Lecture 1: PT 2Adaptive and Innate Immune Responses Flashcards
Q: What is the main function of the innate immune system in infections?
A: It provides an immediate “knock-down” of pathogen load to delay or prevent activation of the adaptive immune system.
Q: Why is activating the adaptive immune response a last resort?
A:
It’s energy-intensive
It creates immunological memory (which can become problematic if directed at self-antigens → autoimmune disease)
Q: What are the key functions of APCs?
A:
Trap/process antigens
Migrate to lymph nodes
Express high levels of MHC I & II
Provide co-stimulation (CD80/86)
Secrete cytokines (e.g., IL-12)
Q: What are plasmacytoid dendritic cells known for?
A: Secreting large amounts of interferon-γ → strong antiviral effect
Q: What triggers APCs to migrate?
A: Chemokines, cytokines, and downregulation of adhesion molecules that keep them in place
Q: What are High Endothelial Venules (HEVs)?
A: Specialized blood vessels in lymph nodes that allow naive lymphocytes to enter the node using L-selectin and integrins.
Q: How do immune cells exit blood vessels and enter tissues?
A: Via adhesion molecule interactions on activated endothelium:
P-selectin/E-selectin → rolling
ICAM-1/VCAM-1 → firm adhesion
PECAM-1 (CD31) → transendothelial migration
Q: What is “lymph node shutdown”?
A: When antigen-presenting cells activate matching lymphocytes, the lymph node temporarily halts entry/exit to allow expansion of specific immune cells.
Q: What are the 4 phases of adaptive immunity?
A:
Recognition
Activation (proliferation & differentiation)
Execution (effector function)
Control (self-limitation & apoptosis)
Q: What are the 3 signals needed for T cell activation?
A:
TCR binds antigen on MHC (I or II)
CD28 binds CD80/86 (co-stimulation)
Cytokine signal (e.g., IL-12 → Th1, IL-4 → Th2, IL-6/IL-23 → Th17)
Q: What is CTLA-4 (CD152)?
A: A negative regulator (“brake”) that binds CD80/86 and limits T cell activation to prevent overactivation
Q: What keeps T cells alive during the immune response?
A: IL-2 and CD28/CD80 interactions upregulate Bcl-2 and Bcl-XL (anti-apoptotic proteins)
Q: What causes T cell apoptosis post-infection?
A: Loss of IL-2 and co-stimulation when APCs stop presenting antigen
Q: What T cells survive?
A: Memory T cells (2–5% of activated population)
Q: How long do peptides stay on MHC?
A: Long duration (slow “off rate”) due to non-covalent but tight binding
Q: How many peptide-MHC complexes are needed to activate a T cell?
A: Only ~0.1% of all MHC molecules need to be peptide-loaded
Th17
induced by
produces
target
function
IL-6 + TGF-β + IL-23
IL-17, IL-22
Neutrophils
Bacteria, fungi
Th1
induced by
produces
target
function
IL-12 + IFN-γ
IFN-γ
Macrophages
intracellular microbes
Th2
induced by
produces
target
function
IL-4
IL-4, IL-5, IL-13
Eosinophils, B cells
Helminths, allergy
Q: How do B cells recognize antigens?
A: Through BCRs (membrane-bound IgM), which bind native, unprocessed antigens
Q: What are the two B cell activation types?
A:
T-dependent: Requires CD4+ T cell help (CD40-CD40L + cytokines) → class switching (IgM → IgG)
T-independent: Responds to polysaccharides/lipids → mostly IgM, short-lived, no memory
Q: What is affinity maturation?
A: Process where repeated antigen exposure leads to higher affinity antibodies via somatic hypermutation and class switching
Q: What cytokines drive class switching?
A:
IFN-γ → IgG2a
IL-4 → IgG1, IgE
TGF-β → IgA
All stimulate IgM
