And

then the integrans are important for telling themsells where to go. And so the uriedis on the integrans and and when they're in the lymph nod and how they leave lymph node and where they know how to, how they know where to go, right? That's all

yeas, there's something we kind of

am ended up because we started following this trouble, so component not following us much. But i still think it's really interesting. And ad hope e some will cleverat with debon, because i think thes theres some very complimentary interest. And, ah, whats he flickla help ourselves ore doing and and how that's being regulated.

I have a question about m t 17 a little bit. I think that sometimes there's this a idea or there there's thing that you've mentioned really well, that, a, there's a question of art seventeens kind of the pathogenic cell am or are they actually, you knowoe lsewillthink about things that they do that are useful. And so my question, when to you about those th seventeens, and, ah, their potential pathogenesis, is that, are they, in those cases, doing something inappropriate? Are they, were they perhaps activated inappropriately? Or is it almost a ripe plant, right place? Thing? Ram

ors a weed in i atei ri eeda weed. Ind a weed in the place that you want id is not a weed. Andea, a weed is just the blont in a place you don't want it. E, no, i think that that's a great question. And i think it's still something that were the field is is still figuring out. Am, why es? One of things that i think about is, well, as, why are most odermmune responses so strongly associated tat 17 cells? You know, why don't you have more ordo imune tch two type diseases, or ordo immune? Am, and so i guess my my sort of philosophical thinking on that is. Am, well, one of the studies wede done in in human t at 17 cells was looking at simulation how they respond to costimulation and tea cel recepti signalling, and finding that, surprisingly, t 17 cells actually rarely like very low levels of cos stimulation, which is in contrast to other tea cells, and in contrast to our thinking that costimulation is signal to to tell a tea cell that they should get activated instead of becoming tolerant. Am, and so andusually pathagans, you know, e, infections that are causing damage are what will drive high cause stimulation. And so that's a safe situation to cause inflammation asyou have a pathagin. So the fact that t at 17 cells seem to almost prefer conditions with loco stimulation. A makes me think that that's part of why order reactive cells are more likely to be t at 17, because you're more likely to see self felf partins in presence of loco stimulation. And then the other thing is this, i do think tha this finding that ile seventene seems to contribute to wound healing type of responses, and that that these cells are mostly present in various surfaces where you do have rapid turnover of tissue. So, you know, you think of central nervous em for example, the brain is not turning over, and there's very few immune cells there, in microbes there, and that's the normal healthy situation. So were is in the gut and the skin, we do have am turn over and ill 17, but it's am yes. So so what are the conditions that allow cells to exist and not cause frank, inflammation? And there is some idea like, it seems like the level of isle one may help to determine that, or isle 23, something besidee kind environment of what else is going on. Am, the metabolic state of the t cells themselves makes a difference to the ones that are highly metaboliclly active ar more likely to cause inflammation. Am, i think that usually the environment is controlling the tisal pathogensity, if that makes sense. Am, but then what makes that go wrong when you have like multiple sperosis, or or serisis, or inordiny disease? I think we still don't have a good understanding of that. So

really, what res probably say about all this is that everything is an immune cell, really. I mean, the we could say that even ones that we thought were structural cells are so. Amune celvs. So

so not only, as you said at the beginning, a, does menology impact everything? Everything is also menologyan

isye, exactly. Everything. Me, knowledge, everything. Meology affects everything and almost every sell yet that's one of the things i find fascinating, is that, am, these stroml cells essentially become immune cells. And and the fact that ile 17 seems to be influencing that so much. Am, i think ye continues to make it interesting, not just in peripheral tissues, but also actually even in the immune sight and the lymph note thes, something wer we're also tryn to understand in the contacts of infection. Then how does that? Am, contribute to outcomes during infection. Because again, there you have this wide range from very mild disease symptoms to very severe disease symptoms, even in the same infection, and even with controlling the infection. So wut? What's kind of regulating that balance? M is something we're becoming more interested and again, here being acty in a microbiology and aminology department and end even closer to people that are thinking about infection all the time, a good opportunity.