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Foundations Clarke > Overview of Host Defenses > Flashcards

Overview of Host Defenses Flashcards

1
Q

What are the body’s two methods to distinguish self from non-self?

A

1) Recognition molecules to identify molecular patterns associated with parasites.
2) Adaptive methods where cells of the immune system are “educated” to identify agents that do not belong in the body while ignoring tissues that belong in the body.

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2
Q

With literally billions of potential foreign invaders, How does genome code for so many antibodies?

A

It can’t. 20K protein-coding genes vs billions of pathogens. But, immune system has ability to “guess” ahead of time.

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3
Q

_______ is an exogenous agent that induces specific immunity following a challenge to the body’s defense systems.
Exogenous agents are Antigens (recognized) that have______ properties (induces immunity)

A

Vaccine.

Immunogen

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4
Q

True or false, all antigens –> antibodies

A

False, the body needs to be “tricked” into making antibodies.

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5
Q

Following a primary infection, what happens.

A

Initial response is an IgM if the challenge represents new and never before recognized antigen. IgM initiates complement action (proteins found in the plasma that bind to foreign objects.

Antibodies are extraordinarily specific but requires time for B-cells to design and produce them. The Lag period between the initial challenge and to a mature response requires approximately 2-weeks. Immunogen induces inflammatory response (getting innate immune system going).

IgG represents an important developmental change for the B-cell. The B-cell is triggered to proliferate, then develop into plasma cells to manufacture immense quantities of immunoglobulin. Production of IgG is a very effective method to eliminate the non-self material.

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6
Q

What happens in a secondary response?

A

IgG drives total antibody force, with IgM accounting for a smaller portion for the immune response. IgM’s are still first on the scene in secondary responses, but IgG’s are ready sooner than they are in primary infections. It is IgG’s that completely kill the infection off

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7
Q

What is anticipation?

A

Each B-cell’s unique recognition ability

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8
Q

True or false, B-cell’s ability to recognize self from non-self is based on respective antigens and is therefor inherent.

A

False, B cells rely on an anticipatory process to recognize

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9
Q

Innate immunity truths

A

Genetically hardwired
Rapid response
Limited repertoire

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10
Q

Acquired Immunity truths

A

Genetic recombination
Protracted response- lag time
Immense repertoire

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11
Q

Effective immunity requires a method to label “decorate” non-self (Complement or Antibody). Effector cells then remove the labeled materials. What two ways can effector cells kill?

A

Effector cells can kill by contact (Cytotoxic T cells, Natural Killer cells, and Eosinophils), or cells that phagocytosis (Neutrophils, Eosinophils, Macrophage).

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12
Q

What is meant by saying the human immune response is “anticipatory”?

A

Each naive lymphocyte (i.e. never exposed to antigen) expresses a single type of antigen receptor (allelic exclusion). Antigen receptor is either an Antibody or T-Cell Receptor. Your body contains >10^7 naïve lymphocytes, thus your system has anticipated >10^7 different antigens, the potential repertoire is actually >10^15 based on the total number of gene segments in our genome.

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13
Q

What is lag time?

A

Time for antigen to be recognized by innate immune processes, transported to immune organs (i.e. lymph nodes), screening by naïve lymphocytes for a match between antigen and antigen receptor, and then expansion of the antigen-specific lymphocyte populations.

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14
Q

What is meant by repertoire?

A

B-cells expressing antigen specific antibody are stimulated to perform somatic hypermutation and class switching ( change from IgM to IgG/IgA/IgE). Somatic hypermutaion greatly enhances the affinity of the anibody but can lead to recognition of totally different antigens. Sometimes self-reactive antibodies result from hypermutation presenting a potential cause for autoimmunity.

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15
Q

What is meant by inducible?

A

Inducible- Lymphocyte response to antigen must be triggered by signals from innate immunity. Inabilities to trigger a lymphocyte response leads to immunodeficiency.

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16
Q

Describe the four types of immunization/ways to develop immunity:

A

Natural Passive - received maternally from placenta or colostrum.
Natural Active - result from infection
Artificial Passive - Antibody transfer from use of antiserum or pooled serum
Artificial Active - Immunization

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17
Q

True or false, passive immunity is long term while active immunity is short term.

A

False, passive immunity is short term while active immunity is long term

18
Q

Example of Active Immunization:
A) Suckling colostrum from breast feeding
B) Injection of snake anti-venom
C) Passage of antibody through the placenta
D) Injection of attenuated influenza virus

A

Injection of attenuated influenza virus

19
Q

Inflammation is essentially the process of _______. True/false, this is more complex in higher level organisms. Why?

A

Flushing out. Complexity increases with higher level organisms (compared to Dr. Clarke’s “tube” example). Increased complexity leads to stringent control of resource usage. Non-cooperative cells do not contribute and are therefor parasites. Inflammation –> flushing out of unwelcome guests.

20
Q

Common cell activities in an organism are:

A

Catabolism
Respiration
Waste Production
Replication

21
Q

Specific Roles for Cells in a Group

A 
Motility
Digestion
Structure
Sensory
Information processing
Defense
Policing
22
Q

How are foreigners identified?

A

Information Content & Discriminating
- Surface molecules are diagnostic of identity. For example Peptidoglycan is an important bacterial cell wall component found only in bacteria. The immune system has developed recognition mechanisms for unique pathogen associated molecular groups or patterns.

23
Q

An antigen recognition molecule must discriminate to successfully target non-self from self. What ways does it do so?

A

Specific Binding
Affinity – usually dependent on contact sites
Avidity – multiple binding sites

24
Q

Binding affinity of antibodies compared to other receptors:

A 
enzymes - 10^-6
Steroid receptors - 10^-7
Peptide hormone receptors - 10^-9
Cytokine receptors - 10^-10
ANTIBODIES - 10^-12 ...VERY HIGH AFFINITY
25
Q

Describe avidity.

A

Affinity is a description of selectivity and strength of interaction.
Avidity produces high binding strength when several low affinity sites work in cooperation to form a strong interaction. Avidity does NOT lead to refined selectivity.

26
Q

Two types of Alert Signals:

A

OUTSIDE - Pathogen Associated Molecular Patterns (PAMP), chemical moiety expressed on surface of worms, fungi etc. THIS MAKES US SICK.
INSIDE - Damage Associated Molecular Patterns

27
Q

Damage Associated Molecular Patterns (DAMP)

A

Occult and obscured from the defense mechanisms (Things that shouldn’t be out of cells)
Danger signal
Damage signal
Recognized by the Innate immune system
Examples: Proteins - Heat Shock proteins
Non-Proteins: Uric acid crystals, ATP, DNA, Heparin sulfate, Hyaluronan fragments
S100 molecules

28
Q

Pathogen Associated Molecular Patterns (PAMP)

A

Molecular moieties (i.e. parts) that are absolutely required for pathogen survival. Recognition system has co-evolved with the appearance of the PAMP, such as Endotoxin (classic - sugar lipid moietyin Lipid A), Flaggelin, dsRNA, CpG DNA, Peptidoglycan & Capping of terminal M6P by golgi.

29
Q

What are Toll Like Receptors (TLR)?

A

Surface molecules with recognition sites for PAMPs, DAMPs and other soluble factors that bind PAMPS (i.e. MD-2/CD14/LBP)). Nine different TLRs have been identified.

30
Q

True or false, TLR4 binds LPS endotoxin, which then triggers a signaling cascade leading to NF-κB and production of Pro-Inflammatory cytokines.

A

False, TLR4 does NOT directly recognize endotoxin but recognizes a serum protein bound with endotoxin. Endotoxin (LPS) is scavenged by a serum protein (LPS binding protein, LBP) and forms a complex with CD14/MD2 on the TLR4 to induce a inflammatory response involving Pro-Inflammatory cytokines.

31
Q

What do intracellular TLRs do?

A

Intracellular Toll Like Receptors bind to…. need to learn.

32
Q 
2. Inflammation induced by urate crystals is an example of:
PAMP
DAMP
Antigen
Immunogen
Kidney problems
A

DAMP

33
Q

Immunological Zones: Skin protects against what?

A 
Parasites
     Protozoans
     Helminthes
     Fungal
     Viral
34
Q

Immunological Zones: Skin protects WITH what?

A 
Langerhan's Cells
Mast Cells
Neutrophils
Macrophage
Eosinophils
35
Q

Immunological Zones: Interstitial protects against what?

A

Virus

Bacteria

36
Q

Immunological Zones: Interstitial protects WITH what?

A

Macrophage
CD4+ Helper T cell
Cytotoxic T cell
Natural Killer Cell

37
Q

Immunological Zones: Mucosal protects against what?

A

Virus

Bacteria

38
Q

Immunological Zones: Mucosal protects WITH what?

A 
Macrophage
Dendritic cell
γδ T cell
B1 Cells
***Primative T & B1 cells act as innate responders – ready to go right away. Limited repetoire. Keep gut flora in check. Not inducible. Really don’t deplete either.
39
Q

What tissues have no adaptive immune respones?

A

Eye and brain have no adaptive responses

40
Q

3 Lines of defense:

A

Epithelium - barriers
Mesoderm - Cellular responses, Flushing, Lyses, Trapping
Endoderm - Cellular Responses, Flushing

41
Q

Temporal response to antigen challenge

A

The pathogen is identified by recognition molecules associated with innate immunity, recognition is driven primarily by complement and Pattern Recognition Receptors (i.e. Toll Like Receptors and NOD Like Receptors). Inflammation provides the first line of defense involving physical (vascular dilation, clotting, flushing) and molecular mechanisms (Complement, chelation of iron) and recruitment of phagocytes (neutrophils). Inflammation is also stimulated by the release DAMP signaling tissue damage. The adaptive response involving production of antibody and effector T cells provides a targeted response. The adaptive response leads to memory of the pathogen. Memory consists of long-lived antibody producing cells and effector T cells that remain in reserve for active recall for subsequent challenges.

42
Q

immunity Summary

A
  • Innate immunity provides sensors for pathogens (TLR’s) and rapid response
  • Adaptive immunity provides high affinity receptors for antigen, production of high affinity requires anticipatory receptors that can be modified (class switching and somatic hypermutation)
  • Memory is a property of adaptive immunity and produced by immunization

Foundations Clarke (2 decks)

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