The design of functional coatings for touchscreens and haptic interfaces is of paramount importance for smartphones, tablets, and computers. Among the functional properties, the ability to suppress or eliminate fingerprints from specific surfaces is one of the most critical. We produced photoactivated anti-fingerprint coatings by embedding 2D-SnSe₂ nanoflakes in ordered mesoporous titania thin films. The SnSe₂ nanostructures were produced by solvent-assisted sonication employing 1-Methyl-2-pyrrolidinone. The combination of SnSe₂ and nanocrystalline anatase titania enables the formation of photoactivated heterostructures with an enhanced ability to remove fingerprints from their surface. These results were achieved through careful design of the heterostructure and controlled processing of the films by liquid phase deposition. The self-assembly process is unaffected by the addition of SnSe₂, and the titania mesoporous films keep their three-dimensional pore organization. The coating layers show high optical transparency and a homogeneous distribution of SnSe₂ within the matrix. An evaluation of photocatalytic activity was performed by observing the degradation of stearic acid and Rhodamine B layers deposited on the photoactive films as a function of radiation exposure time. FTIR and UV-Vis spectroscopies were used for the photodegradation tests. Additionally, infrared imaging was employed to assess the anti-fingerprinting property. The photodegradation process, following pseudo-first-order kinetics, shows a tremendous improvement over bare mesoporous titania films. Furthermore, exposure of the films to sunlight and UV light completely removes the fingerprints, opening the route to several self-cleaning applications.

Regulatory T cells (Tregs) are crucial for the maintenance of immune tolerance and the absence of Tregs results in significant autoantibody production. This suggests that Tregs play a key role in B cell tolerance. The mechanism by which Tregs regulate B cell tolerance has yet to be resolved but has important implications for our understanding of autoimmunity. Using both constitutive and inducible models, we show that the absence of Tregs results in autoantibody production, due to the loss of B cell anergy. Further studies show that this is dependent on the presence of helper T cells. We propose that the absence of Tregs results in the dysregulation of helper T cells that drive the loss of B cell anergy. Interestingly, our studies show the expansion of a CD4+GL7+ population in the absence of Tregs. Subsequent analysis shows that many of these cells express CXCR5 and thus resemble germinal-center TFH cells, an observation confirmed by their expression of Bcl6 and IL-21. We hypothesize that the absence of Tregs drives the expansion of TFH cells that play a role in the loss of B cell anergy. Characterization of this proposed mechanism may unveil new strategies for the treatment or prevention of autoantibody-mediated autoimmune diseases.

Two-dimensional Layered Amorphous Metal Oxide Sensors (LAMOS) represent a new class of 2D amorphous oxide (a-MOx) interfaces with unveiled properties in gas sensing applications. Herein, we report the humidity and gas sensing response of p- and n-type chemoresistive few-layered (2D) amorphous a-SnO₂, a-In₂O₃, and a-Cr₂O₃, discussing their reaction mechanisms using DFT modelling and electrical tests. LAMOS interfaces can be easily prepared by controlled oxidation in air of a large class of exfoliated 2D TMDs, MCs, and TMTH (Transition Metal Dichalcogenides, Chalcogenides, and Trihalides) like WS₂, MoS₂, SnSe₂, In₂Se₃, NiCl₂, and CrCl₃, yielding 2D amorphous a-MOx interfaces. LAMOS platforms preserving all the surface-to-volume advantages of their 2D precursors show excellent gas sensing properties representing a new class of material for gas sensing applications.

Dissecting the mechanisms that support autoantibody production is essential to our understanding of autoimmune diseases such as lupus. Recent work from our laboratory has shown that regulatory T cells (Tregs) play a key role in suppressing autoantibody production by helping to maintain B cell anergy. Our long-term goal is to understand how Tregs regulate B cell anergy. Our studies indicate that helper T cells play a key role as an intermediate between Treg and anergic B cells. Specifically, the absence of Tregs rapidly (within 4 days) drives the expansion of CD4+GL7+ helper T cells. This gross population can be further divided into 2 populations: germinal center follicular T cells (GC-TFH) and a novel non-TFH subset termed TAN cells. These GL7+ helper T cell subsets deliver potent signals to naïve and anergic B cells, inducing significant antibody production from both populations. Recent studies have begun to identify the signals that drive the expansion of GC-TFH and TAN cells in the absence of Tregs. We have shown that treatment of Treg-deficient mice with an agonistic anti-CD137 antibody reduces the expansion of CD4+GL7+ helper T cells (both GC-TFH and TAN cells). This treatment also reduced the expansion of class-switched B cells and abolished autoantibody production. Collectively, our studies indicate that CD137 signaling plays a key role in the expansion of pathogenic helper T cell subsets that support autoimmunity in the absence of Tregs.