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1.
Sci Rep ; 13(1): 22694, 2023 12 20.
Article in English | MEDLINE | ID: mdl-38123643

ABSTRACT

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.


Subject(s)
Mesenchymal Stem Cell Transplantation , Mesenchymal Stem Cells , Urticaria , Animals , Mice , T-Lymphocytes , Mast Cells , Urticaria/chemically induced , Urticaria/therapy , Transforming Growth Factor beta
2.
Front Immunol ; 12: 752888, 2021.
Article in English | MEDLINE | ID: mdl-35069528

ABSTRACT

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.


Subject(s)
Dermatitis, Atopic/immunology , Killer Cells, Natural/immunology , Animals , Antigens, CD1d/immunology , B7-H1 Antigen/immunology , Calcitriol/adverse effects , Calcitriol/analogs & derivatives , Calcitriol/pharmacology , Dermatitis, Atopic/chemically induced , Female , Humans , Mice , T-Lymphocytes, Regulatory/immunology , Th2 Cells/immunology , Transforming Growth Factor beta/immunology , Tumor Necrosis Factor Receptor Superfamily, Member 7/immunology
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