Programa de Doctorado en Ciencias de la Salud, Universidad Veracruzana, Xalapa 91050, Mexico.
Published: November 2021
AI Article Synopsis
Article Abstract
CD38 is a transmembrane glycoprotein expressed by T-cells. It has been reported that patients with systemic lupus erythematosus (SLE) showed increased CD38CD25 T-cells correlating with immune activation and clinical signs. Contrariwise, CD38 deficiency in murine models has shown enhanced autoimmunity development. Recent studies have suggested that CD38 regulatory T-cells are more suppressive than CD38 regulatory T-cells. Thus, we have suggested that CD38 overexpression in SLE patients could play a role in regulating immune activation cells instead of enhancing it. This study found a correlation between CD38 with FoxP3 expression and immunosuppressive molecules (CD69, IL-10, CTLA-4, and PD-1) in T-cells from lupus-prone mice (B6.MRL-Fas/J). Additionally, B6.MRL-Fas/J mice showed a decreased proportion of CD38 Treg cells regarding wild-type mice (WT). Furthermore, Regulatory T-Cells (Treg cells) from mice showed impairment in expressing immunosuppressive molecules and proliferation after stimulation through the T-cell receptor (TCR). Finally, we demonstrated an increased ratio of IFN-γ/IL-10 secretion in splenocytes stimulated with anti-CD3 compared with the WT. Altogether, our data suggest that CD38 represents an element in maintaining activated and proliferative Treg cells. Consequently, CD38 could have a crucial role in immune tolerance, preventing SLE development through Treg cells.
Background: The second-line treatment of neuroendocrine tumors (NETs) of unknown primary origin remains uncertain. This report presented a patient who received octreotide plus IBI-318 plus anlotinib as a second-line treatment for multiple metastatic NETs of unknown primary lesions after the failure of octreotide plus everolimus.
Case Presentation: A 32-year-old male patient presented with elevated CEA (197.
Background: Adoptive therapy with umbilical cord blood (UCB) T-regulatory (Treg) cells can prevent graft vs. host disease (GVHD). We hypothesize that UCB Tregs can treat GVHD and synergize with ruxolitinib, Jak2 inhibitor, to improve outcomes.
Ethnopharmacological Relevance: Diabetic ulcer is a serious diabetes complication and a primary reason for amputations. For many years, the San Huang Xiao Yan (SHXY) recipe has served as a conventional remedy for these ulcers, effectively reducing inflammatory factors and exhibiting considerable therapeutic efficacy. However, the precise mechanism remains incompletely understood.
Background: Small cell lung cancer (SCLC) is a highly fatal malignancy, the complex tumor microenvironment (TME) is a critical factor affecting SCLC progression. Cancer-associated fibroblasts (CAFs) are crucial components of TME, yet their role in SCLC and the underlying mechanisms during their interaction with SCLC cells remain to be determined.
Methods: Microenvironmental cell components were estimated using transcriptome data from SCLC tissue available in public databases, analyzed with bioinformatic algorithms.
Indoleamine 2,3-dioxygenase 1 (IDO1) inhibitors are promising for treating tumors but have limited efficacy due to the immunosuppressive tumor microenvironment. In this study, we develop an orchestrated nanoparticle system using modular peptide assemblies, where the co-assembled sequences are designed for the specific binding to the hydrophobic and hydrophilic domains, guiding the assembly process and enabling the customization of nanoparticle properties. We exploit the modularity of this platform to integrate a hydrophobic ferroptosis precursor, an IDO1 inhibitor, and a hydrophilic peptidic PD-L1 antagonist for optimizing therapeutic outcomes through ferroptosis-enhanced tumor immunotherapy.
