Mod 2: Histology Flashcards
Innate immunity: passive vs active
Adaptive immunity: passive vs active
INNATE
Passive: mom ANTIBODIES move across placenta (IgG to fetus)/in breast milk (IgA to infant)
Active: ANTIBODIES for neutralization, opsonization, precipitation of toxin or pathogen (antidotes)
ADAPTIVE
Passive: immunization WITH BACTERIAL/VIRAL EPITOPES
Active: real-life exposure TO PATHOGEN
Differences b/w innate and adaptive immunity
Innate: both active and passive – Ab introduced to person
Adaptive: both active and passive – exposure to actual pathogen
Innate: no memory cells produced
Adaptive: memory cells produced
Initial vs repeat exposure timeline
More efficient and specific antibody molec during repeat exposure
Initial:
1. Innate immune sys EARLY inflammation (0-4 hrs)
2. Innate immune sys LATE inflammation (4-5 days)
3. Adaptive immune sys (14 days)
4. Pathogen removal/tissue repair
Repeat
- Innate immune sys EARLY inflammation (0-4 hrs)
- Innate immune sys LATE inflammation (2-3 days) SHORTER
- Adaptive immune sys (5-7 days)
- Pathogen removal/tissue repair
MHC I vs MHC II
MHC I: on all nucleated cells of body
MHC II: on phago WBC that have been activated (engulfed a pathogen)
Where are MHC I molec synthesized?
RER TGN (trans golgi network) membrane embedded in plasma membrane **MHC I always produced by our cells**
PRR
What cells are they located on?
Toll receptors -- recognize PAMPs located on: neutrophils periph tissue macrophages periph tissue NK
PAMPs
surface molec with repeated/identical protein (glycoprotein) subunits on pathogens
Proinflammatory cytokines
histamine (basophils, mast cells) – vasodilation, inc cell permeability
prostaglandin (damaged cells) – smooth muscle in blood vessel wall contracts, vasodilation, inc cell permeability
Bonds that hold light chains to heavy chains
heavy chains to heavy chains
disulfide
Structure of heavy and light chains of Ab
Heavy and light chains both have variable and constant region
2 heavy and 2 light chains per antibody
variable region is where antigen epitope binds
Functions of antibodies – initial binding
Neutralization: Ab covers biologically active part of microbe/toxin
Agglutination: Ab cross-links cells – forms clump
Precipitation: Ab cross-links circulating particles to form an insoluble complex
enhance recognition and diminish disease-causing properties
Antibody functions – after binding
Complement fixation: Fc region of antibody binds complement proteins, complement is activated
Opsonization: Fc region of antibody binds to receptors of phago cells, triggering phagocytosis
Activation of NK cells: Fc region of antibody binds to NK cell, triggering release of cytotoxic chemicals
facilitate removal of pathogen
Functions of immune-lymphatic sys
Transport medium (moves WBC and immunesignalling molec b/w blood, periph tissues, immune sys organs)
Circulation of digested/absorbed lipids (from GI tract to heart)
Recognition, degradation, and removal of antigens
MBL vs classic pathway
MBL: day 1, does not require Ab
classic: day 5-7, REQUIRES Ab
Where are complement proteins produced?
liver (they are soluble plasma proteins)
What are the pro-inflammatory cytokines?
C3a
C5a
What opsonizes the pathogen?
C3b
When do monocytes become macrophages?
when exit bloodstream and enter periph tissue
Unique resident pop of macrophages
Langerhan’s: skin/epidermis
Kupfer: liver
Microglia: brain/SC
Cells involved in innate vs adaptive response
Innate:
- -neutrophils
- -monocytes/ macrophages/ dendritic cells
Adaptive:
- -B cells
- -T cells
PAMP – PRR interactions result in…
inflammatory cytokines released
increased numbers of phago cells
number of pathogens dec
CD4+
CD8+
CD4+ on helper T cell
CD8+ on cytotoxic (killer) T cell
NK cells as a “tweaker”
intermediate in specificity
bridge b/w innate and adaptive immune responses
Describe flow of lymph fluid
unidirectional away from periph tissue toward lymph node toward heart returned to blood at brachiocephalic vv