Selected articles September 2014:

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New insights into the expression pattern of T Cell-specific adapter protein in healthy human tissues

 

Expression of the T Cell-specific Adapter Protein in Human Tissues

 

A. D. Pandya, T. B. Leergaard, E. Dissen, G. Haraldsen and A. Spurkland

 

The current study, published in the September issue of the Scandinavian journal of immunology, is the first to address to what extent T cell-specific adapter protein (TSAd) is expressed in various tissues in situ, including lymphoid and non-lymphoid tissue.

 

TSAd is expressed in activated T cells, NK cells and endothelial cells, but due to previous lack of suitable reagents, its tissue expression has not been mapped before. The protein plays a role in cell signalling, proliferation and cellular migration, but its precise role in these processes is yet not well established.

 

The main findings from the current study include:

 

I) In lymphoid tissues, a fraction of CD3 expressing T cells also expressed TSAd.                 

–This may indicate that a particular T cell subset expresses TSAd. It will be more interesting to quest about this subset in future, says Abhilash D. Pandya, PhD student in the group of Anne Spurkland

 

II) In Mucosa-associate lymphoid tissues (MALT), the group observed that all the intraepithelial lymphocytes (IELs, specifically T cells) expressed TSAd.

 

III) In non-lymphoid tissues, they observed TSAd expression in Langerhans’ islets of

pancreas. However, the identity of TSAd expressing islet cells, and the significance

of TSAd expression in these cells is yet to be established.

 

– We did not detect TSAd expression in the endothelium of non-lymphoid organs including liver, kidney, lung and heart as well as in lymphoid tissues, Abhilash D. Pandya says. But we observed TSAd expression in endothelium of blood vessels in skin. This indicates varied expression of TSAd in endothelial cells, based on endothelium of specific tissue. Henceforth, it could be that the TSAd level in some endothelium is normally below the limit of IHC detection.

 

Abhilash D. Pandya developed the tissue specific IHC protocol for the study, and also performed a series of experiments including analysis. He also wrote the manuscript.

– I really enjoyed working on such a novel project, especially to analyse and conclude the results!

 

  

 

 

  

One step closer to solving the riddle of early pregnancy termination.

 

Interaction of Decidual CD56+ NK with Trophoblast Cells during Normal Pregnancy and Recurrent Spontaneous Abortion at Early Term of Gestation

 

N. Sotnikova, D. Voronin, Y. Antsiferova and E. Bukina

 

In this study Natalia Sotnikova and co-workers set out to detail the mechanisms of the interaction of decidual CD56+ NK cells (dNK), infiltrating the maternal part of placenta, and trophoblast cells of foetal origin. They conclude that unbalanced activation of dNK can lead to the impairment of dNK and trophoblast cells interaction during RSA.

 

There is a unique immunological situation in pregnancy when a semiallogenic foetus is implanted and successfully developed within a mother´s womb. This is called the immunological paradox. We do not know exactly why the mother´s immune system does not reject the foetus. Following implantation, the trophoblast cells, which are the primary foetal cells, invade the decidual tissue of placenta of maternal origin and for the pool of so-called extravillous cytotrophoblast cells, which participate in the development of early placenta. At this stage of the pregnancy and unique population of CD56bright NK cells has been shown, but the biological role of these cells has not been demonstrated.

 

The present study was designed to detail the mechanisms of the interaction of dNK and trophoblasts during normal and pathological early pregnancy (first semester recurrent spontaneous abortion, RSA) and to concretize the role of dNK in trophoblast behaviour.

 

– The main finding of our work is proving the cross-talk between decidual CD56+ NK cells and trophoblast in normal and RSA pregnancy, Natalia Sotnikova, head of the laboratory of Clinical immunology at the Federal State Research Institute of Maternity and Childhood in Russia says.

 

From one side the maternal immune system actively recognize foetal antigens and respond to these antigens, but normally this response does not lead to foetus damage. When this physiological process is impaired either due to inadequate maternal response or due to inadequate foetal antigen stimulation the immune balance between mother and foetus is crashed and foetus is rejected.

 

Natalia Sotnikova was the supervisor of the research and she planned the research, participated in the selection of the patients, discussed experiments with co-workers and wrote the manuscript. The work in the lab is not always calm.

 

– We had some rivalry with our colleagues from the Laboratory of Morphology over clinical samples, like who would have the next piece of placenta, but in the end everything was well and everyone got the samples they needed.

 

Natalia Sotnikova is very pleased over the results and the fact that we are now one step closer to solving the riddle of early pregnancy termination.

 

– The fine immune mechanisms participating in this process are very far from complete understanding, but we can confirm that the dramatic stimulation of the functional activity of the maternal decidual CD56+ NK cells by foetal trophoblast cells is one of the mechanisms behind early pregnancy termination.