Monthly Archives: January 2014

5 Cytokines That Are Just Ballin’

I blame Buzzfeed. I really do. But, really, why not have a GIF-studded listicle of cytokines? Am I crazy? 🙂

1) IL-10

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.

IL-10 wants you to know that the party is over.

2) IL-2

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.

The World According to IL-2

3) TGF-β1

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.

TGF-beta1, telling it how it is.


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! 🙂

Dear Th2 Response, Yep. Love, TSLP.

5) IL-33

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!

IL-33 is coming!

Take care now,



My Project, Myself

My project and I? We’re in a good place. We don’t hate each other. This isn’t like the Eminem-Rihanna thing that had begun to happen with my MS thesis. Oh, Lord. Those were dark, drunk days…

I will admit, I was a bit calculative when I picked my current lab: we work with NKT cells, a flavour of immunocyte that isn’t completely understood. Thus, there is a lot to do, lots of questions to ask, lots to answer, and lots of new questions to raise….However, real-talk: I don’t get these cells. I don’t understand them. I don’t understand where their so-called “self” antigens come from. I don’t understand how they get to, y’know, BE. This doesn’t bother me, though, because I imagine that this is part of the process of getting this here PhD. If I knew this already, why in the world would I be in the lab setting up experiments?

My work focuses on the adhesion and migration behaviour of NKT cells in response to differential integrin signaling. The project was born out of this brilliant paper by Dr. Seddon Thomas, whom I admire from afar. In truth, we don’t know what makes NKT cells wanna travel, and if they do, where do they go? Dr. Thomas’s work seems to suggest that NKT cells home to the sinusoids of the liver given the high concentration of ICAM-1 there. I’ll buy it. The paper also suggests that PLZF (zinc-finger protein, transcription factor, controller of cell cycles and fates) is the key regulator of LFA-1 abundance on the NKT cell surface. Sounds good to me…mainly because it opens up all these avenues for the impact of NKT chemokine and integrin/receptor profiles on pathogenesis of inflammatory diseases.

NKT cells are a big deal in asthma. So, what causes them to home to or away from the lung? Is PLZF responsible, again? There are other things. Things I am not at liberty to speak of, but, needless to say, am chuffed about.

So, here we are: my project and I, eyeing each other gingerly, wondering what shall happen next…

Take care now,