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Vocabulary flashcards based on lecture notes about cancer immunology.
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TSAs
Tumor-specific antigens arise from mutations or viral oncogenes; processed by proteasome, transported by TAP1/2, loaded onto MHC I, and presented to CD8+ T cells.
Cross-presentation
Dendritic cells present exogenous tumor antigens on MHC I to activate CD8+ T cells, crucial when tumor cells lose MHC I.
Immune evasion strategies used by tumors
PD-L1 expression, TGF-β secretion, MHC-I loss, Treg recruitment, and IDO expression.
PD-1 inhibition of T cell function
Recruits SHP-2, which dephosphorylates CD3ζ and ZAP-70, inhibiting TCR signaling.
Checkpoint inhibitors
Monoclonal antibodies like Ipilimumab (anti-CTLA-4) and Nivolumab (anti-PD-1) that block T cell inhibition.
CAR-T cell components
scFv for antigen binding, CD3ζ for signaling, and CD28 or 4-1BB for co-stimulation.
Steps in CAR-T therapy
Leukapheresis, gene modification, expansion, lymphodepletion, and reinfusion.
Common complications of CAR-T therapy
Cytokine release syndrome (CRS), neurotoxicity, and B cell aplasia.
How monoclonal antibodies treat cancer
Bind tumor antigens to mediate ADCC, CDC, or block receptor signaling.
T-VEC
An oncolytic HSV virus used in melanoma that lyses tumor cells and enhances immunity.
Phases of cancer immunoediting
Elimination, equilibrium, and escape.
AID in cancer
If dysregulated, it mutates non-Ig genes, contributing to B cell lymphoma.
Suppressive cells in the TME
Tregs, MDSCs, TAMs—these produce IL-10, TGF-β, and suppress T/NK cell function.
Metabolic conditions in the TME that suppress immunity
Hypoxia, lactate, and IDO-mediated tryptophan depletion.
Pyroptosis
Inflammatory, mediated by caspase-1 and gasdermin D; apoptosis is non-inflammatory and silent.