In our latest Journal Club session we discussed a recent publication in the Journal of Immunology. Narumi et al. investigated the role of S100A8/A9 (or Calprotectin) in a tumor environment and discovered a new role of this protein for NK cell activation via interaction with RAGE (receptor of advanced glycation end product).
The study focused on the heterodimeric protein calprotectin, which is formed of the two Ca2+-binding proteins S100A8 and S100A9. Calprotectin can be found in the cytosol of myeloid cells, but not in lymphocytes. Many intracellular and extracellular proinflammatory functions are attributed to calprotectin, essentially regulation of leukocyte adhesion and migration and promotion of cytokine production.
The focus of our journal club this week was a recent paper from Science describing a novel mechanism by which neutrophils deposit chemokine-enriched way-markers to guide CD8+ T cells to the airways during influenza virus infection. (read the full article here http://www.sciencemag.org/content/349/6252/aaa4352.full).
Whilst the role of chemokines in attracting effector immune cells to sites of immune insult is well established, how localized chemokine gradients are produced and maintained is incompletely understood. Likewise, the molecular mechanisms linking neutrophils and T cell recruitment in viral infections is unclear. Lim et al therefore set out to investigate the hypothesis that neutrophils are responsible for generating chemokine gradients that guide influenza-specific CD8+ T cells in the airways.
Written by David Salman, Richard Toshner and Joana Alçada
Edited by Sarah Allden
We recently welcomed Dr Gisli Jenkins, Clinical Associate Professor & Reader in Pulmonary Biology from the University of Nottingham to the IRD Journal Club.
His recent publication “Influenza Promotes Collagen Deposition via αvβ6 Integrin-mediated Transforming Growth Factor β Activation” served as a starting point to discuss various aspects of research in lung fibrosis. The paper explores the relationship between influenza and idiopathic pulmonary fibrosis via transforming growth factor β (TGF-β), a cytokine involved in development, inflammation and wound repair.
The authors hypothesised that influenza-induced epithelial cell damage would stimulate toll-like receptor 3 (TLR3) activity, a receptor that recognizes by-products from viruses such as influenza.