Current teleoperated surgical robots do not provide surgeons with haptic feedback, due in part to the safety risks associated with grounded kinesthetic forces. Ungrounded cutaneous feedback provides an elegant and inherently stable way to refer haptic feedback to the surgeon in such situations. Choosing the most appropriate display, however, is challenging given the substantial number of unique cutaneous displays presented in the literature. In this work, we demonstrate how measuring the space of tactile sensations that a device can create can be employed to objectively compare different cutaneous displays for a specific task. We built four cutaneous displays and compared their ability to render sensations measured while pinching four disparate materials with a biomimetic tactile sensor. As predicted, quantitative tactile rendering errors varied significantly across devices and materials. The results of this comparison can be used to design better cutaneous displays for pinching palpation in robotic surgery. Furthermore, the proposed approach could provide a useful tool for evaluating novel cutaneous devices for various other tactile tasks, providing an objective framework to supplement and guide future human subject studies

Natural killer (NK) cells are an important component of anti-cancer immunity, and their activity is regulated by an array of activating and inhibitory receptors. In mice, the inhibitory NKR-P1B receptor is expressed in NK cells and recognizes the C-type lectin-related protein-b (Clr-b) ligand. NKR-P1B:Clr-b interactions represent a ‘missing-self’ recognition system to monitor cellular levels of Clr-b on healthy and diseased cells. Here, we report an important role for NKR-P1B:Clr-b interactions in tumor immunosurveillance in MMTV-PyVT mice, which develop spontaneous mammary tumors. MMTV-PyVT mice on NKR-P1B-deficient genetic background developed mammary tumors earlier than on wild-type (WT) background. A greater proportion of tumor-infiltrating NK cells downregulate expression of the transcription factor Eomesodermin (EOMES) in NKR-P1B-deficient mice compared to WT mice. Tumor-infiltrating NK cells also downregulated CD49b expression but gain CD49a expression and exhibit effector functions, such as granzyme B upregulation and proliferation in mammary tumors. However, unlike the EOMES + NK cells, the EOMES ‒ NK cell subset is unable to respond to further in vitro stimulation and exhibits phenotypic alterations associated with immune dysfunction. These alterations included increased expression of PD-1, LAG-3, and TIGIT and decreased expression of NKp46, Ly49C/I, CD11b, and KLRG-1. Furthermore, tumor-infiltrating NKR-P1B-deficient NK cells exhibited an elevated dysfunctional immune phenotype compared to WT NK cells. These findings demonstrate that the NKR-P1B receptor plays an important role in mammary tumor surveillance by regulating anti-cancer immune responses and functional homeostasis in NK cells.