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Distinct Mechanisms of CD4+ and CD8+ T-Cell Activation and Bystander Apoptosis Induced by Human Immunodeficien cy Virus Type 1 Virions: J. Virol., Vol. 79, No. 10. (15 May 2005), pp. 6299-6311.Apop tosis of uninfected bystander T cells contributes to T-cell depletion during human immunodeficien cy virus type 1 (HIV-1) infection. HIV-1 envelope/recep tor interactions and immune activation have been implicated as contributors to bystander apoptosis. To better understand the relationship between T-cell activation and bystander apoptosis during HIV-1 pathogenesis, we investigated the effects of the highly cytopathic CXCR4-tropic HIV-1 variant ELI6 on primary CD4+ and CD8+ T cells. Infection of primary T-cell cultures with ELI6 induced CD4+ T-cell depletion by direct cell lysis and bystander apoptosis. Exposure of primary CD4+ and CD8+ T cells to nonreplicating ELI6 virions induced bystander apoptosis through a Fas-independen t mechanism. Bystander apoptosis of CD4+ T cells required direct contact with virions and Env/CXCR4 binding. In contrast, the apoptosis of CD8+ T cells was triggered by a soluble factor(s) secreted by CD4+ T cells. HIV-1 virions activated CD4+ and CD8+ T cells to express CD25 and HLA-DR and preferentially induced apoptosis in CD25+HLA-DR+ T cells in a CXCR4-dependen t manner. Maximal levels of binding, activation, and apoptosis were induced by virions that incorporated MHC class II and B7-2 into the viral membrane. These results suggest that nonreplicating HIV-1 virions contribute to chronic immune activation and T-cell depletion during HIV-1 pathogenesis by activating CD4+ and CD8+ T cells, which then proceed to die via apoptosis. This mechanism may represent a viral immune evasion strategy to increase viral replication by activating target cells while killing immune effector cells that are not productively infected.Geoff rey Holm, Dana Gabuzda

Source: J. Virol., Vol. 79, No. 10. (15 May 2005), pp. 6299-6311.
Progress in solid oxide fuel cell materials: International Materials Reviews, Vol. 50, No. 5. (October 2005), pp. 257-264.K Kendall

Source: International Materials Reviews, Vol. 50, No. 5. (October 2005), pp. 257-264.
Mechanisms of Disease: cancer stem cells[mdash]ta rgeting the evil twin: Nat Clin Prac Oncol, Vol. 5, No. 6. (June 2008), pp. 337-347.Cancer stem cells often represent a minor, highly self-renewing population within the tumor mass and are thought to be the only cells required for both initiation and maintenance of disease. The biology of cancer stem cells, the mechanisms of therapy resistance, and potential future therapeutic interventions in the clinical setting are discussed.Andr eas Trumpp, Otmar Wiestler

Source: Nat Clin Prac Oncol, Vol. 5, No. 6. (June 2008), pp. 337-347.
Prolactin, dendritic cells, and systemic lupus erythematosus: Autoimmunity Reviews, Vol. 7, No. 3. (January 2008), pp. 251-255.Dendri tic cells (DC) play a central role in the induction of autoimmunity in T and B cells. DC express a high level of the major histocompatibi lity complex that interact with the receptors on T cells. Immature DC present antigens efficiently. Prolactin (PRL) participates in DC maturation. Systemic lupus erythematosus (SLE) is characterized by a loss of tolerance to self-antigens and persistent production of autoantibodies . Serum from SLE patients induces normal monocytes to differentiate into DC in correlation with disease activity depending on the actions of interferon-&#x 3b1;, immune complexes, PRL, etc. High serum PRL levels have been found in a subset of SLE patients associated with active disease and organ involvement. It is possible that PRL interacts with DC, skewing its function from antigen presentation to a proinflammator y phenotype with high interferon-&#x 3b1; production. Therefore, SLE is characterized by deficiency of DC functions and abnormal PRL secretion. The relationships between PRL and DC may have a role in the pathogenesis of SLE.L Jara, G Benitez, G Medina

Source: Autoimmunity Reviews, Vol. 7, No. 3. (January 2008), pp. 251-255.
In Vivo Induction of Immune Responses to Pathogens by Conventional Dendritic Cells: Immunity, Vol. 29, No. 3. (19 September 2008), pp. 343-351.Specif ic defense mechanisms against pathogens are fulfilled by different subsets of nonmucosal conventional dendritic cells (DCs), including migratory Langerhans cells (LCs), dermal DCs, and resident CD8+ and CD8? DCs found in lymphoid organs. Dermal DCs capture antigens in the skin and migrate to lymph nodes, where they can transfer the antigens to CD8+ DCs and activate CD4+ T cells. Differential antigen-proces sing machinery grants CD8+ DCs a high efficiency in activating CD8+ T cells through crosspresentat ion, whereas CD8? DCs preferentially trigger CD4+ T cell responses. Recent findings have revealed the important role played by monocyte-deriv ed DCs (mo-DCs), newly formed during infection, in activating CD4+ and CD8+ T cells, regulating immunoglobulin production, and killing pathogens. However, a number of controversial issues regarding the function of different DC subsets during viral, bacterial, and parasitic infections remain to be resolved.M Lopezbravo, C Ardavin

Source: Immunity, Vol. 29, No. 3. (19 September 2008), pp. 343-351.
TRACP Influences Th1 pathways by affecting dendritic cell function.: Journal of bone and mineral research : the official journal of the American Society for Bone and Mineral Research, Vol. 21, No. 9. (September 2006), pp. 1367-1376.TRAC P, a marker of osteoclasts, is also expressed by cells of the immune system. We identified a novel function for TRACP in the dendritic cell. DCs from TRACP knockout mice have impaired maturation and trigger reduced Th1 responses in vivo. We postulate that TRACP has an important role in the presentation of antigens to T cells. INTRODUCTION: TRACP is highly expressed by osteoclasts, activated macrophages, and dendritic cells (DCs). Knockout mice lacking TRACP have an intrinsic defect in osteoclastic resorption and macrophages that display abnormal immunomodulato ry responses and cytokine secretion profiles. Our aim in this study was to investigate the significance of TRACP in the inductive phase of the immune response by examining dendritic cells from TRACP(-/-) mice. MATERIALS AND METHODS: Maturational state and function of leukocyte subsets in mice was assessed by flow cytometry. The ability of the immune system to respond to nonspecific activation and to specific antigen was assessed by delayed type hypersensitivi ty and the presence of isotype-specif ic serum antibody in vivo and T-cell proliferation and cytokine production in vitro. RESULTS: The ability of lipopolysaccha ride (LPS) to upregulate MHC II and CD80 in DCs from TRACP(-/-) mice was reduced compared with wildtype mice, although production of IL-10 by DCs from TRACP-deficien t animals was increased. T- and B-cell responses not involving antigen presentation (anti-CD3, TNP-ficoll) were normal in TRACP(-/-) mice, but responses to T-dependent antigens were impaired. Specifically, TRACP(-/-) mice had defective delayed hypersensitivi ty responses to picryl chloride and reduced proliferative responses to ovalbumin compared with wildtype mice. In response to ovalbumin, but not anti-CD3, T cells from TRACP(-/-) mice produced less interferon-gam ma (IFN-gamma), but there was no difference in IL-4 production: TRACP(-/-) mice also produced less ovalbumin (OVA)-specific IgG2a after immunization. CONCLUSIONS: The finding that DCs from TRACP(-/-) mice have impaired maturation and defective Th1 responses shows that TRACP is important for polarizing responses in naďve T cells to antigen-presen ted dendritic cells.E Esfandiari, M Bailey, CR Stokes, TM Cox, MJ Evans, AR Hayman

Source: Journal of bone and mineral research : the official journal of the American Society for Bone and Mineral Research, Vol. 21, No. 9. (September 2006), pp. 1367-1376.
The direct molecular analysis of metastatic precursor cells in breast cancer: A chance for a better understanding of metastasis and for personalised medicine.: European journal of cancer (Oxford, England : 1990) (18 November 2008)The search for disseminated cancer cells has become a routine procedure in many clinical centres since the pioneering work of Riethmüller and Schlimok was published in the mid 1980s. Until today, clinical studies have mostly focused on the prognostic role of disseminated cancer cells that can be detected in bone marrow samples before manifestation of metastasis. As a more recent development, the field is increasingly concentrating on the prognostic information provided by tumour cells circulating in the peripheral blood instead of analysing the nature of disseminated tumour cells that have successfully homed to a new microenvironme nt and may eventually grow into metastases. This review critically questions that direction and proposes exploiting the unique opportunities provided by the direct molecular analysis of metastatic precursor cells for a better understanding of metastasis, tumour dormancy, therapy target identification , and personalised medicine in an adjuvant therapy setting.Christ oph A Klein

Source: European journal of cancer (Oxford, England : 1990) (18 November 2008)
BRG1-Mediated Chromatin Remodeling Regulates Differentiatio n And Gene Expression Of T Helper Cells.: Molecular and cellular biology (13 October 2008)During T helper cell differentiatio n, distinct programs of gene expression play a key role in defining the immune response to an environmental challenge. How chromatin remodeling events at the associated cytokine loci control differentiatio n is not known. We found that the ATP-dependent remodeling enzyme subunit BRG1 was required for T helper 2 (Th2) differentiatio n and Th2 cytokine transcription. BRG1 binding to cytokine genes was regulated by the extent of differentiatio n, the extent of activation and cell fate. BRG1 was required for some features of the chromatin structure in target genes (DNase I hypersensitivi ty and histone acetylation), suggesting that BRG1 remodeling activity was directly responsible for changes in gene expression. NFAT and STAT6 activity were required for BRG1 recruitment to the Th2 LCR, and STAT6 associated with BRG1 in a differentiatio n-inducible manner, suggesting direct recruitment of BRG1 to the bound loci. Together, these findings suggest BRG1 interprets differentiatio n signals and plays a causal role in gene regulation, chromatin structure, and cell fate.Andrea L Wurster, Michael J Pazin

Source: Molecular and cellular biology (13 October 2008)
Influence of the estrous cycle on the presence and distribution of immune cells in the rat reproductive tract.: American journal of reproductive immunology (New York, N.Y. : 1989), Vol. 39, No. 3. (March 1998), pp. 209-216.PROBLE M: Previous studies have shown that the uterus and vagina contain cells that can present antigen to ovalbumin-spec ific T-cells. The objective of the present study was to systematically characterize the immune cells [major histocompatibi lity complex (MHC) class-II+, macrophages, granulocytes, dendritic cells, and CD8+ cells] present in the uterus and vagina of the rat and to examine their distribution at various stages of the estrous cycle. METHOD OF STUDY: Uterine and vaginal tissues from female rats were selected at various stages of the estrous cycle and were examined by immunohistoche mical analysis. MHC class-II (Ia)-positive cells were detected using the OX-6 monoclonal antibody; macrophages, granulocytes, and dendritic cells were detected by OX-41 monoclonal antibody and CD8-positive T-cells were identified by OX-8 monoclonal antibody. RESULTS: Immunohistoche mical analysis showed cycle-dependen t changes in the immune cell populations in the uterus and vagina. Ia+ cells, macrophages, granulocytes, and dendritic cells were present in large numbers in the stroma of the endometrium and around the glandular epithelium in the uterus at estrus, the stage of the reproductive cycle when estradiol levels are known to be high, relative to those seen at diestrus, when estrogen levels are low and progesterone is the predominant hormone. CD8+ cells were observed in the uterus interspersed between glandular epithelial cells at estrus. Immune cells were more numerous in the vagina, relative to the uterus. OX-6 and OX-41-positive cells were present in greater numbers in the subepithelial layers of the vagina at diestrus, in contrast to estrus. CONCLUSION: This study demonstrates that a variety of immune cells are present in the reproductive tract and that their number and distribution vary in a tissue-specifi c manner with the stage of the estrous cycle.C Kaushic, E Frauendorf, RM Rossoll, JM Richardson, CR Wira

Source: American journal of reproductive immunology (New York, N.Y. : 1989), Vol. 39, No. 3. (March 1998), pp. 209-216.
Environmental estrogens induce mast cell degranulation and enhance IgE-mediated release of allergic mediators.: Environmental health perspectives, Vol. 115, No. 1. (January 2007), pp. 48-52.BACKGROU ND: Prevalence and morbidity of allergic diseases have increased over the last decades. Based on the recently recognized differences in asthma prevalence between the sexes, we have examined the effect of endogenous estrogens on a key element of the allergic response. Some lipophilic pollutants have estrogen-like activities and are termed environmental estrogens. These pollutants tend to degrade slowly in the environment and to bioaccumulate and bioconcentrate in the food chain; they also have long biological half-lives. OBJECTIVES: Our goal in this study was to identify possible pathogenic roles for environmental estrogens in the development of allergic diseases. METHODS: We screened a number of environmental estrogens for their ability to modulate the release of allergic mediators from mast cells. We incubated a human mast cell line and primary mast cell cultures derived from bone marrow of wild type and estrogen receptor alpha (ER-alpha)-def icient mice with environmental estrogens with and without estradiol or IgE and allergens. We assessed degranulation of mast cells by quantifying the release of beta-hexosamin idase. RESULTS: All of the environmental estrogens tested caused rapid, dose-related release of beta-hexosamin idase from mast cells and enhanced IgE-mediated release. The combination of physiologic concentrations of 17beta-estradi ol and several concentrations of environmental estrogens had additive effects on mast cell degranulation. Comparison of bone marrow mast cells from ER-alpha-suffi cient and ER-alpha-defic ient mice indicated that much of the effect of environmental estrogens was mediated by ER-alpha. CONCLUSIONS: Our findings suggest that estrogenic environmental pollutants might promote allergic diseases by inducing and enhancing mast cell degranulation by physiologic estrogens and exposure to allergens.S Narita, RM Goldblum, CS Watson, EG Brooks, DM Estes, EM Curran, T Midoro-Horiuti

Source: Environmental health perspectives, Vol. 115, No. 1. (January 2007), pp. 48-52.

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