For my master thesis, I wrote a small tool that would take and analyze raw genomic high throughput data of various T-cells (chip-seq + rna-seq of th17 to be pre

For my master thesis, I wrote a small tool that would take and analyze raw genomic high throughput data of various T-cells (chip-seq + rna-seq of th17 to be precise) and create a regulatory network in Cytoscape. The basis was a paper relating to The Th17 Project [1]. What I learned is that we are sort of in the very beginnings of understanding how immune cells work (together), how their plasticity works in terms of gene expression at any given point in time. For example, environmental circumstances such as cytokine presence can lead to T-cell types "transforming" to other types which have other effects etc. but it's not well understood how this occurs. A very large amount of genes regulate each other, you get a complicated network of up- and downregulations and it's hard to reproduce and understand what needs to be done to generate a certain type of T-cell with certain characteristics and behavior. And then you haven't even tried doing that in-vivo where you could try to push the immune system to express genes such that many T-cells of type X are generated to enhance or fight inflammation. Because then you just disturbed a complex interacting system with zero idea what the total effect is and whether "the network" is resilient enough to not crash and burn somewhere somehow. It's very very complicated with a huge amount of combinatorics involved so Complex Systems Theory helps to build models helps a bit. [1] http://th17.bio.nyu.edu/pages/index.html http://th17.bio.nyu.edu/pages/index.html