ArticleImmunology2014
Disruption of HLA class II antigen presentation in Burkitt lymphoma: implication of a 47,000 MW acid labile protein in CD4+ T-cell recognition.
Article in Immunology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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Who cites it
13 citing papers in PubMed, 15 citations in OpenAlex.
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- Inhibition of acid ceramidase regulates MHC class II antigen presentation and suppression of autoimmune arthritis.Cytokine · 2020Article
- Calpain mediated expansion of CD4+ cytotoxic T cells in rodent models of Parkinson's disease.Experimental neurology · 2020Article
- A Missing Link between Neuron Specific Enolase Release and Poor Prognosis in Aging Patients with B-cell Lymphoma.Journal of clinical & cellular immunology · 2018Article
- Targeting Enolase in Reducing Secondary Damage in Acute Spinal Cord Injury in Rats.Neurochemical research · 2017Article
- Multiple Defects Impair the HLA Class II Antigen Presentation Capacity of Burkitt Lymphoma.Journal of clinical & cellular immunology · 2016Article
- Large-scale microarray profiling reveals four stages of immune escape in non-Hodgkin lymphomas.Oncoimmunology · 2016Article
- Inhibition of Calpain Activation Protects MPTP-Induced Nigral and Spinal Cord Neurodegeneration, Reduces Inflammation, and Improves Gait Dynamics in Mice.Molecular neurobiology · 2015Article
- Prostate Cancer Immunotherapy: Exploiting the HLA Class II Pathway in Vaccine Design.Journal of clinical & cellular immunology · 2015Article
- Elevation of c-MYC disrupts HLA class II-mediated immune recognition of human B cell tumors.Journal of immunology (Baltimore, Md. : 1950) · 2015Article
- Reduction of myeloid-derived suppressor cells and lymphoma growth by a natural triterpenoid.Journal of cellular biochemistry · 2015Article
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
While Burkitt lymphoma (BL) has a well-known defect in HLA class I-mediated antigen presentation, the exact role of BL-associated HLA class II in generating a poor CD4(+) T-cell response remains unresolved. Here, we found that BL cells are deficient in their ability to optimally stimulate CD4(+) T cells via the HLA class II pathway. This defect in CD4(+) T-cell recognition was not associated with low levels of co-stimulatory molecules on BL cells, as addition of external co-stimulation failed to elicit CD4(+) T-cell activation by BL. Further, the defect was not caused by faulty antigen/class II interaction, because antigenic peptides bound with measurable affinity to BL-associated class II molecules. Interestingly, functional class II-peptide complexes were formed at acidic pH 5·5, which restored immune recognition. Acidic buffer (pH 5·5) eluate from BL cells contained molecules that impaired class II-mediated antigen presentation and CD4(+) T-cell recognition. Biochemical analysis showed that these molecules were greater than 30,000 molecular weight in size, and proteinaceous in nature. In addition, BL was found to have decreased expression of a 47,000 molecular weight enolase-like molecule that enhances class II-mediated antigen presentation in B cells, macrophages and dendritic cells, but not in BL cells. These findings demonstrate that BL likely has multiple defects in HLA class II-mediated antigen presentation and immune recognition, which may be exploited for future immunotherapies.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.