The Experts below are selected from a list of 4653 Experts worldwide ranked by ideXlab platform
David L Woodland - One of the best experts on this subject based on the ideXlab platform.
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the route of priming influences the ability of respiratory Virus specific memory cd8 t cells to be activated by residual antigen
Journal of Experimental Medicine, 2010Co-Authors: Shiki Takamura, Alan D Roberts, Jacob E Kohlmeier, Dawn M Jelleygibbs, Susan Wittmer, David L WoodlandAbstract:After respiratory Virus Infections, memory CD8+ T cells are maintained in the lung airways by a process of continual recruitment. Previous studies have suggested that this process is controlled, at least in the initial weeks after Virus clearance, by residual antigen in the lung-draining mediastinal lymph nodes (MLNs). We used mouse models of influenza and Parainfluenza Virus Infection to show that intranasally (i.n.) primed memory CD8+ T cells possess a unique ability to be reactivated by residual antigen in the MLN compared with intraperitoneally (i.p.) primed CD8+ T cells, resulting in the preferential recruitment of i.n.-primed memory CD8+ T cells to the lung airways. Furthermore, we demonstrate that the inability of i.p.-primed memory CD8+ T cells to access residual antigen can be corrected by a subsequent i.n. Virus Infection. Thus, two independent factors, initial CD8+ T cell priming in the MLN and prolonged presentation of residual antigen in the MLN, are required to maintain large numbers of antigen-specific memory CD8+ T cells in the lung airways.
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cxcr3 directs antigen specific effector cd4 t cell migration to the lung during Parainfluenza Virus Infection
Journal of Immunology, 2009Co-Authors: Jacob E Kohlmeier, Tres Cookenham, Shannon C Miller, Alan Roberts, Jan Pravsgaard Christensen, Allan Randrup Thomsen, David L WoodlandAbstract:Effector T cells are a crucial component of the adaptive immune response to respiratory Virus Infections. Although it was previously reported that the chemokine receptors CCR5 and CXCR3 affect trafficking of respiratory Virus-specific CD8+ T cells, it is unclear whether these receptors govern effector CD4+ T cell migration to the lungs. To assess the role of CCR5 and CXCR3 in vivo, we directly compared the migration of Ag-specific wild-type and chemokine receptor-deficient effector T cells in mixed bone marrow chimeric mice during a Parainfluenza Virus Infection. CXCR3-deficient effector CD4+ T cells were 5- to 10-fold less efficient at migrating to the lung compared with wild-type cells, whereas CCR5-deficient effector T cells were not impaired in their migration to the lung. In contrast to its role in trafficking, CXCR3 had no impact on effector CD4+ T cell proliferation, phenotype, or function in any of the tissues examined. These findings demonstrate that CXCR3 controls Virus-specific effector CD4+ T cell migration in vivo, and suggest that blocking CXCR3-mediated recruitment may limit T cell-induced immunopathology during respiratory Virus Infections.
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cutting edge effector memory cd8 t cells play a prominent role in recall responses to secondary viral Infection in the lung
Journal of Immunology, 2004Co-Authors: Alan D Roberts, David L WoodlandAbstract:The relative contributions of CD62Lhigh (central) memory and CD62Llow (effector) memory T cell populations to recall responses are poorly understood, especially in the respiratory tract. In this study, we took advantage of a dual-adoptive transfer system in the mouse to simultaneously follow the recall response of effector and central memory subpopulations to intranasal Parainfluenza Virus Infection. Using MHC class I and class II multimers, we tracked the responses of Ag-specific CD8+ and CD4+ memory T cells in the same animals. The data show that effector memory T cells mounted recall responses that were equal to, or greater than, those mounted by central memory T cells. Moreover, effector memory T cells were more efficient at subsequently establishing a second generation of memory T cells. These data contrast with other studies indicating that central memory CD8+ T cells are the prominent contributors to systemic Virus Infections.
Alan D Roberts - One of the best experts on this subject based on the ideXlab platform.
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the route of priming influences the ability of respiratory Virus specific memory cd8 t cells to be activated by residual antigen
Journal of Experimental Medicine, 2010Co-Authors: Shiki Takamura, Alan D Roberts, Jacob E Kohlmeier, Dawn M Jelleygibbs, Susan Wittmer, David L WoodlandAbstract:After respiratory Virus Infections, memory CD8+ T cells are maintained in the lung airways by a process of continual recruitment. Previous studies have suggested that this process is controlled, at least in the initial weeks after Virus clearance, by residual antigen in the lung-draining mediastinal lymph nodes (MLNs). We used mouse models of influenza and Parainfluenza Virus Infection to show that intranasally (i.n.) primed memory CD8+ T cells possess a unique ability to be reactivated by residual antigen in the MLN compared with intraperitoneally (i.p.) primed CD8+ T cells, resulting in the preferential recruitment of i.n.-primed memory CD8+ T cells to the lung airways. Furthermore, we demonstrate that the inability of i.p.-primed memory CD8+ T cells to access residual antigen can be corrected by a subsequent i.n. Virus Infection. Thus, two independent factors, initial CD8+ T cell priming in the MLN and prolonged presentation of residual antigen in the MLN, are required to maintain large numbers of antigen-specific memory CD8+ T cells in the lung airways.
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cutting edge effector memory cd8 t cells play a prominent role in recall responses to secondary viral Infection in the lung
Journal of Immunology, 2004Co-Authors: Alan D Roberts, David L WoodlandAbstract:The relative contributions of CD62Lhigh (central) memory and CD62Llow (effector) memory T cell populations to recall responses are poorly understood, especially in the respiratory tract. In this study, we took advantage of a dual-adoptive transfer system in the mouse to simultaneously follow the recall response of effector and central memory subpopulations to intranasal Parainfluenza Virus Infection. Using MHC class I and class II multimers, we tracked the responses of Ag-specific CD8+ and CD4+ memory T cells in the same animals. The data show that effector memory T cells mounted recall responses that were equal to, or greater than, those mounted by central memory T cells. Moreover, effector memory T cells were more efficient at subsequently establishing a second generation of memory T cells. These data contrast with other studies indicating that central memory CD8+ T cells are the prominent contributors to systemic Virus Infections.
Mark Von Itzstein - One of the best experts on this subject based on the ideXlab platform.
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exploring inhibitor structural features required to engage the 216 loop of human Parainfluenza Virus type 3 hemagglutinin neuraminidase
MedChemComm, 2017Co-Authors: Ibrahim Mustafa Eldeeb, Larissa Dirr, Patrice Guillon, Mark Von ItzsteinAbstract:Human Parainfluenza Virus type-3 is a leading cause of acute respiratory Infection in infants and children. There is currently neither vaccine nor clinically effective treatment for Parainfluenza Virus Infection. Hemagglutinin-neuraminidase glycoprotein is a key protein in viral Infection, and its inhibition has been a target for inhibitor development. In this study, we explore the structural features required for Neu2en derivatives to efficiently lock-open the 216-loop of the human Parainfluenza Virus type-3 hemagglutinin-neuraminidase protein.
Patrice Guillon - One of the best experts on this subject based on the ideXlab platform.
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exploring inhibitor structural features required to engage the 216 loop of human Parainfluenza Virus type 3 hemagglutinin neuraminidase
MedChemComm, 2017Co-Authors: Ibrahim Mustafa Eldeeb, Larissa Dirr, Patrice Guillon, Mark Von ItzsteinAbstract:Human Parainfluenza Virus type-3 is a leading cause of acute respiratory Infection in infants and children. There is currently neither vaccine nor clinically effective treatment for Parainfluenza Virus Infection. Hemagglutinin-neuraminidase glycoprotein is a key protein in viral Infection, and its inhibition has been a target for inhibitor development. In this study, we explore the structural features required for Neu2en derivatives to efficiently lock-open the 216-loop of the human Parainfluenza Virus type-3 hemagglutinin-neuraminidase protein.
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Exploring Human Parainfluenza Virus Type‑1 Hemagglutinin–Neuraminidase as a Target for Inhibitor Discovery
2014Co-Authors: Ibrahim M. El-deeb, Patrice Guillon, Moritz Winger, Tanguy Eveno, Thomas Haselhorst, Jeffrey C. Dyason, Mark Von ItzsteinAbstract:Human Parainfluenza Virus type 1 is the major cause of croup in infants and young children. There is currently neither vaccine nor clinically effective treatment for Parainfluenza Virus Infection. Hemagglutinin–neuraminidase glycoprotein is a key protein in viral Infection, and its inhibition has been a target for 2-deoxy-2,3-didehydro-d-N-acetylneuraminic acid (Neu5Ac2en)-based inhibitor development. In this study, we explore the effect of C-5 modifications on the potency of Neu5Ac2en derivatives that target the human Parainfluenza type-1 hemagglutinin–neuraminidase protein. Our study demonstrates that the replacement of the Neu5Ac2en C-5 acetamido moiety with more hydrophobic alkane-based moieties improves the inhibitory potency for both hemagglutinin–neuraminidase functions. These findings shed light on the importance of C-5 substitution on Neu5Ac2en in the design of novel sialic acid-based inhibitors that target human Parainfluenza type-1 hemagglutinin–neuraminidase
Jacob E Kohlmeier - One of the best experts on this subject based on the ideXlab platform.
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the route of priming influences the ability of respiratory Virus specific memory cd8 t cells to be activated by residual antigen
Journal of Experimental Medicine, 2010Co-Authors: Shiki Takamura, Alan D Roberts, Jacob E Kohlmeier, Dawn M Jelleygibbs, Susan Wittmer, David L WoodlandAbstract:After respiratory Virus Infections, memory CD8+ T cells are maintained in the lung airways by a process of continual recruitment. Previous studies have suggested that this process is controlled, at least in the initial weeks after Virus clearance, by residual antigen in the lung-draining mediastinal lymph nodes (MLNs). We used mouse models of influenza and Parainfluenza Virus Infection to show that intranasally (i.n.) primed memory CD8+ T cells possess a unique ability to be reactivated by residual antigen in the MLN compared with intraperitoneally (i.p.) primed CD8+ T cells, resulting in the preferential recruitment of i.n.-primed memory CD8+ T cells to the lung airways. Furthermore, we demonstrate that the inability of i.p.-primed memory CD8+ T cells to access residual antigen can be corrected by a subsequent i.n. Virus Infection. Thus, two independent factors, initial CD8+ T cell priming in the MLN and prolonged presentation of residual antigen in the MLN, are required to maintain large numbers of antigen-specific memory CD8+ T cells in the lung airways.
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cxcr3 directs antigen specific effector cd4 t cell migration to the lung during Parainfluenza Virus Infection
Journal of Immunology, 2009Co-Authors: Jacob E Kohlmeier, Tres Cookenham, Shannon C Miller, Alan Roberts, Jan Pravsgaard Christensen, Allan Randrup Thomsen, David L WoodlandAbstract:Effector T cells are a crucial component of the adaptive immune response to respiratory Virus Infections. Although it was previously reported that the chemokine receptors CCR5 and CXCR3 affect trafficking of respiratory Virus-specific CD8+ T cells, it is unclear whether these receptors govern effector CD4+ T cell migration to the lungs. To assess the role of CCR5 and CXCR3 in vivo, we directly compared the migration of Ag-specific wild-type and chemokine receptor-deficient effector T cells in mixed bone marrow chimeric mice during a Parainfluenza Virus Infection. CXCR3-deficient effector CD4+ T cells were 5- to 10-fold less efficient at migrating to the lung compared with wild-type cells, whereas CCR5-deficient effector T cells were not impaired in their migration to the lung. In contrast to its role in trafficking, CXCR3 had no impact on effector CD4+ T cell proliferation, phenotype, or function in any of the tissues examined. These findings demonstrate that CXCR3 controls Virus-specific effector CD4+ T cell migration in vivo, and suggest that blocking CXCR3-mediated recruitment may limit T cell-induced immunopathology during respiratory Virus Infections.
