Selected articles September 2015

 

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Previously unknown role for IRF4 in liver transplant rejection

 

Inhibition of Interferon Regulatory Factor 4 Attenuates Acute Liver Allograft Rejection in Mice

 

W. Zhao, Z. Zhang, Q. Zhao, M. Liu and Y. Wang

 

In this study, published in the September issue of Scandinavian Journal of Immunology, a Chinese research group shows that interferon regulatory factor 4 (IRF4) plays a crucial rule in regulating acute liver allograft rejection.

 

Acute liver allograft rejection is a serious complication after liver transplantation. IRF4 is expressed predominantly in the immune system and plays an important role in its development and function. However the role of IRF4 in liver transplantation has not been investigated before.

 

Wei Zhao is the first author of this paper and was in charge of experiments, analysis and interpretation of the data.

 

– In this study, we show that inhibition of IRF4 attenuates acute liver allograft rejection in mice, she says.

 

This effect of IRF4 is associated with promoted M2 macrophage differentiation; the study show an up regulation of the M2 numbers in liver of recipients treated with IRF4 siRNA.

 

The results in this study suggest that IRF4-inhibition reprogrammed macrophages to the M2, thereby favoring a ”graft protecting” status rather than progressive inflammation and destruction. IRF4 siRNA treatment increases IL-10 production and promotes M2 macrophage differentiation both in vitro and in vivo.

 

 

 

 

Limited cutaneous SSc and diffuse cutaneous SSc – more than two sites of the same coin

 

Increased Serum Levels of the IL-33 Neutralizing sST2 in Limited Cutaneous Systemic Sclerosis

 

A. Wagner, M. Köhm, A. Nordin, E. Svenungsson, J.M. Pfeilschifter and H. H. Radeke

 

In this study performed by German and Swedish researchers it is shown that the soluble receptor for IL-33, sST2 is elevated in late phase limited cutaneous systemic sclerosis (lcSSc) as compared to patients with shorter disease duration or with the diffuse subtype of SSc. The researchers demonstrate that sST2 and not IL-33 is significantly increased in serum of lcSSc patients with disease duration over 9 years.

 

Annika Wagner was a PhD in the group of Professor Radeke when this study was undertaken and was responsible for the recruitment of the German patients and control subjects. She also prepared major part of serum and plasma samples, performed the ELISA measurements and did some of the statistical analyses.

 

– Our results give an additional hint towards the hypothesis that limited cutaneous SSc and diffuse cutaneous SSc seem to be more than two sites of the same coin. The ongoing discussion if lcSSc and dcSSc are two complete different diseases may give us the opportunity to gain a deeper understanding of the pathophysiology of lcSSc and dcSSc. This might result in an earlier diagnosis of the "two forms of SSc" and may give the physicians new opportunities to improve SSc treatment.

 

Data raised within this trial highlight the functional interaction of IL-33 and its neutralizing receptor sST2 in pathological processes of SSc and stresses the role of sST2 as a progression marker of lcSSc.

 

Annika Wagner, who is a trained biologist appreciated the work with this study and was happy to get a deeper insight into clinical research.

 

– And I got the chance to learn capillaroscopy at a workshop by the capillarscopy expert professor Cutolo, that was amazing, she concludes.