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When a pathogen infects your body, the T cells at the site of infection are a vital part of your immune response. However, in order to complete this function the T cells need to stop at the infection site, resisting the blood flow. It’s known that a T cell’s ability to stop in the blood vessels is controlled by diacylglycerol kinases (DGKs). These are known to activate guanine nucleotide exchange factors (GEFs) and Ras proximity 1 (Rap1) molecules, which in turn activate integrin lymphocyte function associated antigen-1 (LFA-1).

Now, Dooyoung Lee and colleagues from the University of Pennsylvania have determined how the level of DKGs regulate T cell arrest in vessels. Using flow chamber assays and in silico models, they show that loss of DGKs actually increases a T cell’s ability to stop in vessels, possibly due to an increase in in LFA-1 binding affinity. Future experiments should deduce the exact effects of DGK deficiency on T cell arrest.

This article is a good example of how well experimental work and computer models can be integrated to solve biological questions. It’s also free* for the next four weeks:

Diacylglycerol kinase zeta negatively regulates CXCR4-stimulated T lymphocyte firm arrest to ICAM-1 under shear flow
Dooyoung Lee, Jiyeon Kim, Michael T. Beste, Gary A. Koretzky and Daniel A. Hammer
DOI: 10.1039/C2IB00002D

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