The natural cytotoxicity receptors (NCRs) NKp30, NKp44, and NKp46 are thought to be NK lineage restricted. Herein we show that IL-15 induces NCR expression on umbilical cord blood (UCB) T cells. NCRs were mainly on CD8(+) and CD56(+) UCB T cells. Only NKp30 was functional as demonstrated by degranulation, IFN-gamma release, redirected killing, and apoptosis. Since NCRs require adaptor proteins for function, the expressions of these adaptors were determined. The adaptors used by NKp30 and NKp46, FcepsilonR1gamma and CD3zeta, were detected in UCB T cells. There was a near absence of DAP12, the adaptor for NKp44, consistent with a hypofunctional state. NKp46 was on significantly fewer UCB T cells, possibly accounting for its lack of function. Adult peripheral blood (PB) T cells showed minimal NCR acquisition after culture with IL-15. Since UCB contains a high frequency of naive T cells, purified naive T cells from adult PB were tested. Although NKp30 was expressed on a small fraction of naive PB T cells, it was nonfunctional. In contrast to UCB, PB T cells lacked FcepsilonR1gamma expression. These results demonstrate differences between UCB and PB T cells regarding NCR expression and function. Such findings challenge the concept that NCRs are NK cell specific.
Download full-text PDF |
Source |
---|---|
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2614673 | PMC |
http://dx.doi.org/10.4049/jimmunol.181.7.4507 | DOI Listing |
Z Rheumatol
January 2025
Medizinische Klinik 2, Schwerpunkt Rheumatologie/Klinische Immunologie, Universitätsklinikum Würzburg, Oberdürrbacher Str. 6, 97080, Würzburg, Deutschland.
Neutropenia in rheumatoid arthritis (RA) is a problem that often needs to be addressed. Side effects of basic antirheumatic treatment, infections or substrate deficiencies are common causes; however, T‑cell large granular lymphocytic (T-LGL) leukemia, a mature T‑cell neoplasm, can also lead to autoimmune cytopenia. The T‑LGL leukemia can be associated not only with RA but also with other autoimmune diseases or neoplasms.
View Article and Find Full Text PDFFront Pharmacol
January 2025
Department of Pathophysiology, College of Basic Medical Sciences, China Medical University, Shenyang, Liaoning, China.
Introduction: The risk of kidney fibrosis is significantly elevated in individuals with diabetes, chronic nephritis, trauma, and other underlying conditions. Concurrently, human umbilical cord blood-derived mesenchymal stem cells (hUCB-MSCs) and their extracellular vesicles (MSC-Exos) have gained prominence in regenerative medicine. In light of these observations, we are undertaking a meta-analysis to elucidate the influence of hUCB-MSCs and MSC-Exos on kidney fibrosis.
View Article and Find Full Text PDFCell J
January 2025
Department of Regenerative Medicine, Cell Science Research Center, Royan Institute for Stem Cell Biology and Technology, ACECR, Tehran, Iran. Email:
Cell-based therapy has shown promising outcomes in the treatment of cerebral palsy (CP). However, there is no consensus on a standard therapeutic protocol regarding the source of cells, optimal cell dose, timing and frequency of cell injections, route of administration, or the use of combination therapy. This lack of consensus necessitates a comprehensive investigation to clarify these crucial yet undefined factors in cell-based therapy for CP patients.
View Article and Find Full Text PDFArch Dermatol Res
January 2025
Division of Gastroenterology and Hepatology, 200 1st Street SW, Rochester, MN, 55905, USA.
Background: Celiac disease (CeD) has shown an association with autoimmune disorders including vitiligo and alopecia areata (AA). Ritlecitinib, a JAK3 and TEC kinase family inhibitor, has been approved for treatment of patients with AA and is in late-stage development for vitiligo. Ritlecitinib inhibits cytotoxic T cells, NK cells, and B cells which play a role in the pathogenesis of CeD.
View Article and Find Full Text PDFNat Rev Rheumatol
January 2025
Leeds Institute of Rheumatic and Musculoskeletal Medicine, University of Leeds, Leeds, UK.
B cell depletion with rituximab, a chimeric monoclonal antibody that selectively targets B cells by binding CD20, has been used off label in severe and resistant systemic lupus erythematosus (SLE) for over two decades. Several biological mechanisms limit the efficacy of rituximab, including immunological reactions towards the chimeric molecule, increased numbers of residual B cells, including plasmablasts and plasma cells, and a post-treatment surge in B cell-activating factor (BAFF) levels. Consequently, rituximab induces remission in only a proportion of patients, and safety issues limit its use.
View Article and Find Full Text PDFEnter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!