Tag Archives: ICAM-1

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,