Chapter 17: Adaptive Immunity: Specific Defenses of the Host

adaptive immunity

“specific” immunity or resistance to SPECIFIC pathogens (get rid of only CERTAIN pathogens → very picky)

• develop later for specific microbe (acquired via infetion/vaxx → inject pathogens)

• specific recognition & response to specific microbe (discriminates)

• has immunological memory (encountered before)

• slower immune response

• 3rd line of Host Defenses

immunology

study of host defenses against foreign substances (antigens)

antigen (Ag)

= foreign invader = pathogen

substance that stimulates a certain immune response → antibody production (ex. pathogens, foreign substance, vaccines)

antibody (Ab)

protective proteins made by the host in response to certain antigens

• aka immunoglobulins (Ig) = Ab

humoral immunity

fights invaders/threats OUTSIDE of the cell (extracellular Ag’s)

• involves B cells indirectly making antibodies that help destroy pathogens (mark for destruction)

cell-mediated (cellular) immunity (CMI)

attacks antigens that have entered the cell (intracellular Ag’s → usually animal virus)

• produces T cells that recognize parts of antigens that get processed by phagocytosis & will destroy antigen

B cells & T cells

• B cells mature in bone marrow

• T cells mature in thymus

• after B/T cells mature = migrate to lymphoid tissue (lymph nodes, spleen, etc.)

antigen’s (Ag’s)

substances cause production of antibodies (turn on immune system → humoral immunity)

• most Ag’s have external components that interact w/ antibodies (Y) (antigenic determinants)

Ab’s

globular proteins called immunoglobulins (Ig)

• recognize/bind to antigenic determinants → form Ag-Ab complex

• only “mark” Ag for destruction

Ab’s structure

four proteins (4*) chains (subunits) form a “Y-shape” (2 identical light/2 identical heavy chains joined together)

antibodies

• variable regions: at ends of arms

  • bind to antigenic determinants

• constant region: the stem

  • IgG, IgM, IgA, IgD, IgE

IgG

• structure: monomer

• location: blood, lymph, intestine

• fxn: enhances phagocytosis & neutralizes toxins/viruses

• abundance: MOST abundant in blood serum

• misc: long-lived (3 weeks), provides long-term protection, crosses placenta (transplacental passage)

IgM

• structure: pentamer

• location: blood vessels

• fxn: clumping (agglutination of pathogens → engulf several @ one time)

• abundance: 6% of serum antibodies

• misc: largest Ab, primary response to infection, short lived (if ↑ IgM ↓ IgG = new infection)

IgA

• structure: mostly dimer in secretions → tears, saliva, breast milk (can be monomer when on mucosal lining)

• location: mucus membrane surfaces/secretions

• fxn: prevent attachment of pathogens to mucus membranes

• abundance: MOST abundant in body (b/c mucus membrane) & 13% of serum antibodies

IgD

• structure: monomer

• location: blood, lymph, on B cells

• fxn: may be involved in self-tolerance (ability to tolerate yourself so won’t attack yourself)

• abundance: 0.02% of serum antibodies

IgE

• structure: monomer

• location: on mast cells/basophils, in blood

• fxn: cause release histamines from mast cells/basophils → allergies & destruction of parasitic worm infections (by ADCC)

• abundance: 0.002% of serum antibodies

Ig abundance (body)

A G M D E

Ig abundance (blood)

G A M D E

clonal selection & clonal expansion of B cells (big picture)

b cells → plasma cells → antibodies

clonal selection