Embryonic-stem-cell-derived mesenchymal stem cells relieve experimental contact urticaria by regulating the functions of mast cells and T cells.

Contact urticaria (CU) is an inflammatory skin disorder triggered by specific substances upon skin contact, leading to immediate acute or chronic manifestations characterized by swelling and redness. While mesenchymal stem cells (MSCs) are increasingly recognized for their therapeutic potential in immune diseases, research on the efficacy and mechanisms of stem cell therapy for urticaria remains scarce. This study investigates the regulatory role of embryonic-stem-cell-derived multipotent MSCs (M-MSCs) administered in a CU mouse model. Therapeutic effects of M-MSC administration were assessed in a Trimellitic anhydride-induced contact urticaria model, revealing significant inhibition of urticarial reactions, including ear swelling, itchiness, and skin lesion. Moreover, M-MSC administration exerted control over effector T cell activities in major lymphoid and peripheral tissues, while also suppressing mast cell degranulation in peripheral tissues. Notably, the inhibitory effects mediated by M-MSCs were found to be TGF-ß-dependent. Our study demonstrates the capacity of M-MSCs to regulate contact urticaria in a murine model, harmonizing the activation of inflammatory T cells and mast cells. Additionally, we suggest that TGF-ß derived from M-MSCs could play a pivotal role as an inhibitory mechanism in contact urticaria.

Complementary Analysis for Undetectable Microplastics from Contact Lenses to Aquatic Environments via Fourier Transform Infrared Spectroscopy.

Although microplastics (MPs) are intrinsically toxic and function as vectors for organic micropollutants, their discharge from wastewater treatment plant effluents and human activity remains unknown owing to the limitations of detection and treatment technologies. It is imperative to quantify MPs from human activities involving the consumption of various plastic products. This study warns that contact lenses can generate MPs and nanoplastics (NPs) after being discharged into aquatic environments. Identification via micro-Fourier transform infrared spectroscopy revealed that the fragmented particles (from a few tens to a few hundred micrometres) could not be detected as poly(2-hydroxyl methacrylate), the component of contact lenses, owing to changes in its chemical properties. After the degradation process, the median size of the contact lens particles decreased from 313 to 85 µm. Approximately 300,600 g of contact lens waste is discharged into sewage systems daily in the United States of America (USA), where 45 million people wear contact lenses and throw away one-fifth of them every day. Contact lens waste (1 g) has the potential to release 5653.3-17,773.3 particles of MPs. This implies that the currently reported MP amounts in the environmental matrix exclude significant amounts of MPs and NPs from discharged contact lenses. The identification method should be examined, and a registration of the disposal process should be established.

CD1dhiPD-L1hiCD27+ Regulatory Natural Killer Subset Suppresses Atopic Dermatitis.

Effector and regulatory functions of various leukocytes in allergic diseases have been well reported. Although the role of conventional natural killer (NK) cells has been established, information on its regulatory phenotype and function are very limited. Therefore, the objective of this study was to investigate the phenotype and inhibitory functions of transforming growth factor (TGF)-ß-producing regulatory NK (NKreg) subset in mice with MC903-induced atopic dermatitis (AD). Interestingly, the population of TGF-ß-producing NK cells in peripheral blood monocytes (PBMCs) was decreased in AD patients than in healthy subjects. The number of TGF-ß+ NK subsets was decreased in the spleen or cervical lymph node (cLN), but increased in ear tissues of mice with AD induced by MC903 than those of normal mice. We further observed that TGF-ß+ NK subsets were largely included in CD1dhiPD-L1hiCD27+ NK cell subset. We also found that numbers of ILC2s and TH2 cells were significantly decreased by adoptive transfer of CD1dhiPD-L1hiCD27+ NK subsets. Notably, the ratio of splenic Treg per TH2 was increased by the adoptive transfer of CD1dhiPD-L1hiCD27+ NK cells in mice. Taken together, our findings demonstrate that the TGF-ß-producing CD1dhiPD-L1hiCD27+ NK subset has a previously unrecognized role in suppressing TH2 immunity and ILC2 activation in AD mice, suggesting that the function of TGF-ß-producing NK subset is closely associated with the severity of AD in humans.