Blog posts

CD8+ T cells follow neutrophil snail trails in virus-infected airways

Written by Caroline Anderson

Edited by John MacKey

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.

Influenza Promotes Collagen Deposition via αvβ6 Integrin-mediated Transforming Growth Factor β Activation

Journal club with Gisli Jenkins from 21/9/15

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.

A novel role for Tregs in providing active TGF-β for immune regulation

Written by William Branchett

Edited by Judith Secklehner and Caroline Anderson 

The immune system has a huge capacity for destruction which, if unrestrained, can cause collateral damage to host tissue. Immune responses must therefore have ‘off’ switches to limit their magnitude and avoid inflammatory disease. Conversely, pathogens and tumours can hijack these mechanisms of immune regulation to favour their own survival. Understanding of immune regulation may therefore allow the design of drugs to manipulate overly exuberant or insufficient immune responses.

Transforming growth factor β (TGF-β) is a multi-functional cytokine that can dampen immune responses, in part by suppressing the pro-inflammatory activity of effector CD4+ T cells (Teffs).