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A role for IL-15 in the migration of effector CD8 T cells to the lung airways following influenza infection.

Authors: Verbist, KC  Cole, CJ  Field, MB  Klonowski, KD 
Citation: Verbist KC, etal., J Immunol. 2011 Jan 1;186(1):174-82. Epub 2010 Nov 22.
Pubmed: (View Article at PubMed) PMID:21098221
DOI: Full-text: DOI:10.4049/jimmunol.1002613

The cytokines generated locally in response to infection play an important role in CD8 T cell trafficking, survival, and effector function, rendering these signals prime candidates for immune intervention. In this paper, we show that localized increases in the homeostatic cytokine IL-15 induced by influenza infection is responsible for the migration of CD8 effector T cells to the site of infection. Moreover, intranasal delivery of IL-15-IL-15Ralpha soluble complexes (IL-15c) specifically restores the frequency of effector T cells lost in the lung airways of IL-15-deficient animals after influenza infection. Exogenous IL-15c quantitatively augments the respiratory CD8 T cell response, and continued administration of IL-15c throughout the contraction phase of the anti-influenza CD8 T cell response magnifies the resultant CD8 T cell memory generated in situ. This treatment extends the ability of these cells to protect against heterologous infection, immunity that typically depreciates over time. Overall, our studies describe what to our knowledge is a new function for IL-15 in attracting effector CD8 T cells to the lung airways and suggest that adjuvanting IL-15 could be used to prolong anti-influenza CD8 T cell responses at mucosal surfaces to facilitate pathogen elimination.


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RGD Object Information
RGD ID: 4994196
Created: 2011-03-01
Species: All species
Last Modified: 2011-03-01
Status: ACTIVE


RGD is funded by grant HL64541 from the National Heart, Lung, and Blood Institute on behalf of the NIH.