... and since we've set out on the topic, there are many curious things that are immunomodulators / immunosuppressants / anti-inflammatory, such as the cis-isomer of urocanic acid which is found on human skin. The ultraviolet radiation in sunlight changes trans-urocanic acid into cis-urocanic acid, which is immunomodulatory via serotonin receptor 5-HT2A. Paper:
https://doi.org/10.1073/pnas.0603119103 ... another one on the molecular basis for how it works:
https://doi.org/10.1016/j.bmcl.2009.07.143(Urocanic acid is a funny name. According to Wikipedia, Urocanic acid was first isolated in 1874 by the chemist Max Jaffé from the urine of a dog,[8][9] hence the name (Latin: urina = urine, and canis = dog). Cis- and trans-urocanic acid literally mean "this side dog-pee acid" and "that-side dog pee acid", respectively. Weird! I almost wish I could unlearn the fact as it's somewhat distracting, heh.)
And similarly, many substances which activate serotonin receptor 5-HT2A are immunosuppressors and antiinflammatory, substances which are more known for, uh, inflaming the ... er ... senses?: https://doi.org/10.3389/fimmu.2015.00358
A receptor by name Sigma-1 is mentioned the, *ahem*, 5-HT2A agonist paper. It's thought to be immunomodulatory. Have you seen the study that indicates that the SSRI fluvoxamine helps against severe cases of COVID-19? http://dx.doi.org/10.1001/jama.2020.22760
Turns out that fluvoxamine is apparently has the strongest effect on the Sigma-1 receptor among the known SSRIs. https://doi.org/10.3389/fphar.2021.652688
As far as I understand this: Apparently serotonin can both induce inflammation as well as reduce it, depending on what receptors it hits, i.e. in what tissue it is. And blood platelets store serotonin at high densities. I hadn't heard about any of this until recently. Most surprising to me was that the organ responsible for the brunt of breaking down excess serotonin for disposal are ... the lungs!
There are theories - which seem biologically plausible to me - that in COVID-19, there is inflammation and endothelial injury to the lungs, which causes platelets to release serotonin, the lungs' ability to clear serotonin is impaired, and that this forms a feedback loop of excess serotonin buildup and further inflammation. https://dx.doi.org/10.2139/ssrn.3800402 ... and that blocking serotonin receptors using 5-HT2A agonists helps recover severe cases of COVID-19. There is anecdotal evidence and biological plausibility. They say it's hard to get this studied properly, i.e. to get funding and attention.