Hla-i Downregulation
Hla-i Downregulation - Related Videos
08:07
Personalized Peptide Arrays for Detection of HLA Alloantibodies in Organ Transplantation
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Cited by 2 •
2017
Mismatches in human leukocyte antigen (HLA) sequences between organ donor and recipient pairs are the major cause of antibody-mediated rejection in organ transplantation. Here we present the use of custom antigen arrays that are based on individual donors' HLA sequences to probe anti-donor HLA alloantibodies in organ recipients.
03:15
A Peptide Array-Based Detection of Anti-donor HLA Alloantibodies in Organ Recipients
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2025
This video demonstrates an assay to detect anti-donor HLA alloantibodies in organ recipients. A peptide array is synthesized to represent potential epitopes for antibody-mediated organ rejection. The array is incubated with the recipient's serum, containing alloantibodies that bind to their target epitopes. Antibody binding is detected using chemiluminescence to identify donor-specific HLA epitopes that incite alloantibody reactivity.
01:15
Receptor Downregulation in MVBs
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2023
Multivesicular bodies (MVBs) are mature endosomes that sort ubiquitinated proteins and then fuse with lysosomes to degrade the sorted proteins. Epidermal growth factor (EGF) and its receptor (EGFR) form a complex that can be internalized through endocytosis, sorted into an MVB, and later degraded. The EGFR can initiate signaling pathways that lead to cell proliferation, migration, and differentiation. Overexpression of EGFR stimulates cells to proliferate. Excessive EGFR activation may...
07:18
HLA-Ig Based Artificial Antigen Presenting Cells for Efficient ex vivo Expansion of Human CTL
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Cited by 17 •
2011
A new DC independent method for induction and expansion of antigen-specific T cells is described. HLA A2-Ig based artificial Antigen Presenting Cells (aAPC) are loaded with HLA-A2 restricted peptides to efficiently expand CTL of diverse antigen specificity. This technology holds great potential for CTL-based adoptive immunotherapy.
10:16
SorLA and CLC:CLF-1-dependent Downregulation of CNTFRα as Demonstrated by Western Blotting, Inhibition of Lysosomal Enzymes, and Immunocytochemistry
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Cited by 1 •
2017
The present protocol describes how Western blotting and immunocytochemistry combined with inhibition of lysosomal enzymes can be used to demonstrate the downregulation of Ciliary Neurotrophic Factor Receptor-α (CNTFRα), which is conveyed by the interaction between Cytokine-like Factor-1 (CLF-1) and the endocytic receptor sorLA.
FAQs
Changes in HLA gene regulation can reduce the amount of HLA-I displayed at the cell surface without necessarily involving the antigen-processing machinery. The resulting decrease limits presentation of intracellular peptides to CD8+ T cells, making tumor cells less recognizable to this branch of the immune response. Distinguishing regulatory changes from processing defects helps clarify how immune escape develops.
Beta-2 microglobulin and TAP transporters are key antigen-processing components that support effective HLA-I peptide presentation. Defects in either component can reduce surface display even when other parts of the HLA system remain present. Examining these components therefore helps researchers determine whether impaired presentation reflects a structural or transport-related problem rather than altered HLA gene regulation alone.
Reduced HLA-I can weaken recognition by cytotoxic CD8+ T cells because fewer intracellular peptides are presented for immune surveillance. However, the same change can also affect natural killer cell responses, so its net immune consequence is not limited to T-cell evasion. Cancer studies must therefore consider both immune pathways when interpreting the significance of HLA-I loss.
A useful investigation separates reduced surface HLA-I expression from defects in the supporting antigen-processing pathway. Researchers can consider altered HLA gene regulation alongside the status of beta-2 microglobulin and TAP transporters, then relate these findings to immune recognition. This framework helps connect a molecular abnormality with the likely extent of tumor-cell visibility to cytotoxic lymphocytes.
HLA-I status can provide information about how readily tumor cells may be recognized by cytotoxic T cells. When reduced expression or associated processing defects are identified, the finding may mark a tumor with altered immune visibility. As a biomarker, it can help researchers characterize immune escape mechanisms and investigate whether HLA-I status relates to treatment response.
Because many immune-recognition effects depend on peptide display, reduced HLA-I may influence how effectively cytotoxic T cells detect tumor cells during immunotherapy. Assessing this pathway can therefore help explain variable treatment responses and identify limitations in immune visibility. In cancer research, such information supports efforts to predict outcomes and explore strategies for improving therapeutic effectiveness.