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Keller, Michael D.
Blood, 11/2018, Letnik: 132, Številka: 22Journal Article
In this issue of Blood, Brigida et al1 demonstrate that null mutations in ARPC1B result in combined immunodeficiency because of defects in T-cell migration, lymphoproliferation, and formation of the immune synapse, and further show that these abnormalities may be rescued by transduction of wild-type ARPC1B.
