Background: The role of TAM receptors are well characterised in autoimmunity and cancer biology. Their role in infectious diseases is now being elucidated. The goal of this study is to characterise TAM receptor expression profiles of various innate immune components at homeostasis as well as in various infection models. The hypothesis of this study is that up-regulation of TAM receptors, AXL and MerTK are responsible for the de-sensitisation of airway macrophages to bacteria following influenza infection. Furthermore, I hypothesise that TAM receptors may be involved in limiting innate immune activation at homoeostasis. Methods: Using a murine model, we characterised TAM receptor expression on various innate populations in the lung following viral (influenza A) and bacterial (Streptcoccus pneumoniae) infections. We also investigated the role of AXL in influenza/bacteria single and co-infection using AXL-/- mice. Results: AXL and MerTK are differentially expressed by innate populations in the lung depending on their location. Monocytes and neutrophils which infiltrate into the alveolar space during influenza infection significantly up-regulate TAM receptor expressions. Lack of AXL significantly potentiates innate immunity by upregulating the release of inflammatory cytokines in vitro. Conclusion: Up-regulation of AXL following a viral infection may explain the exacerbation of secondary bacterial complications as its upregulation limits the innate inflammatory responses.
- Copyright © 2013 by The American Association of Immunologists, Inc.