T resident helper cells promote humoral responses in the lung

Influenza is a deadly and costly infectious disease, even during flu seasons when an effective vaccine has been developed. To improve vaccines against respiratory viruses, a better understanding of the immune response at the site of infection is crucial. After influenza infection, clonally expanded...

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Bibliographic Details
Published in:Science immunology 2021-01, Vol.6 (55)
Main Authors: Swarnalekha, Nivedya, Schreiner, David, Litzler, Ludivine C, Iftikhar, Saadia, Kirchmeier, Daniel, Künzli, Marco, Son, Young Min, Sun, Jie, Moreira, Etori Aguiar, King, Carolyn G
Format: Article
Language:English
Subjects:
Animals
Disease Models, Animal
Female
Humans
Immunity, Mucosal
Influenza A virus - immunology
Influenza Vaccines - administration & dosage
Influenza Vaccines - immunology
Influenza, Human - immunology
Influenza, Human - prevention & control
Influenza, Human - virology
Lung - immunology
Lung - pathology
Lung - virology
Male
Mice
Mice, Transgenic
Proto-Oncogene Proteins c-bcl-6 - genetics
Proto-Oncogene Proteins c-bcl-6 - metabolism
T-Lymphocyte Subsets - immunology
T-Lymphocyte Subsets - metabolism
T-Lymphocytes, Helper-Inducer - immunology
T-Lymphocytes, Helper-Inducer - metabolism
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Summary:Influenza is a deadly and costly infectious disease, even during flu seasons when an effective vaccine has been developed. To improve vaccines against respiratory viruses, a better understanding of the immune response at the site of infection is crucial. After influenza infection, clonally expanded T cells take up permanent residence in the lung, poised to rapidly respond to subsequent infection. Here, we characterized the dynamics and transcriptional regulation of lung-resident CD4 T cells during influenza infection and identified a long-lived, dependent population that we have termed T resident helper (T ) cells. T cells arise in the lung independently of lymph node T follicular helper cells but are dependent on B cells, with which they tightly colocalize in inducible bronchus-associated lymphoid tissue (iBALT). Deletion of in CD4 T cells before heterotypic challenge infection resulted in redistribution of CD4 T cells outside of iBALT areas and impaired local antibody production. These results highlight iBALT as a homeostatic niche for T cells and advocate for vaccination strategies that induce T cells in the lung.
ISSN:2470-9468
2470-9468
DOI:10.1126/sciimmunol.abb6808