Immune system ↗Dendritic cells sample tissue
Immature dendritic cells take up material continuously; innate activation changes migration, processing, costimulation, and cytokine output.
IMMUNE / 04
Match a clone.
Build a memory.
Adaptive immunity requires more than antigen binding. Location, MHC, costimulation, helper signals, inhibitory checkpoints, and tissue context determine whether a specific clone expands, tolerates, or stops.
Intracellular peptides reach CD8 cells
MHC I displays selected peptides from intracellular proteins, with cross-presentation allowing dendritic cells to prime some CD8 responses.
Endosomal peptides reach CD4 cells
MHC II on professional antigen-presenting cells displays selected peptides from engulfed or endosomal material.
A second signal controls commitment
T-cell receptor recognition without appropriate costimulation may fail, induce anergy, or contribute to tolerance rather than expansion.
Rare cells meet efficiently
Lymphatic delivery, specialized stromal zones, chemokines, and recirculation bring antigen-bearing cells together with diverse naive lymphocytes.
Helper programs coordinate
CD4 T cells differentiate into overlapping states that support macrophage activation, antibody responses, barrier defense, granulocytes, or regulation.
Cytotoxic cells inspect MHC I
Activated CD8 T cells can release perforin and granzymes or use death-receptor pathways against matching infected or abnormal cells.
B cells bind intact antigen
The B-cell receptor recognizes native structures, internalizes antigen, and presents derived peptide to matching helper T cells.
Affinity and class are refined
Mutation, selection, helper signals, and class switching generate higher-affinity antibodies with different effector functions.
Antibody is secreted at scale
Short- and long-lived plasma cells produce antibody that can neutralize, opsonize, activate complement, or recruit cellular killing.
Activation stays conditional
CTLA-4, PD-1, regulatory cells, suppressive cytokines, antigen loss, and withdrawal of growth signals limit continued activity.
Most effector cells disappear
After antigen and inflammatory signals decline, apoptosis reduces the expanded population and helps end tissue disruption.
B cells preserve recognition options
Memory B cells can rapidly reactivate, present antigen, and enter new rounds of differentiation or maturation after re-exposure.
T cells occupy distinct compartments
Central, effector, and tissue-resident memory populations differ in location, recirculation, speed, and effector readiness.
Antibody can persist without re-exposure
Selected plasma cells survive in specialized niches and continue secreting antibody, although durability varies by antigen and response.
Specificity does not guarantee safety
Central and peripheral control must restrain self-reactive clones; autoantibody or T-cell presence has disease-specific meaning.