Exam questions 12, 13 Flashcards
Cytokine action on cells
A cytokine acts on a cell if the cell expresses the corresponding receptor. TNF binds TNFR, activating NF-κB or triggering apoptosis.
Cytokine response detection methods
qRT-PCR/PCR (mRNA detection), ELISA (protein levels), Flow Cytometry (intracellular proteins), Bioassays (functional activity).
IL-1β production mechanism
Pro-IL-1β is transcribed via NF-κB, cleaved by caspase-1, and secreted after inflammasome activation.
Cytokine regulation methods
Short half-life, decoy receptors, antagonists (e.g., IL-1Ra), post-translational modifications.
T lymphocytes and antigen encounter
T cells meet antigens in lymph nodes, transported by APCs from the infection site.
B vs T cell antigen recognition
B cells recognize native antigens, T cells recognize processed antigens on MHC.
B-cell activation (TD and TI antigens)
TD requires T-helper cell interaction, TI activates B-cells via BCR crosslinking or co-receptors.
Thymic T-cell selection
Positive selection for self-MHC recognition, negative selection to eliminate self-reactive T-cells.
TCR gene rearrangement
TCR β-chain undergoes V-DJ joining, α-chain V-J joining, RAG proteins mediate recombination, allelic exclusion.
MHC I and MHC II expression
MHC I on all nucleated cells for intracellular antigens, MHC II on APCs for extracellular antigens.
MHC I vs MHC II peptides
MHC I binds short peptides (8-10 amino acids), MHC II binds longer peptides (13-18 amino acids).
MHC molecules as “protein fingerprints”
MHC presents peptides from the cell’s protein turnover, reflecting its environment.
MHC molecules as “promiscuous”
MHC molecules bind various peptides fitting structural constraints.
MHC prediction algorithms
Based on anchor residues and peptide spacing for computational predictions.
KIRs on NK cells
KIRs inhibit NK cells by recognizing MHC I molecules
NK cell killing mechanism
NK cells induce apoptosis via perforin/granzyme release and death receptor activation.
Cardinal signs of inflammation
Heat (calor), Redness (rubor), Swelling (tumor), Pain (dolor), Loss of function (functio laesa).
Host defense in wound infection
Complement activation, neutrophil recruitment, cytokine release, antigen presentation, adaptive immunity activation.
Adaptive response to mycobacteria
Th1 response with IFN-γ, IL-12, macrophage activation, CTL activation for infected cells.
Desirable vaccine properties
Immunogenicity, long-term memory, safety.
Adjuvant effect
Enhances immune response by activating PRRs and stimulating cytokine production.
TLR-induced pathways
MyD88 pathway activates NF-κB for inflammation, TRIF pathway activates IRF for type I interferons.
Autoimmune hemolytic anemia mechanism
Autoantibodies target RBCs
Hypogammaglobulinemia
Deficiency in antibody production, leading to recurrent bacterial infections.
Wound infection host defense steps
Complement activation, neutrophil recruitment, cytokine release, antigen presentation, adaptive immunity.
LPS recognition by immune cells
LPS binds TLR4-MD2 complex, activating NF-κB and IRF3 for cytokine production.
IL-1β production
TLR activation induces pro-IL-1β, inflammasome activation cleaves it to mature IL-1β.
Adjuvancy explanation
Enhances immune response by stimulating PRRs and providing co-stimulatory signals.
KIRs function on NK cells
Inhibit NK activity through MHC I recognition
NK cell target killing mechanisms
Perforin/granzyme pathway and death receptor activation induce apoptosis in target cells.
B-cell activation by thymus-dependent antigens
T-helper cell interaction and CD40-CD40L signaling trigger B-cell activation and differentiation.
Antibody structure and function
Y-shaped structure, Fab region for antigen binding, Fc for effector functions (e.g., opsonization, complement activation).
Class switching mechanism
AID deaminates cytosines, DNA breaks are repaired, leading to new antibody isotype.
TCR diversity mechanisms
V(D)J recombination during T-cell development, junctional diversity via N-nucleotide addition.
Effector T-cell subsets
CD4+ T-cells: Th1, Th2, Th17, Treg. CD8+ T-cells: Cytotoxic T lymphocytes (CTLs).
Th1 vs Th2 balance
Th1 promotes cell-mediated immunity, Th2 promotes humoral immunity.
Immune response against viruses
Th1 responses and CTL-mediated killing of infected cells.
Type I interferons in antiviral defenses
Induces antiviral states, enhances NK and CTL activity, upregulates MHC I.
