Maintenance of size and function of influenza virus hemagglutinin specific transgenic T‐cell clone during life
Immunization induces less protective immunity against infectious diseases in old compared to young subjects. We have studied the effect of age on the in vitro and in vivo function of murine transgenic T cells expressing a receptor for influenza hemagglutinin 110‐120 peptide. During aging the transge...
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Published in | Journal of cellular and molecular medicine Vol. 5; no. 4; pp. 388 - 396 |
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Main Authors | , , |
Format | Journal Article |
Language | English |
Published |
Oxford, UK
Blackwell Publishing Ltd
01.10.2001
John Wiley & Sons, Inc |
Subjects | |
Online Access | Get full text |
ISSN | 1582-1838 1582-4934 |
DOI | 10.1111/j.1582-4934.2001.tb00173.x |
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Abstract | Immunization induces less protective immunity against infectious diseases in old compared to young subjects. We have studied the effect of age on the in vitro and in vivo function of murine transgenic T cells expressing a receptor for influenza hemagglutinin 110‐120 peptide. During aging the transgenic T cells undergo the age‐associated shift from naive to memory phenotype but maintain, despite thymic involution, their number as well as their cytokine production and proliferative responses induced by the hemagglutinin 110‐120 peptide in vitro. The maintenance of the size and functions of transgenic T cells during the aging may be related to low expression of CTLA‐4 molecules known to exhibit a negative regulatory effect subsequent to interaction with costimulatory molecules as well as of stimulation of T cells by unknown cross reactive endogenous factors but not by nominal antigen since innate immunity prevents natural infection with influenza virus of murine species. This suggests that the impaired immunity induced by immunization in old subjects reflects defects in the development and maintenance of T cell memory and not in the expression of effector activity. |
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AbstractList | Immunization induces less protective immunity against infectious diseases in old compared to young subjects. We have studied the effect of age on the in vitro and in vivo function of murine transgenic T cells expressing a receptor for influenza hemagglutinin 110-120 peptide. During aging the transgenic T cells undergo the age-associated shift from naive to memory phenotype but maintain, despite thymic involution, their number as well as their cytokine production and proliferative responses induced by the hemagglutinin 110-120 peptide in vitro. The maintenance of the size and functions of transgenic T cells during the aging may be related to low expression of CTLA-4 molecules known to exhibit a negative regulatory effect subsequent to interaction with costimulatory molecules as well as of stimulation of T cells by unknown cross reactive endogenous factors but not by nominal antigen since innate immunity prevents natural infection with influenza virus of murine species. This suggests that the impaired immunity induced by immunization in old subjects reflects defects in the development and maintenance of T cell memory and not in the expression of effector activity.Immunization induces less protective immunity against infectious diseases in old compared to young subjects. We have studied the effect of age on the in vitro and in vivo function of murine transgenic T cells expressing a receptor for influenza hemagglutinin 110-120 peptide. During aging the transgenic T cells undergo the age-associated shift from naive to memory phenotype but maintain, despite thymic involution, their number as well as their cytokine production and proliferative responses induced by the hemagglutinin 110-120 peptide in vitro. The maintenance of the size and functions of transgenic T cells during the aging may be related to low expression of CTLA-4 molecules known to exhibit a negative regulatory effect subsequent to interaction with costimulatory molecules as well as of stimulation of T cells by unknown cross reactive endogenous factors but not by nominal antigen since innate immunity prevents natural infection with influenza virus of murine species. This suggests that the impaired immunity induced by immunization in old subjects reflects defects in the development and maintenance of T cell memory and not in the expression of effector activity. Immunization induces less protective immunity against infectious diseases in old compared to young subjects. We have studied the effect of age on the in vitro and in vivo function of murine transgenic T cells expressing a receptor for influenza hemagglutinin 110-120 peptide. During aging the transgenic T cells undergo the age-associated shift from naive to memory phenotype but maintain, despite thymic involution, their number as well as their cytokine production and proliferative responses induced by the hemagglutinin 110-120 peptide in vitro. The maintenance of the size and functions of transgenic T cells during the aging may be related to low expression of CTLA-4 molecules known to exhibit a negative regulatory effect subsequent to interaction with costimulatory molecules as well as of stimulation of T cells by unknown cross reactive endogenous factors but not by nominal antigen since innate immunity prevents natural infection with influenza virus of murine species. This suggests that the impaired immunity induced by immunization in old subjects reflects defects in the development and maintenance of T cell memory and not in the expression of effector activity. Immunization induces less protective immunity against infectious diseases in old compared to young subjects. We have studied the effect of age on the in vitro and in vivo function of murine transgenic T cells expressing a receptor for influenza hemagglutinin 110‐120 peptide. During aging the transgenic T cells undergo the age‐associated shift from naive to memory phenotype but maintain, despite thymic involution, their number as well as their cytokine production and proliferative responses induced by the hemagglutinin 110‐120 peptide in vitro . The maintenance of the size and functions of transgenic T cells during the aging may be related to low expression of CTLA‐4 molecules known to exhibit a negative regulatory effect subsequent to interaction with costimulatory molecules as well as of stimulation of T cells by unknown cross reactive endogenous factors but not by nominal antigen since innate immunity prevents natural infection with influenza virus of murine species. This suggests that the impaired immunity induced by immunization in old subjects reflects defects in the development and maintenance of T cell memory and not in the expression of effector activity. |
Author | Bona, C. A. Radu, D. L. Weksler, M. E. |
AuthorAffiliation | 1 Department of Microbiology, Mount Sinai School of Medicine, New York, NY USA 2 Department of Medicine, Weill Medical College of Cornell University, New York, NY USA |
AuthorAffiliation_xml | – name: 2 Department of Medicine, Weill Medical College of Cornell University, New York, NY USA – name: 1 Department of Microbiology, Mount Sinai School of Medicine, New York, NY USA |
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SubjectTerms | Aging Aging - immunology Animals Cell size Costimulator CTLA-4 protein Effector cells Female Hemagglutinin Glycoproteins, Influenza Virus - immunology Hemagglutinin Glycoproteins, Influenza Virus - metabolism Hemagglutinins immunity Immunization Immunological memory Infectious diseases Influenza Influenza virus Innate immunity Interferon-gamma - metabolism Interleukin-4 - metabolism Lymphocytes Lymphocytes T Male Memory cells Mice Mice, Inbred BALB C Mice, Transgenic Orthomyxoviridae - metabolism Peptides Peptides - immunology Peptides - metabolism Phenotypes Receptors, Antigen, T-Cell, alpha-beta - immunology Receptors, Antigen, T-Cell, alpha-beta - metabolism Spleen - cytology Survival Rate T-Lymphocytes - immunology T-Lymphocytes - physiology Thymic involution Thymus transgenic |
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Title | Maintenance of size and function of influenza virus hemagglutinin specific transgenic T‐cell clone during life |
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