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Your search keyword '"Hadley, Annette"' showing total 19 results
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19 results on '"Hadley, Annette"'

3. Attrition of memory CD8 T cells during sepsis requires LFA-1

Author

Serbanescu, Mara A, primary, Ramonell, Kimberly M, additional, Hadley, Annette, additional, Margoles, Lindsay M, additional, Mittal, Rohit, additional, Lyons, John D, additional, Liang, Zhe, additional, Coopersmith, Craig M, additional, Ford, Mandy L, additional, and McConnell, Kevin W, additional

Published
2016
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4. CXCR4 blockade decreases CD4+ T cell exhaustion and improves survival in a murine model of polymicrobial sepsis.

Author

Ramonell, Kimberly M., Zhang, Wenxiao, Hadley, Annette, Chen, Ching-wen, Fay, Katherine T., Lyons, John D., Klingensmith, Nathan J., McConnell, Kevin W., Coopersmith, Craig M., and Ford, Mandy L.

Subjects
CHEMOKINE receptors, SEPTICEMIA treatment, T cells, CD4 antigen, MULTIPLE organ failure, ANTI-inflammatory agents, ANIMAL models in research
Abstract

Sepsis is a dysregulated systemic response to infection involving many inflammatory pathways and the induction of counter-regulatory anti-inflammatory processes that results in a state of immune incompetence and can lead to multi-organ failure. CXCR4 is a chemokine receptor that, following ligation by CXCL12, directs cells to bone marrow niches and also plays an important role in T cell cosignaling and formation of the immunological synapse. Here, we investigated the expression and function of CXCR4 in a murine model of polymicrobial sepsis. Results indicate that CXCR4 is selectively upregulated on naïve CD4+ and CD8+ T cells and CD4+ central memory T cells following the induction of sepsis, and that CXCR4 antagonism resulted in a significant decrease in sepsis-induced mortality. We probed the mechanistic basis for these findings and found that CXCR4 antagonism significantly increased the number of peripheral CD4+ and CD8+ T cells following sepsis. Moreover, mice treated with the CXCR4 antagonist contained fewer PD-1+ LAG-3+ 2B4+ cells, suggesting that blockade of CXCR4 mitigates CD4+ T cell exhaustion during sepsis. Taken together, these results characterize CXCR4 as an important pathway that modulates immune dysfunction and mortality following sepsis, which may hold promise as a target for future therapeutic intervention in septic patients. [ABSTRACT FROM AUTHOR]

Published
2017
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5. Heterogeneity among viral antigen-specific CD4+ T cells and their de novo recruitment during persistent polyomavirus infection1

Author

Lin, Eugene, Kemball, Christopher C., Hadley, Annette, Wilson, Jarad J., Hofstetter, Amelia R., Pack, Christopher D., and Lukacher, Aron E.

Subjects
CD4-Positive T-Lymphocytes, Polyomavirus Infections, viruses, Antigens, Polyomavirus Transforming, Epitopes, T-Lymphocyte, Article, Mice, Inbred C57BL, Mice, Cell Movement, Chronic Disease, Animals, Capsid Proteins, Female, Antigens, Viral, Tumor, Polyomavirus
Abstract

Virus-specific CD4(+) T cells optimize antiviral responses by providing help for antiviral humoral responses and CD8(+) T cell differentiation. Although CD4(+) T cell responses to viral infections that undergo complete clearance have been studied extensively, less is known about virus-specific CD4(+) T cell responses to viruses that persistently infect their hosts. Using a mouse polyomavirus (MPyV) infection model, we previously demonstrated that CD4(+) T cells are essential for recruiting naive MPyV-specific CD8(+) T cells in persistently infected mice. In this study, we defined two dominant MPyV-specific CD4(+) T cell populations, one directed toward an epitope derived from the nonstructural large T Ag and the other from the major viral capsid protein of MPyV. These MPyV-specific CD4(+) T cells vary in terms of their magnitude, functional profile, and phenotype during acute and persistent phases of infection. Using a minimally myeloablative-mixed bone marrow chimerism approach, we further show that naive virus-specific CD4(+) T cells, like anti-MPyV CD8(+) T cells, are primed de novo during persistent virus infection. In summary, these findings reveal quantitative and qualitative differences in the CD4(+) T cell response to a persistent virus infection and demonstrate that naive antiviral CD4(+) T cells are recruited during chronic polyomavirus infection.

Published
2010

8. Gamma Interferon Controls Mouse Polyomavirus Infection In Vivo

Author

Wilson, Jarad J., primary, Lin, Eugene, additional, Pack, Christopher D., additional, Frost, Elizabeth L., additional, Hadley, Annette, additional, Swimm, Alyson I., additional, Wang, Jun, additional, Dong, Ying, additional, Breeden, Cynthia P., additional, Kalman, Daniel, additional, Newell, Kenneth A., additional, and Lukacher, Aron E., additional

Published
2011
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19. MHC Class lb-Restricted CD8 T Cells Differ in Dependence on CD4 T Cell Help and CD28 Costimulation over the Course of Mouse Polyomavirus Infection.

Author

Hofstetter, Amelia R., Ford, Mandy L., Sullivan, Lucy C., Wilson, Jarad J., Hadley, Annette, Brooks, Andrew G., and Lukacher, Aron E.

Subjects
*MAJOR histocompatibility complex, *T cells, *POLYOMAVIRUS diseases, *CAPSIDS, *VIRUS diseases, *LABORATORY mice
Abstract

We recently identified a protective MHC class lb-restricted CD8 T cell response to infection with mouse Polyomavirus. These CD8 T cells recognize a peptide from aa 139-147 of the VP2 viral capsid protein bound to the nonpolymorphic H-2Q9 molecule, a member of the Qa-2 family of &bgr;2m-associated MHC class Ib molecules. Q9:VP2.139-specific CD8 T cells exhibit an unusual inflationary response characterized by a gradual expansion over 3 mo followed by a stable maintenance phase. We previously demonstrated that Q9:VP2.139-specific CD8 T cells are dependent on Ag for expansion, but not for long-term maintenance. In this study, we tested the hypothesis that the expansion and maintenance components of the Q9:VP2.139-specific T cell response are differentially dependent on CD4 T cell help and CD28 costimulation. Depletion of CD4+ cells and CD28/CD40L blockade impaired expansion of Q9:VP2.139-specific CD8 T cells, and intrinsic CD28 signaling was sufficient for expansion. In contrast, CD4 T cell insufficiency, but not CD28/CD40L blockade, resulted in a decline in frequency of Q9:VP2.139-specific CD8 T cells during the maintenance phase. These results indicate that the Q9:VP2.139-specific CD8 T cell response to mouse Polyomavirus infection depends on CD4 T cell help and CD28 costimulation for inflationary expansion, but only on CD4 T cell help for maintenance. [ABSTRACT FROM AUTHOR]

Published
2012
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