## Th17 cells

In a previous post I mentioned T-cells of types Th1 and Th2 and discussed their possible role in multiple sclerosis and a mathematical model for their dynamics. Both of these are types of helper T-cells carrying the molecule CD4 on their surface. In the recent past another class of CD4+ T-cells, the Tregs (regulatory T-cells) have been widely studied. In a way they are a new and more precise incarnation of the old idea of suppressor T-cells which had lived a rather shadowy existence. Tregs are associated with the surface molecule CD25 and express the transcription factor Foxp3. They may be of central importance in autoimmune disease. Now a new class of T-cells has come onto the scene. These are the Th17 cells. As far as I know there are no T-cells with the names Th4 to Th16. The name Th3 has been used for a type of regulatory T-cells but does not seem to have gained much prominence. The name Th17 has a different origin – it is due to the fact that these cells secrete the cytokine interleukin 17. Th17 cells have been implicated in a variety of immune-mediated diseases such as psoriasis, rheumatoid arthritis, multiple sclerosis, inflammatory bowel disease and asthma. These cells were only identified in 2006 when IL-17 had already been around for ten years.

In some cases Th1 and Th17 cells seem to work side by side with similar effects. For instance both seem to be having harmful effects in rheumatoid arthritis (RA). The analogue of IL-17 for the Th1 cells is tumour necrosis factor $\alpha$. Antibodies against TNF$\alpha$ are now used therapeutically in the treatment of RA and some other autoimmune diseases which are usually considered as associated with Th1 cells. So what about MS? There Th1 and Th17 cells seem to be at work. Surprisingly, antibodies against TNF$\alpha$ seem to have a neligible or harmful effect on MS patients. This might give some new insight into the differences between diseases with superficially similar mechanisms. Of course one may think of using antibodies against IL-17 as treatments for autoimmune diseases. In which cases will the results be the same as when TNF$\alpha$ is targeted and in which cases different? My hope is that divergent results could lead to deeper insights into the workings of the immune system. Perhaps it could be possible to identify some essential networks of players (cells and/or cytokines) which are susceptible to theoretical analysis.