BLG 307 Lecture Notes - Prokaryote, Lamprey, Tlr7

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28 Jan 2013

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Innate Immunity (Principles, Patterns, Receptor Signaling) L2/p.1
Innate Immunity-prepared to mount a fast, stereotyped defense against attack (rapid, general)
Adaptive Immunuity-specific, learned, response to a specific attack (slower, specific)
Need efficiency, and accuracy, (prevent self destruction), quick initiation, in dealing with pathogens
Inflamation-fundamental host response to injury
-sends activated immune cells to site, sequesters pathogens, limits damage, initiates repair
Calor = Heat Dalor = Pain Rubor = Redness Tumor = Swelling
-due to inflammatory mediators effect on microvasculature at injury or infection site.
Innate Immune Response- preexisting ability to recognize broad structural patterns as foreign
-Cells (mac/neut/NKC) use germline encoded receptors to recognize patterns.
-Various weapons to kill general classes of pathogens
- Release mediators to induce adaptive immune system
Adaptive Im. Response- learned ability after initial exposure to rec. precise molecular structures as
-Cells (B/T) use receptors rearranged in devt to rec. specific antigens from specific
-Activated AI cells respond to kill specific antigens.
-clonal distribution- delay until the cell with the right receptor reaches site of infection.
Some Disadvantages of AI
1. Expansion/Differentiation recquired Allows pathogen time to proliferate
2. Somatically generated diversity Receptors not inherited
3. Random specificity (some anti-self) Need context to Id self vs. nonself
Innate IS evolved first (older jawless fish “lamprey” have no AI system
COMPONENTS OF THE INNATE I.S. (Barrier Functions/Rec of Path Structures/Effector
-skin, airway, GI tract, genitourinary tract = potential sites for pathogen entry
-Primary Defense = epithelial cell layer joined by tight junctions
-secrete defensins (small +ve antimicrobial peptides) bind to acidic mol in bacterial cell walls
(disrupt memb)
SKIN-largest and most exposed epithelia
-thickness and dry surface prevent colonizartion
MUCUOSAL SURFACES- mucus layer decreases pathogen adhesion (antibacterial peptides)
-provides constant flow to limit pathogen exposure time (don’t have time to divide)
LUNGS- movt by mucus by cilia (pathogens don’t have time to divide)
Normal Flora (bacteria) in skin and gut also help.
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B. RECOGNITION OF PATHOGENIC STRUCTURES- limited set of structural motifs
Effector Mechanisms 1. Inflammationn
2. Acute Phase Response
3. Opsonization
4. Phagocytsis
5. Sounding the alarm-cytokine signals
PAMPs and PRRs
A. PAMPs (Pathogen Associated Molecular Patterns)on viruses, fungi, and bacteria
1. LPS – on bacterial wall of Gram negative rod shaped bacteria
2. Bacterial DNA- sequence CpG
3. N-formyl methionine-first AA of bacteria
4. dsRNA of viruses
5. Yeast cell wall structural units
PAMP Properties
1. Expressed by pathogens and not by host (primary requirement)
2. Structurally Invarient (b/c bacteria/viruses mutate easily)
3. Required for Survival or Pathogenicity
4. Usually polysaccharides or polynucleotides (not proteins)
5. Repeating Structural motif
Best Known PAMP example is LPS (gram negative cell walls)
-lipid portion (in bacterial cell membrane) -core polysaccharide -repeating terminal sugar residues
-although structurally heterogeneous some invariant parts
-repeating polysaccharide motif, necessary for survival
B. PRRs (Pattern Recognition Receptors)-on immune system
-germline encoded, not rearranged
-extracellular proteins, signaling receptors, endocytic receptors (independent evolution)
-PAMP of a pathogen binds/activates PRP of macrophageactivates innate immune response
1.Extracellular PRRS
Fxns: (1) opsonization = alteration of foreign target cell to promote phagocytosis
(2) activation of complement cascade
(a) CPR (C-Reactive Protein) (opsonization?)
-acute phase responseproduction and secretion of proteins involved in immune activation and wound
from the liver into circulation.
-serum marker of inflammation (depends on length of insult)
-binds to phosphocholine on bacterial cell walls
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