Effector T cells migrate into the inflamed tissue will increase tissue damage and lead to deterioration of inflammatory diseases. Researchers from the University of Pennsylvania found that the lack of adapter proteins and CRK CRK-like T cells appear adhesion, chemotaxis decline characteristics, and proved by experiments CRK family of proteins capable freezer of selectively regulating t-cell adhesion and the effect site the ability to migrate, and proposed methods of treatment of graft versus host disease (GVHD) for CRK protein family or can be developed against. Recently, the results of this study in the prestigious Journal of Clinical JCI published online.
The researchers found that the use of conditions knockout mice, and after missing CRK CRK-like protein, T-cell adhesion, chemotaxis are declining, and found CRK CRK-like and there are a lot of these two proteins functionally redundant, overexpression of either, can lead to both defects in T cell function was restored deletion results. The researchers found by studying the mechanism, CRK can exchange factor C3G and adhesion molecules reside CASL synergies with RAP guanine nucleotide activating integrin regulatory GTPase RAP1. CRK protein essential for effector T cell migration to sites of inflammation, but does not affect the effector T cells migrate to the lymphoid organs.
In summary, the article found CRK protein family of adapter proteins to the site of inflammation T cell migration and adhesion selective regulation. The research on the development of great significance for promoting the treatment of GVHD.
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