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Immunity Commons™

Open Access. Powered by Scholars. Published by Universities.®

2006

Articles 1 - 5 of 5

Full-Text Articles in Immunity

Characterization Of Host Cell Death Induced By Chlamydia Trachomatis, Songmin Ying, Silke F. Fischer, Matthew A. Pettengill, Debye Conte, Stefan A. Paschen, David M. Ojcius, Georg Hacker Nov 2006

Characterization Of Host Cell Death Induced By Chlamydia Trachomatis, Songmin Ying, Silke F. Fischer, Matthew A. Pettengill, Debye Conte, Stefan A. Paschen, David M. Ojcius, Georg Hacker

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Chlamydia are obligate intracellular bacteria that modulate apoptosis of the host cell. Strikingly, chlamydial infection has been reported both to inhibit and to induce apoptosis. Although the ability to inhibit apoptosis has been corroborated by the identification of cellular targets, confirmation of cell death induction has been complicated by a mixture of apoptotic features and atypical cell death during infection, as well as by differences in the experimental techniques used to measure cell death. Here we use a panel of well-established approaches in the study of apoptosis to define the form of cell death induced by Chlamydia trachomatis infection. Infected …

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Recruitment Of Bad By The Chlamydia Trachomatis Vacuole Correlates With Host-Cell Survival, Philippe Verbeke, Lynn Welter-Stahl, S. Ying, J. Hansen, Georg Hacker, Toni Darville, David M. Ojcius May 2006

Recruitment Of Bad By The Chlamydia Trachomatis Vacuole Correlates With Host-Cell Survival, Philippe Verbeke, Lynn Welter-Stahl, S. Ying, J. Hansen, Georg Hacker, Toni Darville, David M. Ojcius

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Chlamydiae replicate intracellularly in a vacuole called an inclusion. Chlamydial-infected host cells are protected from mitochondrion-dependent apoptosis, partly due to degradation of BH3-only proteins. The host-cell adapter protein 14-3-3β can interact with host-cell apoptotic signaling pathways in a phosphorylation-dependent manner. In Chlamydia trachomatis-infected cells, 14-3-3β co-localizes to the inclusion via direct interaction with a C. trachomatis-encoded inclusion membrane protein. We therefore explored the possibility that the phosphatidylinositol-3 kinase (PI3K) pathway may contribute to resistance of infected cells to apoptosis. We found that inhibition of PI3K renders C. trachomatis-infected cells sensitive to staurosporine-induced apoptosis, which is accompanied by mitochondrial cytochrome c …

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Fms-Like Tyrosine Kinase 3 Ligand Recruits Plasmacytoid Dendritic Cells To The Brain, James Curtin, Gwendalyn King, Carlos Barcia, Chunyan Liu, Francois Hubert, Carole Guillonneau, Regis Josien, Ignacio Anegon, Pedro Lowenstein, Maria Castro Mar 2006

Fms-Like Tyrosine Kinase 3 Ligand Recruits Plasmacytoid Dendritic Cells To The Brain, James Curtin, Gwendalyn King, Carlos Barcia, Chunyan Liu, Francois Hubert, Carole Guillonneau, Regis Josien, Ignacio Anegon, Pedro Lowenstein, Maria Castro

Articles

The lack of professional afferent APCs in naive brain parenchyma contributes to the systemic immune ignorance to Ags localized exclusively within the brain. Dendritic cells (DCs) appear within the brain as a consequence of inflammation, but no molecular mechanisms accounting for this influx have been described. In this study we demonstrate that Fms-like tyrosine kinase 3 ligand (Flt3L) recruits plasmacytoid DCs (pDCs; >50-fold; p < 0.001) to the brain parenchyma. These pDCs expressed IFN-alpha, the hallmark cytokine produced by pDCs, indicating recruitment and activation in situ of bona fide pDCs within the brain parenchyma. Flt3L did not increase the numbers of conventional DCs, macrophages, or B, T, NK, NKT, or microglial cells within the brain. Our data demonstrate that Flt3L reconstitutes a crucial afferent component of the immune response, namely, professional APCs within the brain parenchyma, and this could counteract the intrinsic systemic immune ignorance to Ags localized exclusively within the brain.

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Intercellular Spreading Of Porphyromonas Gingivalis Infection In Primary Gingival Epithelial Cells, Özlem Yilmaz, Philippe Verbeke, Richard J. Lamont, David M. Ojcius Jan 2006

Intercellular Spreading Of Porphyromonas Gingivalis Infection In Primary Gingival Epithelial Cells, Özlem Yilmaz, Philippe Verbeke, Richard J. Lamont, David M. Ojcius

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Porphyromonas gingivalis, an important periodontal pathogen, is an effective colonizer of oral tissues. The organism successfully invades, multiplies in, and survives for extended periods in primary gingival epithelial cells (GECs). It is unknown whether P. gingivalis resides in the cytoplasm of infected cells throughout the infection or can spread to adjacent cells over time. We developed a technique based on flow cytofluorometry and fluorescence microscopy to study propagation of the organism at different stages of infection of GECs. Results showed that P. gingivalis spreads cell to cell and that the amount of spreading increases gradually over time. There was a …

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Premature Induction Of An Immunosuppressive Regulatory T Cell Response During Acute Simian Immunodeficiency Virus Infection, Jacob D. Estes, Qingsheng Li, Matthew R. Reynolds, Stephen W. Wietgrefe, Lijie Duan, Timothy Schacker, Louis J. Picker, David I. Watkins, Jeffrey D. Lifson, Cavan Reilly, John V. Carlis, Ashley T. Haase Jan 2006

Premature Induction Of An Immunosuppressive Regulatory T Cell Response During Acute Simian Immunodeficiency Virus Infection, Jacob D. Estes, Qingsheng Li, Matthew R. Reynolds, Stephen W. Wietgrefe, Lijie Duan, Timothy Schacker, Louis J. Picker, David I. Watkins, Jeffrey D. Lifson, Cavan Reilly, John V. Carlis, Ashley T. Haase

Qingsheng Li Publications

Here we report the results of an investigation into the possibility that one mechanism responsible for the establishment of persistent human immunodeficiency virus infection is an early regulatory T (Treg) cell response that blunts virus- specific responses. Using the simian immunodeficiency virus (SIV)–infected rhesus macaque model, we show that, indeed, viral replication and immune activation in lymphatic tissue drive a premature immunosuppressive response, with dramatic increases in the frequencies of CD4+CD25+FOXP3+ Treg cells, transforming growth factor–β1+ cells, interleukin–10+ cells, and indoleamine 2,3-dioxygenase+CD3+ cells.When we compared SIV infection with rhesus cytomegalovirus (RhCMV) …

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