Phagocytic antigen-presenting cells (APCs) are involved in innate and adaptive immune responses to bacteria. Adaptive responses to bacteria involve processing of bacterial antigens for presentation by class II major histocompatibility complex (MHC II) molecules and class I MHC (MHC I) molecules to stimulate CD4(+) and CD8(+) T cells, respectively. To examine the role of phagosomes in processing of antigens for presentation by MHC II molecules to CD4(+) T cells, phagosomes have been biochemically and functionally analyzed by a variety of techniques that include flow analysis (flow organellometry), SDS-PAGE/Western blotting, and an antigen-presenting organelle assay. Using these techniques, we have demonstrated that phagosomes containing latex beads or Mycobacterium tuberculosis (MTB) contain components of the MHC II processing pathway and support the formation of peptide-MHC II complexes.
Download full-text PDF |
Source |
|---|---|
| http://dx.doi.org/10.1007/978-1-59745-157-4_23 | DOI Listing |
Publication Analysis
Top Keywords
Similar Publications
Norepinephrine (NE) promotes activated B cells to identify and kill effector CD8 T cells through FasL/Fas pathway in spleen mononuclear cells isolated from experimental autoimmune encephalomyelitis (EAE).
Brain Behav Immun
January 2025
Department of Neurobiology, School of Basic Medical Sciences, Harbin Medical University, Harbin 150081, Heilongjiang, PR China; The Key Laboratory of Myocardial Ischemia, Harbin Medical University, Ministry of Education, Harbin 150081, Heilongjiang, PR China. Electronic address:
It has been reported that the nervous system can regulate immune reactions through various mechanisms. However, the role of splenic sympathetic nerve activity in the autoimmune reactions during the pathogenesis of experimental autoimmune encephalomyelitis (EAE) remained unclear. Here, we blocked the activity of the splenic sympathetic nerve and found that the number of adaptive immune cells, such as CD4 T cells, CD8 T cells and B cells, were upregulated.
View Article and Find Full Text PDFIn silico functional analysis of the human, chimpanzee, and gorilla MHC-A repertoires.
Immunogenetics
January 2025
Theoretical Biology and Bioinformatics, Department of Biology, Faculty of Science, Utrecht University, Utrecht, The Netherlands.
T cells recognize peptides displayed on the surface of cells on MHC molecules. Genetic variation in MHC genes alters their peptide-binding repertoire and thus influences the potential immune response generated against pathogens. Both gorillas and chimpanzees show reduced diversity at their MHC class I A (MHC-A) locus compared to humans, which has been suggested to be the result of a pathogen-mediated selective sweep.
View Article and Find Full Text PDFTargeting EGFR-binding protein SLC7A11 enhancing antitumor immunity of T cells via inducing MHC-I antigen presentation in nasopharyngeal carcinoma.
Cell Death Dis
January 2025
Department of Pathology, The Xiangya Hospital, Central South University, 410008, Changsha, Hunan, China.
Approximately 80% of nasopharyngeal carcinoma (NPC) patients exhibit EGFR overexpression. The overexpression of EGFR has been linked to its potential role in modulating major histocompatibility complex class I (MHC-I) molecules. We discovered that EGFR, operating in a kinase-independent manner, played a role in stabilizing the expression of SLC7A11, which subsequently inhibited MHC-I antigen presentation.
View Article and Find Full Text PDFCell type-specific upregulation of NKG2D ligand MICA in response to APTO253.
Ann Transl Med
December 2024
Institute for Tumor Immunology, Center for Tumor Biology and Immunology, Philipps-University Marburg, Marburg, Germany.
One of the most important targets for natural killer (NK) cell-mediated therapy is the induction of natural killer group 2D ligand (NKG2D-L) expression. APTO253 is a small molecule that selectively kills acute myeloid leukemia (AML) cells, and it has been reported that APTO253 can induce Krüppel-like factor 4 (KLF4) expression and downregulate c-MYC expression. Recently, we discovered a novel role of APTO253 in modulating the NK cell response by inducing surface expression of NKG2D-Ls, especially MHC class I polypeptide-related sequence A (MICA), in AML cells.
View Article and Find Full Text PDFRECQL4 affects MHC class II-mediated signalling and favours an immune-evasive signature that limits response to immune checkpoint inhibitor therapy in patients with malignant melanoma.
Clin Transl Med
January 2025
Department of Dermatology and Allergy, University Hospital of Munich, Ludwig-Maximilian-University, Munich, Germany.
Background: Cancer immunotherapy has transformed metastatic cancer treatment, yet challenges persist regarding therapeutic efficacy. RECQL4, a RecQ-like helicase, plays a central role in DNA replication and repair as part of the DNA damage response, a pathway implicated in enhancing efficacy of immune checkpoint inhibitor (ICI) therapies. However, its role in patient response to ICI remains unclear.
View Article and Find Full Text PDFWant AI Summaries of new PubMed Abstracts delivered to your In-box?
Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!