We investigated the capacity of CD25(+) T regulatory cells (Treg) to modulate T cell responses to nickel, a common cause of allergic contact dermatitis. CD4(+) T cells isolated from the peripheral blood of six healthy, nonallergic individuals showed a limited capacity to proliferate in response to nickel in vitro, but responsiveness was strongly augmented (mean increment +/- SD, 240 +/- 60%) when cells were depleted of CD25(+) Treg. Although CD25(+) Treg were anergic to nickel, a small percentage up-regulated membrane CTLA-4 upon nickel exposure. CD25(+) Treg strongly and dose-dependently inhibited nickel-specific activation of CD25(-) T lymphocytes in coculture experiments in a cytokine-independent, but cell-to-cell contact-dependent, manner. Approximately 30% of circulating CD25(+) Treg expressed the cutaneous lymphocyte-associated Ag (CLA), and CLA(+)CD25(+) Treg were more efficient than CLA(-)CD25(+) cells in suppressing nickel responsiveness of CD25(-) T cells. The site of a negative patch test in response to nickel showed an infiltrate of CD4(+)CLA(+) cells and CD25(+) cells, which accounted for approximately 20% of the total T cells isolated from the tissue. Skin-derived T cells suppressed nickel-specific responses of peripheral blood CD25(-) T cells. In addition, 60 +/- 14% of peripheral blood CD25(+) Treg expressed the chemokine receptor CCR7 and strongly inhibited naive T cell activation in response to nickel. Finally, CD25(+) T cells isolated from peripheral blood of nickel-allergic patients showed a limited or absent capacity to suppress metal-specific CD4(+) and CD8(+) T cell responses. The results indicates that in healthy individuals CD25(+) Treg can control the activation of both naive and effector nickel-specific T cells.
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http://dx.doi.org/10.4049/jimmunol.171.11.5760 | DOI Listing |
JCI Insight
December 2024
Department of Microbiology and Immunology, McGill University, Montreal, Quebec, Canada.
Deficits in IL-2 signaling can precipitate autoimmunity by altering the function and survival of FoxP3+ regulatory T cells (Tregs) while high concentrations of IL-2 fuel inflammatory responses. Recently, we showed that the non-beta IL-2 SYNTHORIN molecule SAR444336 (SAR'336) can bypass the induction of autoimmune and inflammatory responses by increasing its reliance on IL-2 receptor α chain subunit (CD25) to provide a bona fide IL-2 signal selectively to Tregs, making it an attractive approach for the control of autoimmunity. In this report, we further demonstrate that SAR'336 can support non-beta IL-2 signaling in murine Tregs and limit NK and CD8+ T cells' proliferation and function.
View Article and Find Full Text PDFImmunopharmacol Immunotoxicol
December 2024
College of Nursing and Health Sciences, Jazan University, Jazan, Saudi Arabia.
Rhino-Orbital-Cerebral Mucormycosis (ROCM) cases increased sharply in India during the second COVID-19 wave. Due to uncontrolled hyperglycemia, prolonged steroid use, and high ferritin levels, the immune system was dysregulated throughout this surge. Our study examined post-COVID-19 ROCM patients' T regulatory cell (Treg), T helper 17 cell (Th17) and Myeloid derived suppressor cell (MDSC) levels before and after three months of treatment.
View Article and Find Full Text PDFCell Biochem Biophys
December 2024
Affiliated Hospital of North Sichuan Medical College, Nanchong, Sichuan, China.
To investigate the regulatory mechanism of indoleamine 2, 3-dioxygenase (IDO) in T lymphocyte differentiation and its role in promoting the growth of gastric cancer (GC) cells through the PI3K/Akt/mTOR pathway. GC cell lines (MFC and NCI-N87) and PBMC cells were co-cultured and IDO inhibitor 1-methyl-tryptophan (1-MT) was added. The proliferation was detected by CCK-8, the apoptosis was detected by flow cytometry, and the contents of TNF-α, IL-1β, IL-6, IL-8, and INF-γ were detected by ELISA.
View Article and Find Full Text PDFImmunol Invest
December 2024
Immunology Department and Center of Neuroscience, Fujian Medical University, Fuzhou, Fujian, PR China.
Background: Phospholipase D2 (PLD2) enzymes are expressed on the cytoplasmic membrane of bacteria, fungi, plants, and animals. Recently, extensive research has linked PLD2 to the chronic inflammatory activity of cells. Allergic asthma is a chronic airway inflammation disease.
View Article and Find Full Text PDFPhotochem Photobiol Sci
December 2024
Allergy Immunology, Murdoch Children's Research Institute, Royal Children's Hospital, Melbourne, VIC, Australia.
Higher prevalence of multiple sclerosis at higher latitudes is associated with reduced sunlight during childhood. Alterations in inflammatory Th17 and regulatory T cells (Treg) are associated with autoimmunity. In Hobart, Australia (latitude 42.
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