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BIOL 1104 (30)

Innate Immunity

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BIOL 1104
Tamy Superle

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 V. ADAPTIVE IMMUNITY 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 foreign. -Cells (B/T) use receptors rearranged in devt to rec. specific antigens from specific path. -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 Mechanisms) A. BARRIER FXNS -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. 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 SEE NEXT LECTURE L2/p.2 PAMPs and PRRs A. PAMPs (Pathogen Associated Molecular Patterns) –on viruses, fungi, and bacteria Examples 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 macrophageactivates 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 responseproduction and secretion of proteins involved in immune activation and wound healing from the liver into circulation. -serum marker of inflammation (depends on length of insult) -binds to phosphocholine on bacterial cell walls (b) MBL (Mannan binding lectin) -acute phase response protein made in liver -binds mannose residues (fucose) on yeast and bacterial cell walls through several clusters of carb rec domain. -sugars on mammalian cell surface but have different spacing of binding domains -grouping of binding domains on
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