Study guide

Immunity and Infection: IM250 Study Guide

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Course
IMM250 (IMM250)

Institution
University Of Toronto (U Of T )

Complete study guide for Immunity and Infection: IM250; these documents contain detailed notes and diagrams/figures to go along with the notes. Included are also study questions and highlights of the most important topics. Bonus: I received a 92% (4.0 GPA) in this course using these notes.

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Uploaded on October 13, 2019
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Lecture 1: The Immune System From historical to modern perspectives
The Immune System
 Immune system: a system of tissues, cells and soluble products that recognize, attack and destroy entities that can endanger
our health when they enter our bodies
 Four major classes of pathogens:
1. Bacteria (e.g. salmonella)
2. Virus (e.g. rhinovirus)
3. Fungi
4. Parasite (e.g. malaria)
Immune Response
 There are 4 stages of immune system and 3 challenges associated with each step
1. Recognition: pathogens are highly varied in structure and evolve quickly
2. Response: pathogens replicate or produce toxins quickly
3. Returning to resting: collateral damage to healthy tissue caused by immune response
Smallpox
 Disease caused by virus variola major - no animal reservoir
o Causes small fluid filed vesicles on skin
 Variolation: inoculation with material from small pox pustule to produce immunity
o vaccination
o Very bad because it spread disease even more
o Edward Jenner paved the road for vaccination when he realized cowpox (attenuated version of small pox) could
produce immunity
Germ Theory of Disease
 Louis Pasteur & Robert Koch began isolating and characterizing organisms that could only bee see under a microscope
 The germ theory proposed that microbe are organisms too small to be seen by eye, and some cause specific diseases
 Koch developed techniques for cultivating pure cultures of bacteria
Louis Pasteur
 Realized he could induce acquired immunity in chickens
 He made two major discoveries;
1. Fermentation
2. Pasteurization
 Disproved the spontaneous generation of microorganism
Cellular v Humoral Immunology; A Century-Long Dispute
 Metchnikoff theorized and demonstrated that human white blood cells similarly engulf and destroy pathogens like bacteria
o Demonstrated that phagocytes represent a first line of defence
o He was a cellularity; believed that phagocytes, not antibodies, played a prominent role in immunity
 Paul Ehrlich was a humoralist and believed soluble anti-toxins(antibodies) were responsible for immunity
o Anti-toxins (according to Ehrlich)
 Anti-toxins were receptors with lock and key structure
 Bind to infectious agent to a anti-toxin would cause release and production of more the anti-toxin receptors
 He thought that cells express several different anti-toxins which is false
o MacFarlane revised Ehrlich theory with clonal selection hypothesis:
 Each lymphocyte makes one kind of antibody
 “Antigens” stimulate the clonal proliferation of lymphocytes that make an antibody that recognizes a
particular antigen
Lymphocytes
 Two major types of lymphocytes that look the same up until they mature:
1. B cell: Produce antibodies
i. Differentiate into plasma cells
2. T cell: produce cytokines
i. Help antibody production
Strategies used by Immune Cells
 There are several strategies used by immune cells to eliminate infectious agents or protect against infection
o Killer cells which induce cell death in virally-infected cells
o Pre-existing antibodies block access of the virus to its cellular receptor
 Protecting target cells from infection
o Phagocytes ingest extrasellar bacteria

, o Degranulating cells (e.g. neutrophil) release granules containing toxic molecules to kill antibody coated parasites

Lecture 2: Innate Immunity: First Line of
Defense
Requirements
 There are 8 requirements for infectious disease:
1. Reservoir
2. Transmission to host
3. Invasion through a portal of entry
4. Adherence to host tissue
5. Infection
6. Temporary evasion of host defenses
7. Disease: interference with normal host function
8. Exit and transmission
Clinical and subclinical infection
 Most of the time our innate mechanisms of defense are sufficing to avoid the establishment of infection → sub-clinical
infection
 When the immune system is defective, same microbes that are normally controlled cause opportunistic infections
 Pathogens causing acute infections are cleared by innate and adaptive effectors
What is a pathogen
 A bacteria, virus, or microbe that posse’s inherent ability to cross anatomical barriers and causing disease in healthy person
o Posses genes encoding virulence factors that increase their effectiveness
 Flagella
 Adhesion
 Effector proteins: proteins from the bacteria that hijack host cell
proteins to allow bacterial entry
and survival inside the cell
 toxins
Koch's Postulate
 Contains 4 postulates:
1. Pathogen has to be in all diseased individuals and not healthy organisms
2. Pathogen is isolated from diseased individual and grown in culture
3. Put pathogen in healthy individual
4. Remove pathogen and see if it identical to original causing factor
Pylori
 Causes ulcers - proven by Marshall
 Used to be part of normal microbiota but in late 90s became eradicated through antibiotics
Microbes and Humans
 Infectious disease can come about in several ways:
1. Some bacteria are entirely adapted to the pathogenic way of life in humans.
2. Some bacteria acquire extra virulence factors making them pathogenic
3. Some bacteria from the normal flora can cause disease if they gain access to deep tissues by trauma
4. In immunocompromised patients, many free-living bacteria an can cause disease
Growing recognition of the link between microbes and chronic diseases
 Ulcer shows ink between pylori and stomach cancer
 Cervical cancer can be caused by papilloma virus
Drug-resistant microbes
 Nosocomial (hospital acquire) infections are antibiotic resistant
 There are 3 factors that contribute to hospital acquired infections:
1. Surgery's
2. Immunocompromised hosts
3. Contamination (chain of transmission)
Antibiotic resistance
 excessive use in farming
 Excessive and unnecessary antibiotics given to patients

,  Patients not completing cycle
First Line Defense Strategies
 There re two types of barriers in first line of defense:
1. Chemical and biological barriers:
i. Lysozyme
a. Enzyme that breaks the cell wall of bacteria by attacking the bond that keeps together the two
sugar components of peptidoglycan
ii. Antimicrobial peptides of skin and gut kill microbes
iii. Stomach acid and enzymes inhibit bacterial growth
iv. Microbiota outcompete pathogenic microbes in body
2. Physical barriers:
i. Mucus and cilia
ii. Epithelial cells of skin and mucosal surfaces
a. Skin epithelium is also multilayered
ii. Gut mucus keeps particles and microbes at a safe distance from epithelial layer
Defensins
 Natural peptide antibiotic that is cationic which disrupts pathogen membrane layer by creating a pore
Innate Immunity Receptors
 Innate immune cells recognize conserved features of infectious pathogens called PAMPs & MAMPs
o PAMPs & MAMPS are recognized using PRR (PATTERN RECOGNTION RECEPTORS)
PAMPS
 Components of the bacterial cell wall represent a source of pamp (e.g. LPS on gram negative bacteria)
 PAMPs are conserved molecular structures present on pathogens
o On bacteria: LPS, peptidoglycan, flagellin
o On viruses: ssRNA, dsRNA
o On fungi: several glycans
o On parasites: GPI anchors
 Bacteria can be differentiated into 2 groups based on the gram stain of cell wall:
o Gram +ve stain purple with crystal violet while gram +ve stain red
Gram +ve & -ve staining
 Gram +ve cell walls have a single membrane enclosed by thick cross-linked sugars these sugars take up dye and make
bacteria appear purple
 Gram -ve bacteria have a thin cell wall which can take up purple but easily washed out and takes up counter stain (red)

Toll
 Toll-like Receptors (TLRs) were the first PPR discovered
 The human toll is TLR4 and it is the receptor for LPS

Human TLRs: cellular location and ligands
 TLR1/2/6/4/5 are membrane receptors
 TLR3/7/8/9 are intracellular receptors
 Ligand → receptor → recruits’ adaptor → kinase phosphorylates → intimidate signalling molecules → metabolic change,
cell movement, or gene transcription

Recognition of LPS and signalling through TLR-4
 LPS → TLR4 → IKK(adaptor) → IkappaB degrades (kinase activity) → NFkappaB enters cytosol and will induce
transcription of pro-inflammatory cytokines

Lecture 3: The acute inflammatory response: Cellular and humoral mediators of
innate defense
Cellular and humoral mediators of innate defense
 Cells of the innate system = phagocytes, mast cells, NK cells
o All use phagocytosis
 Secreted mediators of the innate system = cytokines & complement system
 Innate and adaptive immunity work together to clear infections;

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