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 inJournal of cellular and molecular medicine Vol. 5; no. 4; pp. 388 - 396
Main Authors Radu, D. L., Weksler, M. E., Bona, C. A.
Format Journal Article
LanguageEnglish
Published Oxford, UK Blackwell Publishing Ltd 01.10.2001
John Wiley & Sons, Inc
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ISSN1582-1838
1582-4934
DOI10.1111/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.
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
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Snippet 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...
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...
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StartPage 388
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
URI https://onlinelibrary.wiley.com/doi/abs/10.1111%2Fj.1582-4934.2001.tb00173.x
https://www.ncbi.nlm.nih.gov/pubmed/12067472
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https://www.proquest.com/docview/18371825
https://www.proquest.com/docview/71309605
https://pubmed.ncbi.nlm.nih.gov/PMC6740224
Volume 5
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