Selected articles October 2015
New link between TL1A and pro-inflammatory cytokines in inflammatory bowel disease
TL1A as a Potential Local Inducer of IL17A Expression in Colon Mucosa of Inflammatory Bowel Disease Patients
T. J. Ślebioda, A. Bojarska-Junak, M. Stanisławowski, M. Cyman, P. M. Wierzbicki, J. Roliński, K. Celiński and Z. Kmieć
In a study in the October issue of Scandinavian Journal of immunology a group of researchers from Poland show that in humans the tumor necrosis factor superfamily member TL1A may contribute to intestinal inflammation by local induction of expression of pro-inflammatory cytokine IL-17A. They also show that TL1A and its receptor DR3 is expressed not only on mononuclear cells present in intestinal lamina propria but also on enterocytes.
– The role of TL1A in inflammatory bowel disease is very complex and still remains not entirely explained, says dr Tomasz Slebioda, post-doctoral researcher at the Department of Histology at the Medical University of Gdansk.
The present study aimed to establish a link between expression of TL1A and selected TL1A-induced pro-inflammatory cytokines involved in the pathogenesis of inflammatory bowel disease. In addition, the researchers wanted to investigate a connection between serum concentration of TL1A in patients with inflammatory bowel disease and activation of peripheral blood T cells.
Tomasz Slebioda designed the study and conducted most of the research and especially enjoyed the ability to continue and expand the studies which he started as a PhD student at the University of Southampton (UK) under the supervision and direction of Prof. Aymen Al-Shamkhani.
– It has to be emphasized, however, that this publication is a result of successful cooperation with a team of medical doctors and scientists from Medical University of Lublin in Poland, he says.
In summary, the data presented in this publication indicate that TL1A may contribute to pathogenesis of inflammatory bowel diseases via local but not systemic induction of IL-17A but not IL-4, IL-13 or IFN-gamma.
Novel mechanism by which Varicella-zoster virus suppresses the antiviral response of the host
Suppressor of Cytokine Signaling 3 Expression Induced by Varicella-Zoster Virus Infection Results in the Modulation of Virus Replication
E.-J. Choi, C.-H. Lee and O. S. Shin
Here, a group of Korean researchers demonstrate that the expression of suppressor of cytokine signaling (SOCS)3 impaired host control of Varicella-zoster virus, resulting in modulation of type I IFN signaling and viral replication.
Varicella-zoster virus is an important viral pathogen that is responsible for causing varicella (chickenpox) hand herpes zoster (shingles). The virus has been shown to suppress early anti-viral innate immune responses, but the exact mechanisms are not yet well understood.
– In this study, we used three different cell types, keratinocytes, fibroblasts, and macrophages to investigate VZV-induced anti-viral responses, Eun-Jin Choi says.
Eun-Jin Choi is the first author of the study and is a post doc in the lab of infection and immunology at Korea University.
– It was intriguing to observe distinct characteristics of immune responses against Varicella-zoster virus infection, depending on the cell types, she says.
Taken together, the data presented in this publication indicate that Varicella-zoster virus-induced expression of SOCS3 represents a viral evasion mechanism and suggest that type I IFN signaling may be modulated by SOCS3-mediated immune suppression. This is a novel mechanism by which Varicella-zoster virus suppresses the anti-viral response of the host and paves a path to efficient virus replication.