Cleaning and disinfection are important operations in food processing because of the significant contributions to product hygiene and food safety. The transfer of residues from surfaces into a product and the contamination with adhering microorganisms must therefore be avoided with sufficient certainty. Traditional methods for the removal of adherents and inactivation of microorganisms are based on thermal, mechanical, or chemical principles and are known to be time-and energy-consuming. This has resulted in a search for alternative methods that show prospective potential for their use in food-processing plants. This review gives an overview on such methods, which are based on physical principles. In dry-ice cleaning, for example, carbon dioxide snow pellets are blasted onto a surface to remove adherents through a combined action of thermal and mechanical effects, followed by dissolution of these adherents. Ice-pigging is a procedure where an ice/ water mixture is forced through pipes, heat exchangers, or other equipment to carry off adhered substances. Another method for physical cleaning, mainly described in context with membrane filtration, is to use vibration in the ultrasonic frequency domain to reduce fouling and to stabilize permeate flux. Radiation from various sources (UV lamps, radionuclides, X-ray tubes) differs in its applicability and disinfection efficiency because of differences in energy and penetration depth. Cold plasma treatment is another promising technology that is currently under investigation for cleaning and disinfection of surfaces of inorganic and organic materials.

Cassava starch was debranched using pullulanase and the linear glucans recrystallized by incubation at 60°C or by temperature cycling at 120/60°C, and further subjected to heat‐moisture treatment (HMT). Resistant starch (RS III) contents increased from 21.4 g/100 g in the debranched starch (DS) to 67.3 g/100 g in the debranched starch incubated at 60°C (DRS) and 47.8 g/100 g in the debranched starch subjected to temperature cycling (DCS), and further to 84.8 g/100 g and 88.4% g/100 g in HMT‐DRS and HMT‐DCS, respectively. Total crystallinity varied between 31.4‐59.8% and the crystalline type was C in DS and DRS and A in DCS, HMT‐DRS and HMT‐DCS. The melting properties were characterized by broad endotherms, but the exact melting region and enthalpy were dependent on recrystallization method. The main endothermic peaks of DS and DRS occurred at 103.9 and 109.8°C, respectively, whereas DCS exhibited split endotherms at 113.6 and 138.1°C. Heat‐moisture treatment broadened the endotherms and increased their enthalpies. Scanning electron micrographs revealed surface topography differences related to size and aggregation of individual crystalline bodies.

CD4+Foxp3+ Treg cells are essential for maintaining self-tolerance and preventing excessive immune responses. In the context of Th1 immune responses, co-expression of the Th1 transcription factor T-bet with Foxp3 is essential for Treg cells to control Th1 responses. T-bet-dependent expression of CXCR3 directs Treg cells to the site of inflammation. However, the suppressive mediators enabling effective control of Th1 responses at this site are unknown. In this study, we determined the signature of CXCR3+ Treg cells arising in Th1 settings and defined universal features of Treg cells in this context using multiple Th1-dominated infection models. Our analysis defined a set of Th1-specific co-inhibitory receptors and cytotoxic molecules that are specifically expressed in Treg cells during Th1 immune responses in mice and humans. Among these, we identified the novel co-inhibitory receptor CD85k as a functional predictor for Treg-mediated suppression specifically of Th1 responses, which could be explored therapeutically for selective immune suppression in autoimmunity.

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The results suggest that self-perceived dental irregularity and negative impact of dental esthetics might affect oral health, whereas previous extensive orthodontic treatment may have favorable effects by improving dental health compliance.

Foxp3 + regulatory T (Treg) cells are essential for maintaining peripheral tolerance and preventing autoimmunity. While genetic factors may predispose for autoimmunity, additional environmental triggers, such as viral infections, are usually required to initiate the onset of disease. Here, we show that viral infection with LCMV results in type I IFN-dependent Treg cell loss that is rapidly compensated by the conversion and expansion of Vβ5 + conventional T cells into iTreg cells. Using Vβ5-deficient mice, we show that these Vβ5 + iTreg cells are dispensable for limiting anti-viral immunity. Rather, the delayed replenishment of Treg cells in Vβ5-deficient mice compromises suppression of microbiota-dependent activation of CD8 + T cells, resulting in colitis. Importantly, recovery from clinical symptoms in IBD patients is marked by expansion of the corresponding Vβ2 + Treg population in humans. Collectively, we provide a link between a viral trigger and an impaired Treg cell compartment resulting in the initiation of immune pathology.

Regulatory T cells (Tregs) maintain peripheral self-tolerance and limit immune mediated pathology. Like effector T cells, Tregs can specialize in TH1-dominated immune responses and co-express T-bet together with Foxp3. This allows for expression of CXCR3 and efficient homing to sites of TH1 responses. However, whether such functional specialization is paralleled by memory generation among Tregs is unknown. In this study, we investigated the ability of polyclonal Tregs to form functional memory in response to viral infection. Using adoptive transfer models to compare infection-experienced Tregs generated upon acute Lymphocytic Choriomeningitis Virus (LCMV) WE and Vaccinia Virus (VV) infections with naive Tregs, we observed no differences in their phenotype or their in vivo maintenance. When comparing functional properties of infection-experienced and naive Tregs, we found no differences in in vitro suppressive capacity nor in their ability to limit the effector response upon homologous, systemic or local re-challenge in vivo. Our results suggest that no functional Treg memory is generated in the context of systemic LCMV or VV infection, but we cannot rule out the possibility that the generation of Treg memory may be possible in other contexts.

Regulatory T cells (Tregs) prevent excessive immune responses and limit immune pathology upon infections. To fulfill this role in different immune environments elicited by different types of pathogens, Tregs undergo functional specialization into distinct subsets. During acute type 1 immune responses, type 1 Tregs are induced and recruited to the site of ongoing Th1 responses to efficiently control Th1 responses. However, whether a similar specialization process also takes place following chronic infections is still unknown. In this study, we investigated Treg specialization in persistent viral infections using lymphocytic choriomeningitis virus (LCMV) and murine cytomegalovirus (MCMV) infection as models for chronic and latent infections, respectively. We identify CD85k as a Th1-specific co-inhibitory receptor with sustained expression in persistent viral infections and show that recombinant CD85k inhibits LCMV-specific effector T cells. Furthermore, expression of the CD85k ligand ALCAM is induced on LCMV-specific and exhausted T cells during chronic LCMV infection. Finally, we demonstrate that type 1 Tregs arising during chronic LCMV infection suppress Th1 effector cells in an ALCAM-dependent manner. These results extend the current knowledge of Treg specialization from acute to persistent viral infections and reveal an important functional role of CD85k in Treg-mediated suppression of type 1 immunity.