γδ T cells are considered to be innate-like lymphocytes that respond rapidly to stress without clonal selection and differentiation. Here we use next-generation sequencing to probe how this paradigm relates to human Vδ2neg T cells, implicated in responses to viral infection and cancer. The prevalent Vδ1 T cell receptor (TCR) repertoire is private and initially unfocused in cord blood, typically becoming strongly focused on a few high-frequency clonotypes by adulthood. Clonal expansions have differentiated from a naive to effector phenotype associated with CD27 downregulation, retaining proliferative capacity and TCR sensitivity, displaying increased cytotoxic markers and altered homing capabilities, and remaining relatively stable over time. Contrastingly, Vδ2+ T cells express semi-invariant TCRs, which are present at birth and shared between individuals. Human Vδ1+ T cells have therefore evolved a distinct biology from the Vδ2+ subset, involving a central, personalized role for the γδ TCR in directing a highly adaptive yet unconventional form of immune surveillance.

Over the past few years, the scientific community, as well as the world's coatings industry has seen the introduction of oxide/polymer-based superhydrophobic surfaces and coatings with exceptional water repellency. Online videos have caught the public's imagination by showing people walking through mud puddles without getting their tennis shoes wet or muddy, and water literally flying off coated surfaces. This article attempts to explain the basics of this behavior and to discuss and explain the latest superhydrophobic technological breakthroughs. Since superhydrophobic surfaces and coatings can fundamentally change how water interacts with surfaces, and the fact that earth is a water world, it can legitimately be said that this technology has the potential to literally change the world.

Vδ2+ T cells form the predominant human γδ T-cell population in peripheral blood and mediate T-cell receptor (TCR)-dependent anti-microbial and anti-tumour immunity. Here we show that the Vδ2+ compartment comprises both innate-like and adaptive subsets. Vγ9+ Vδ2+ T cells display semi-invariant TCR repertoires, featuring public Vγ9 TCR sequences equivalent in cord and adult blood. By contrast, we also identify a separate, Vγ9− Vδ2+ T-cell subset that typically has a CD27hiCCR7+CD28+IL-7Rα+ naive-like phenotype and a diverse TCR repertoire, however in response to viral infection, undergoes clonal expansion and differentiation to a CD27loCD45RA+CX3CR1+granzymeA/B+ effector phenotype. Consistent with a function in solid tissue immunosurveillance, we detect human intrahepatic Vγ9− Vδ2+ T cells featuring dominant clonal expansions and an effector phenotype. These findings redefine human γδ T-cell subsets by delineating the Vδ2+ T-cell compartment into innate-like (Vγ9+) and adaptive (Vγ9−) subsets, which have distinct functions in microbial immunosurveillance.

Background & AimsMucosal-Associated Invariant T (MAIT) cells are innate-like T cells characterised by the invariant TCR-chain, Vα7.2-Jα33, and are restricted by MR1, which presents bacterial vitamin B metabolites. They are important for antibacterial immunity at mucosal sites; however, detailed characteristics of liver-infiltrating MAIT (LI-MAIT) and their role in biliary immune surveillance remain unexplored.MethodsThe phenotype and intrahepatic localisation of human LI-MAIT cells was examined in diseased and normal livers. MAIT cell activation in response to E. coli-exposed macrophages, biliary epithelial cells (BEC) and liver B cells was assessed with/without anti-MR1.ResultsIntrahepatic MAIT cells predominantly localised to bile ducts in the portal tracts. Consistent with this distribution, they expressed biliary tropic chemokine receptors CCR6, CXCR6, and integrin αEβ7. LI-MAIT cells were also present in the hepatic sinusoids and possessed tissue-homing chemokine receptor CXCR3 and integrins LFA-1 and VLA-4, suggesting their recruitment via hepatic sinusoids. LI-MAIT cells were enriched in the parenchyma of acute liver failure livers compared to chronic diseased livers. LI-MAIT cells had an activated, effector memory phenotype, expressed α4β7 and receptors for IL-12, IL-18, and IL-23. Importantly, in response to E. coli-exposed macrophages, liver B cells and BEC, MAIT cells upregulated IFN-γ and CD40 Ligand and degranulated in an MR1-dependent, cytokine-independent manner. In addition, diseased liver MAIT cells expressed T-bet and RORγt and the cytokines IFN-γ, TNF-α, and IL-17.ConclusionsOur findings provide the first evidence of an immune surveillance effector response for MAIT cells towards BEC in human liver; thus they could be manipulated for treatment of biliary disease in the future.

This study reports concentrations of BDEs 47, 99, 100, 153, and 154 in outdoor air [median sigmaPBDE (sum of BDEs 47, 99, 100, 153, and 154) = 18 pg m(-3)] in air from a range of office and home indoor microenvironments (median sigmaPBDE = 762 pg m(-3)) and vegan and omnivorous duplicate diet samples (median sigmaPBDE = 154 and 181 pg g(-1) dryweightforvegan and omnivorous diets, respectively). Median daily human exposure to sigmaPBDE via inhalation is 6.9 ng/person and 90.5 ng/person via diet but the relative significance of these pathways may vary considerably between individuals. Median concentrations in indoor air were higher in workplace (sigmaPBDE = 1082 pg m(-3)) than in domestic (sigmaPBDE = 128 pg m(-3)) microenvironments, and substantial differences in concentrations in air from different rooms in the same office building were found. When data from the only mechanically ventilated room was excluded, a significant positive correlation (p < 0.001) was observed between PBDE concentrations and both the number of electrical appliances and polyurethane foam-containing chairs. Concentrations of sigmaPBDE and BDEs 47 and 99 were significantly higher (p < 0.1) in omnivorous diet samples than in vegan diet samples, implying that while plant-based foods contribute appreciably, higher exposure occurs via ingestion of animal-based comestibles.

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Concentrations and chiral signatures of polychlorinated biphenyls (PCBs) were measured in outdoor air (using polyurethane foam (PUF)--disk passive samplers) and surface soil samples taken at approximately monthly intervals over 1 year at 10 locations on a rural-urban transect across the West Midlands of the U.K. In both air and soil, concentrations clearly decrease with increasing distance from the city center, supporting the existence of an urban "pulse", that indicate the West Midlands conurbation to be a source of PCBs to the wider environment. Concentrations of PCBs in outdoor air samples in this study are well below those reported previously for indoor air in the West Midlands. This, combined with comparison of chiral signatures in outdoor air and soil with those in samples of indoor air taken in the West Midlands, suggest strongly that the principal contemporary source of PCBs in this conurbation is ventilation of indoor air and not volatilization from soil. Future reductions in PCB concentrations in outdoor air and ultimately human exposure appear best achieved by action to remove remaining sources of PCBs from existing structures.

γδ T cells are unconventional lymphocytes commonly described as ‘innate-like’ in function, which can respond in both a T cell receptor (TCR)-independent and also major histocompatibility complex (MHC)-unrestricted TCR-dependent manner. While the relative importance of TCR recognition had remained unclear, recent studies revealed that human Vδ1 T cells display unexpected parallels with adaptive αβ T cells. Vδ1 T cells undergo profound and highly focussed clonal expansion from an initially diverse and private TCR repertoire, most likely in response to specific immune challenges. Concomitantly, they differentiate from a Vδ1 T cell naïve (Tnaïve) to a Vδ1 T cell effector (Teffector) phenotype, marked by the downregulation of lymphoid homing receptors and upregulation of peripheral homing receptors and effector markers. This suggests that an adaptive paradigm applies to Vδ1 T cells, likely involving TCR-dependent but MHC-unrestricted responses to microbial and non-microbial challenges.