosphoethanolamine-labeled liposomes. Curosurf and both saturated surfactant PC species downregulated CD14 expression and upregulated CD206. HLA-DR and CD80 were upregulated by Curosurf and palmitoylmyristoyl-PC, whereas dipalmitoyl-PC showed no effect. The latter upregulated TLR2 and TLR4 expression, whereas Curosurf and palmitoylmyristoyl-PC had no effect. PC species tested were incorporated in comparable amounts by macrophages. Curosurf and PC species inhibited phagocytosis of E. coli. Scavenger receptor CD36, CD68, SR-A, and LOX-1 mRNA expression was upregulated by Curosurf, whereas PC species only upregulated SR-A. Curosurf and palmitoylmyristoyl-PC inhibited alphaCD3-induced T cell proliferation by 50%, whereas dipalmitoyl-PC and palmitoyloleoyl-PC showed no effect. These data identify individual surfactant PC species as modifiers of macrophage differentiation and suggest differential effects on innate and adaptive immune functions. 相似文献
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G T Brice A E Mayne K Leighton F Villinger J S Allan A A Ansari 《Journal of medical primatology》1999,28(2):49-56
Dysfunction of T lymphocytes is well documented in HIV-1-infected individuals; however, the mechanisms responsible for the noted dysfunction are not well understood. CD40L is an important costimulatory molecule that helps initiate immune responses, and there is controversy regarding whether or not expression of CD40L is compromised in HIV-1-infected individuals. We have utilized the SIV infection of experimentally infected (disease-susceptible) and naturally infected (disease-resistant) nonhuman primates as animal models of human AIDS to address this issue. Little is known concerning the expression of CD40L in nonhuman primates. Studies were conducted to determine the frequency, density, phenotype, and kinetics of CD40L expression by in vitro activated peripheral blood mononuclear cells (PBMCs) from different species of uninfected and SIV-infected monkeys. Data obtained show marked differences in the density and phenotypic lineage that expresses CD40L in lymphoid cells from the three species examined. However, no detectable differences were noted in the frequency and density of CD40L expression by in vitro activated lymphoid cells from uninfected and SIV-infected disease-susceptible rhesus macaques and seropositive as compared to seronegative disease-resistant sooty mangabeys. These data suggest that phenotypic expression of CD40L is not compromised due to SIV infection. 相似文献
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Whereas B7-1/B7-2 and CD28/cytotoxic T lymphocyte-associated antigen-4 (CTLA-4) serve as the main switches regulating the
clonal composition of activated naive T cells, other B7 family members fine-tune the expansion and properties of activated
T cells. Inducible costimulatory molecule (ICOS)-B7h promotes T-dependent antibody isotype switching and expansion of effector
cells. Effector T cells trafficking into inflamed tissues interact with antigen-presenting cells there and are regulated by
PD-1 and its ligands. B7-H3 and B7x could control the interaction between effector T cells and the peripheral tissues. The
different varieties of regulatory T cells could regulate both naive T cell activation and effector function through costimulatory
receptor/ligands. 相似文献
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Dendritic cells are innate sentinels of the immune system and potent activators of naÏve T cells. Mechanisms must exist to enable these cells to achieve maximal activation of T cells specific for microbial antigens, while avoiding activation of T cells specific for self‐antigens. Here we discuss how a combination of signals from pattern recognition receptors and T cells co‐ordinates subcellular trafficking of antigen with both major histocompatibility complex class I and class II molecules and T‐cell costimulatory molecules, resulting in the preferential presentation of microbial peptides within a stimulatory context. 相似文献
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Cbl family ubiquitin ligases act as key negative regulators of TCR signaling. Knockout mice lacking Cbl-b and c-Cbl show augmented T cell activation and CD28-independent IL-2 production. In order to study Cbl function directly in post-thymic T cells, a DN Cbl adenovirus was generated for transduction of T cells from Coxsackie/adenovirus receptor (CAR) transgenic (Tg) mice. We show that dominant negative (DN) Cbl-transduced CD4+ T cells exhibited enhanced IL-2 production upon TCR/CD28 engagement compared with empty adenoviral vector-transduced cells. This augmentation was reflected at both IL-2 mRNA and protein level, and correlated with increased protein phosphorylation of Vav, Akt, ERK, and p38MAPK. Our results indicate that introduction of dominant negative Cbl can potentiate activation of post-thymic CD4+ T cells, which argues for development of strategies to interfere with Cbl function as a method of immunopotentiation. 相似文献
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