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- Murphy, Colin, 1983, et al.
(author)
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Plasmonic Temperature-Programmed Desorption
- 2021
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In: Nano Letters. - : American Chemical Society (ACS). - 1530-6992 .- 1530-6984. ; 21:1, s. 353-359
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Journal article (peer-reviewed)abstract
- Temperature-programmed desorption (TPD) allows for the determination of the bonding strength and coverage of molecular mono- or multilayers on a surface and is widely used in surface science. In its traditional form using a mass spectrometric readout, this information is derived indirectly by analysis of resulting desorption peaks. This is problematic because the mass spectrometer signal not only originates from the sample surface but also potentially from other surfaces in the measurement chamber. As a complementary alternative, we introduce plasmonic TPD, which directly measures the surface coverage of molecular species adsorbed on metal nanoparticles at ultrahigh vacuum conditions. Using the examples of methanol and benzene on Au nanoparticle surfaces, the method can resolve all relevant features in the submonolayer and multilayer regimes. Furthermore, it enables the study of two types of nanoparticles simultaneously, which is challenging in a traditional TPD experiment, as we demonstrate specifically for Au and Ag.
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- Serwas, NK, et al.
(author)
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Human DEF6 deficiency underlies an immunodeficiency syndrome with systemic autoimmunity and aberrant CTLA-4 homeostasis
- 2019
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In: Nature communications. - : Springer Science and Business Media LLC. - 2041-1723. ; 10:1, s. 3106-
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Journal article (peer-reviewed)abstract
- Immune responses need to be controlled tightly to prevent autoimmune diseases, yet underlying molecular mechanisms remain partially understood. Here, we identify biallelic mutations in three patients from two unrelated families in differentially expressed in FDCP6 homolog (DEF6) as the molecular cause of an inborn error of immunity with systemic autoimmunity. Patient T cells exhibit impaired regulation of CTLA-4 surface trafficking associated with reduced functional CTLA-4 availability, which is replicated in DEF6-knockout Jurkat cells. Mechanistically, we identify the small GTPase RAB11 as an interactor of the guanine nucleotide exchange factor DEF6, and find disrupted binding of mutant DEF6 to RAB11 as well as reduced RAB11+CTLA-4+ vesicles in DEF6-mutated cells. One of the patients has been treated with CTLA-4-Ig and achieved sustained remission. Collectively, we uncover DEF6 as player in immune homeostasis ensuring availability of the checkpoint protein CTLA-4 at T-cell surface, identifying a potential target for autoimmune and/or cancer therapy.
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