NDLI: Inchoate CD8+ T Cell Responses in Neonatal Mice Permit Influenza Induced Persistent Pulmonary Dysfunction

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Inchoate CD8+ T Cell Responses in Neonatal Mice Permit Influenza Induced Persistent Pulmonary Dysfunction

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Inchoate CD8+ T Cell Responses in Neonatal Mice Permit Influenza Induced Persistent Pulmonary Dysfunction

Content Provider	World Health Organization (WHO)-Global Index Medicus
Author	Ding, Liren Troxclair, Dana Ripple, Michael Balakrishna, Shrilatha You, Dahui Ahlert, Terry A. Cormier, Stephania A. Sandquist, Dane
Description	Country affiliation: United States Author Affiliation: You D ( Department of Pharmacology and Experimental Therapeutics, Louisiana State University Health Sciences Center, New Orleans, LA 70112, USA.)
Abstract	Influenza infection remains a significant cause of pulmonary morbidity and mortality worldwide, with the highest hospitalization and mortality rates occurring in infants and elder adults. The mechanisms inducing this considerable morbidity and mortality are largely unknown. To address this question, we established a neonatal mouse model of influenza infection to test the hypothesis that the immaturity of the neonatal immune system is responsible for the severe pulmonary disease observed in infants. Seven-day-old mice were infected with influenza A virus (H1N1) and allowed to mature. As adults, these mice showed enhanced airway hyperreactivity, chronic pulmonary inflammation, and diffuse emphysematous-type lesions in the lungs. The adaptive immune responses of the neonates were much weaker than those of adults. This insufficiency appeared to be in both magnitude and functionality and was most apparent in the CD8(+) T cell population. To determine the role of neonatal CD8(+) T cells in disease outcome, adult, naive CD8(+) T cells were adoptively transferred into neonates before infection. Neonatal mice receiving the adult CD8(+) T cells had significantly lower pulmonary viral titers and greatly improved pulmonary function as adults (airway resistance similar to SHAM). Additional adoptive transfer studies using adult CD8(+) T cells from IFN-gamma-deficient mice demonstrated the importance of IFN-gamma from CD8(+) T cells in controlling the infection and in determining disease outcome. Our data indicate that neonates are more vulnerable to severe infections due to immaturity of their immune system and emphasize the importance of vaccination in infants.
ISSN	00221767
e-ISSN	15506606
Journal	The Journal of Immunology
Issue Number	5
Volume Number	181
Language	English
Publisher	The American Association of Immunologists
Publisher Date	2008-09-01
Publisher Place	United States
Access Restriction	Open
Subject Keyword	Cd8-positive T-lymphocytes Immunology Influenza A Virus, H1n1 Subtype Lung Diseases Therapy Adoptive Transfer Animals Animals, Newborn Transplantation Disease Models, Animal Interferon-gamma Pathology Virology Mice Mice, Knockout Pneumonia Pulmonary Emphysema Respiratory Hypersensitivity Research Support, N.i.h., Extramural Discipline Immunology
Content Type	Text
Resource Type	Article
Subject	Immunology and Allergy Immunology

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Inchoate CD8+ T Cell Responses in Neonatal Mice Permit Influenza Induced Persistent Pulmonary Dysfunction1

Airway-Resident Memory CD8 T Cells Provide Antigen-Specific Protection against Respiratory Virus Challenge through Rapid IFN-Î³ Production.

An unexpected antibody response to an engineered influenza virus modifies $CD8^{+}$ T cell responses

IFN-Î³ from CD4 T cells is essential for host survival and enhances CD8 T cell function during Mycobacterium tuberculosis infection.

Reduced interferon-α production by dendritic cells in type 1 diabetes does not impair immunity to influenza virus

Tim-3 directly enhances CD8 T cell responses to acute Listeria monocytogenes infection.

CD8 T cells use IFN-Î³ to protect against the lethal effects of a respiratory poxvirus infection.

CD4+ T cell-dependent IFN-Î³ production by CD8+ effector T cells in Mycobacterium tuberculosis infection.

IFN-gamma receptor signaling regulates memory CD8+ T cell differentiation.

Inchoate CD8+ T Cell Responses in Neonatal Mice Permit Influenza Induced Persistent Pulmonary Dysfunction

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Inchoate CD8+ T Cell Responses in Neonatal Mice Permit Influenza Induced Persistent Pulmonary Dysfunction1

Airway-Resident Memory CD8 T Cells Provide Antigen-Specific Protection against Respiratory Virus Challenge through Rapid IFN-Î³ Production.

An unexpected antibody response to an engineered influenza virus modifies $CD8^{+}$ T cell responses

IFN-Î³ from CD4 T cells is essential for host survival and enhances CD8 T cell function during Mycobacterium tuberculosis infection.

Reduced interferon-α production by dendritic cells in type 1 diabetes does not impair immunity to influenza virus

Tim-3 directly enhances CD8 T cell responses to acute Listeria monocytogenes infection.

CD8 T cells use IFN-Î³ to protect against the lethal effects of a respiratory poxvirus infection.

CD4+ T cell-dependent IFN-Î³ production by CD8+ effector T cells in Mycobacterium tuberculosis infection.

IFN-gamma receptor signaling regulates memory CD8+ T cell differentiation.

Inchoate CD8+ T Cell Responses in Neonatal Mice Permit Influenza Induced Persistent Pulmonary Dysfunction