This is a fun session that reviews highlights of the rheumatology literature over the last year. I won’t go into the clinical stuff because I’m not sure I agree with the selections, but the basic science stuff was interesting. This is a field I’m really not familiar with and therefore I really can’t go into all the details. But here’s the summary:

So there’s a new cell structure that’s been called the inflammasone that was described this year. It acts through a molecular path mediated by something called NALP3. This path induces an inflammatory molecule known as interleukin-1-beta. Why is this interesting? Because this path is shared by some crystal diseases, like gout, and some hereditary diseases, like something called Neonatal Onset Multisystem Inflammatory Disease (NOMIS), a hereditary inflammatory disease of childhood. This is interesting because we have an interleukin blocking drug (anakinra) and when it was used in NOMIS – based on this new discovery – the disease pretty much melted away. That’s a nice clinical use of a basic science discovery.

Then, a regulatory path termed the ‘sialylation switch’ was described. It turns out that immunoglobulins, the classic method of inducing inflammation, can be ‘turned off’ if they are sialylated (adding a certain molecule). That’s kind of neat because it means that immunoglobulins can be both inflammation-inducing, and inflammation-depressing. This has future therapeutic potential – I think you can see it. If you can somehow sialylate immunoglobulins that cause inflammatory disease, maybe you can turn off the reaction.

Finally, we heard about the non-inflammatory effect of complement. Complements are another classical mediator of inflammation. Here complement was shown to help induce neovascularization (the creation of new blood vessels) in age-related macular degeneration. Once again, this was not an effect that was know of before, and again has potential therapeutic consequences. Maybe treating macular degeneration with anti-inflammatory drugs is useful.