I blame Buzzfeed. I really do. But, really, why not have a GIF-studded listicle of cytokines? Am I crazy? 🙂
You know how inflammation can be a clusterf**k sometimes? Well, IL-10, and the other cytokines of that family are the ones that lay down the law. When inflammation needs to be quieted, IL-10 will insert its bad 18.5 kDa self into the fray, and, via a JAK1-STAT3 signaling axis will induce the anergy of IL-2 dependent Th1 cells. IL-10 is the friend who knows when your rager of a party has run its course, the friend who will save your IL-2-drunk ass from alcohol poisoning. In a nutshell, this is IL-10.
Interleukin 2 is a 133 amino acids of a roaring good time. IL-2 is the milkshake that brings almost all the important inflammtory cells to the yard. As antigenically/mitogenically stimulated T-cells crank out IL-2, it brings about its own proliferation by turning on IL-2 producing genes in T-cells and macrophages, but also causing IL-2 receptor upregulation on T-cells, B-cells, macrophages, and NK cells. Basically, IL-2 is what drives a robust adaptive response to any nasties who think they know what’s up. Really, bacteria/viruses/anything else, IL-2 always knows what’s up. Don’t even. Like, nope. “Cause IL-2 does not give a shit.
Transforming Growth Factor Beta is the belle of the ball, one of the reigning divas of the immune response, a major Prom Queen candidate… One of the reasons for this is that the cytokine is super-involved: it has important roles in cell fate determination, angiogenesis, morphogenesis and regulation of certain hormones, just to name a few things off of the top of my head. In the immune response, however, TFG-beta is involved in both the initiation and resolution of inflammation, like its buddy IL-10, up there. While TGF-beta has several productive interactions with T-cells, NK cells and macrophages, my favourite TGF-beta trick involves its interactions with the extra-cellular matrix wherein in brings about fibrosis. This is an important consequence for, say, wound-healing. The signaling axis involved is the sort of thing I want to party with forever.
TSLP is slowly emerging as THE Queen Bitch of the Th2 immune response–sorry, IL-4. Love ya, but, yeah…
Thymic Stromal Lymphopoeitin is involved in basophil development, the proliferation of dendritic cells armed with a Th2 programme or even a tolerogenic one, the homeostasis of NKT and CD4+ T-cell populations, and also this fascinating phenomenon known as The Atopic March. This is, well, “a process”, shall we say, that causes allergic diseases to progress: from, say, atopic dermatitis to allergic asthma or allergic rhinitis or both. TSLP is purported to be the one cytokine that fine tunes the Th2 response to seemingly leap from one organ to the next. Disclaimer: I don’t strictly understand the machinations of the Atopic March; take my explanation slightly salted! 🙂
Interleukin-33 is your epithelial cells’ way of letting you know that shit is going down. IL-33, under necrotizing circumstances, will be released from the dying cells and induce a potent cytotoxic T-cell response. IL-33 is one to watch out for, really, because, structurally, it has similarities with the IL-1 Family of cytokines, but it doesn’t *need* to be cleaved by Caspase 1 to be active. It also has a nuclear localization signal which suggests more “traditional” cytokine-y roles. But what are they, really? IL-33 is seen as important in both allergic diseases, as well as good ol’ antimicrobial defence. The destiny and secrets of this cytokine (alarmin?) seem very promising, indeed!
Take care now,