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BHCS1006 > Immonology > Flashcards

Immonology Flashcards

1
Q

Define Innate Immunity.

A

Specialized cells and molecules that induce a rapid response to eliminate pathogens. It’s composed of barriers, macrophages, mediators, etc…

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2
Q

List the components of the innate immunity.

A 
Epithelial barriers
Antimicrobial peptides 
Complement 
Cytokines
Phagocytic cells 
Receptors 
NK cells
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3
Q

What are examples of surface barriers to infection?

A

Skin, GI tract, respiratory tract, etc…

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4
Q

Why is innate immunity important?

A

Innate is not antigen specific but rather diverse and recognizes general patters.

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5
Q

List 3 epithelial barrier to infection.

A

Mechanical; epithelial cells joined by tight junctions.
Chemical; enzymes(e.g. lysozyme) and surfactant proteins in the lung.
Microbiology; produce antibacterial substances.

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6
Q

Define the complement system and identify the 3 ways complement removes microbes.

A

Complement is a defense system consisting of multiple proteins produced by the liver.
3 ways of removing microbes; Opsonization, Inflammation, Cytolysis.

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7
Q

Define Opsonization, Inflammation, Cytolysis and their respective roles in the Complement System.

A

Opsonization; mechanisms of tagging pathogens for elimination.
Inflammation; mechanism of signaling cytokines.
Cytolysis; rupturing of a cell membrane.

Classical pathway; involved antibodies.
Lectin pathway; direct recognition of carbohydrates on a pathogen.
Alternative pathway; recognizes pathogen through alternative scavenger proteins.
- All pathways go through a central component (C3) which then determines one of three responses (Opsonization, Inflammation, Cytolysis).

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8
Q

Outline the process of triggering the innate immune responses.

A

Injury/infection occur -> type of cytokine(chemotaxis or inflammation) - Chemotaxis recruits the cells to fight infection, inflammation activates to kill pathogens. The cytokines allow for increased permeability of blood vessels which allows for the requirement of more cells resulting in swelling.

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9
Q

Define Cytokines and outline their roles and characteristics.

A

Cytokines(e.g. IL-1)are molecules that are used for cell signaling, or cell-to-cell communication.

  • All cytokines can activate an acute phase response.
  • Cytokines can recruit cells via chemotaxis using soluble Chemokines (e.g. IL-8 which recruits phagocytes).
  • Anti-inflammatory (e.g. IL-10).
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10
Q

Describe the acute phase response.

A

Acute phase response is associated with the induction of fever (which creates a bad environment for pathogens). The IL-1 & IL-6 are the main triggers for the active phase response and the production of acute phase proteins that recognize and respond to pathogens(e.g. CRP biochemical marker of inflammation), which leads to activation of complement (Opsonization).

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11
Q

List the sights of inflammation.

A

Heat, swelling, redness, pain, loss of function.

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12
Q

Outline the emigration of neutrophils.

A

Margination -> rolling -> integrity activation by Chemokines -> stable adhesion -> migration through endothelium.

(VIEW SLIDES FOR VISUAL)

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13
Q

List the cells of innate immunity.

A 
Neutrophils 
Monocytes
Eosinophils 
NK cells
Macrophages 
Mast cells
Dendritic cells
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14
Q

Outline the process of phagocytosis.

A

Phagocytosis is an active process installed by binding to a pathogen, where its then internalized.
Phagocyte receives the pathogen -> engulfs the phagosome -> fuses with lysosome containing acid hydrolase -> destroy pathogen -> exocytosis.

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15
Q

Detail the function of macrophages in inflammation and their interactions with up to 4 substances.

A

Macrophages can:

  • produce cytokines(e.g. IL-1, IL-6)
  • be response to lipids(e.g. prostaglandins)
  • produce killing molecules (e.g. ROS & NO)
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16
Q

How is inflammation controlled or resolved?

A

Inflammation is regulated through anti-inflammatory molecules such as:

  • Cytokines (e.g. IL-10, IL-4)
  • Drugs (e.g. NSAIDs[aspirin])
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17
Q

Define sepsis and its characteristics.

A

Life-threatening organ dysfunction due to a dysregulated host response to infection. Sepsis is characterized by overwhelming inflammatory cytokine production.

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18
Q

How does the immune system detect pathological molecules?

A

PAMPs can recognize:

- LPS(i.e. Gram- bacteria), Lipoteichoic acid(i.e. Gram+), peptidoglycan, bacterial DNA, etc…

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19
Q

Define PAMPs.

A

Pathogen-associated molecular patterns (PAMPs) are recognized by pattern-recognition receptors (PRRs), which play a key role in innate immunity in the recognition of pathogens or of cellular injury.

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20
Q

Define PRR. Examples?

A

Pattern Recognition Receptors (PRRs) are proteins capable of recognizing molecules frequently found in pathogens (the so-called Pathogen-Associated Molecular Patterns—PAMPs). Examples include:

  • Toll-like Receptors (TLR)
  • Nod-like Receptors (NLR)
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21
Q

Define TLRs and Outline their function.

A

Toll-like receptors (TLRs) are proteins that are involved in host defence against pathogens. TLRs act as primary sensors of microbes and activate signalling pathways that lead inflammation. There is a wide range or TLRs(e.g. TLR4 which recognizes LPS).

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22
Q

Define NLRs and Outline their function.

A

NLRs recognize peptidoglycan which is a constituent of Gram positive and negative bacteria.

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23
Q

Define adaptive immunity.

A

Adaptive Immunity is highly specific and because it is acquired its is typically slow reaction however upon secondary exposure to a pathogen the reaction quickens due to immunological memory.

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24
Q

Define humoral immunity.

A
  • Humoral immunity is the principle defense against extracellular microbes.
    • Extracellular microbes; include fungi, helminths, and some bacteria. As such the microbes themselves are accessible to circulatory soluble mediators (e.g. antibodies))
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25
Q

What mediates humoral immunity and what are the effector responses generated to deal with extracellular pathogens?

A

Th2 and B cells mediate humoral immunity. Effector responses include:
Macrophages suppression
Antibody production
Eosinophil activation

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26
Q

Draw or recall the focal process of humoral immunity.

A

Depending on how the extracellular resident pathogen is processed by the APC, it programs a Naive CD4+ T Cell to differentiate into the appropriate helper subset(Th2 Subset) that drives humoral responses. Predominately, Th2, through the production of IL-4, can modulate the differentiation and activation of B Cells to produce a range of antibodies with different functions. Additionally, Th2, through the production of IL-4 & IL-10, can play a role in suppressing macrophage pro-inflammatory behavior. And finally, through the production of IL-5, the activation of eosinophils for immune responses against helminths.

27
Q

Outline the function of CD4+ helper T cells (Th).

A

Th2 cells promote the generation of B-cell antibodies, macrophage suppression & allergic/anti-helminth parasite responses.

28
Q

Draw, example, or recall the method of activation of Th2 cells.

A

MHC II presented on the surface of an APC and how it can antigenically activate the Helper T Cell. What is needs is MHC presenting antigenic peptide being presented to the T Cell Receptor in conjunction of CD4 (This is known as the antigen stimulus[its MHC II restricted signal]). The other signal ‘Co-stimulatory’, is the co-stimulatory ligand (B7). This B7 presenting on the APC expresses and activates CD28. (It is the culmination of the antigen stimulus and the co-stimulus that ensures the activation of the Th2 Cell).

29
Q

Draw/Outline the development of Th2 subset.

A

The APC present antigen in the context of MHC II, on conjunction with the co-stimulatory signal and it drives Naive CD4+ T-Cells to differentiate and proliferate towards Th2 Cells (this is antigen dependent and also driven by the soluble cytokine IL-4) that are functionally differentiated and activated to help drive humoral responses. In this process the final result can be a range of functionally activated Th2 cells such as IL-4,IL-5, etc…, however, some cells do not undergo this process and become Long-term Memory T-cells (used in secondary exposure).

30
Q

What effector pathway is the primary immune reaction, explain? (Humoral)

A

Antibody production is the predominate reaction in humoral immunity is how Th2 activate B-cells to produce antibodies, the secreteble soluble molecules, that help fight extracellular resident pathogens and this is determined by the production of IL-4 by the Th2 cells and by the types of antibody that is produced by these B-cells which will determine the overall immune response.

31
Q

Discuss/Describe the structural function of antibodies.

A
32
Q

Identify and describe each antibody isotope and their functions.

A
33
Q

What is isotope class switching? Examples?

A

B-Cell are able to exhibit Isotype Class Switching, which essentially allows for the switching of immunoglobulin isotypes, in order to tailor the immune response to whatever pathogen that may be present.
Examples:
- IL-4 induced IgE and IgG
- IL-2/IL-4/IL-5 induces IgM

34
Q

Define cell mediated immunity (CMI).

A
  • Principle defense against intracellular microbes.
    • Intracellular microbes (virus & some bacteria) survive and proliferate inside host cells and are hence inaccessible to circulating antibodies.
35
Q

What is CMI mediated by? And what are the effector pathways?

A

T lymphocytes mediate CMI. Effector pathways include:
Tc prodn
DTH response

36
Q

Describe/Draw the focal process of CMI.

A

Intracellular resident pathogens are processed by APC, and when talking about Naive CD4+ T-Cells, this antigen that’s processed from these intracellualr resident pathogens that are restricted to presneted by MHC II molecules in conjunction with co-stimulatory signals and an appropriate cytokine environment, the naive t cells different and proliferate into the subset Th1. It is this subset that is most important for CMI; Th1 drive a range of responses, from macrophage activation, cytotoxic T-Cell proliferation, neutrophil activation, etc… With regards to CMI, it’s mechanisms 1 and 2 that predominate.

37
Q

Identify the role of CD4+ helper T cells in CMI.

A

Th1 cells promote the generation of Tc and DTH reactions.

38
Q

Outline/Draw the development of Th1 subset.

A

The APC present antigen in the context of MHC II, on conjunction with the co-stimulatory signal and it drives Naive CD4+ T-Cells to differentiate and proliferate towards Th1 Cells (this is antigen dependent and also driven by the soluble cytokine IL-12 & IFNy ) that are functionally differentiated and activated to help drive CMI responses. In this process the final result can be a range of functionally activated Th1 cells such as IL-2, IFNy, etc…, however, some cells do not undergo this process and become Long-term Memory T-cells (used in secondary exposure).

**Should be noted that these process are very similar to humoral responses aside from the cytokine environment (IL-12, IFNy)*

39
Q

Define CD8+ cytotoxic T cells and their function.

A

CD8+ Tc kill target cells bearing endogenously derived Ag presented by MHC I.

The first main mechanism is the activation of cytotoxic T-Cells where helper cells are defined by CD4+. Cytotoxic T-Cells have a phenotypic marker called CD8 (so anything expressing CD8 is likely to be a cytotoxic T-cell). Effectively what the cytotoxic T-Cells do is they gang up on target cells and kill them (This is a restricted response; in the case of CD8, they are activated by antigenic peptide presented by MHC I ).

40
Q

Define Tc cells.

A

CD8+ Tc kill target cells bearing endogenously derived Ag presented by MHC I. The first main mechanism is the activation of cytotoxic T-Cells where helper cells are defined by CD4+. Cytotoxic T-Cells have a phenotypic marker called CD8 (so anything expressing CD8 is likely to be a cytotoxic T-cell). Effectively what the cytotoxic T-Cells do is they gang up on target cells and kill them (This is a restricted response; in the case of CD8, they are activated by antigenic peptide presented by MHC I ).

41
Q

Outline the process of activation of Tc cells.

A
42
Q

Briefly outline the two ways cytotoxic T cells are activated.

A

Dependently;

Independently;

43
Q

Define DTH, how they function, and why they might be used instead of Tc cells.

A

Delayed-type hypersensitivity responses often generated against pathogens living inside the macrophages themselves.
Functions;
- Recruit monocytes to site of infection
- Keep monocytes/Macrophages at site of infection
- Activate monos/Macrophages to kill intracellular pathogens.

DTH may be used instead of Tc cells as its a more destructive immune response.

44
Q

Outline/Draw the cellular features of the DTH response.

A

The first mechanism is all about IFNy that is produced by Th1 that activates the macrophages enabling them to be pro-inflammatory, alongside this they can phagocytose microbes and infected cells.

  1. Activation of CD4+ Th Cells
  2. Migration of effector Th1 Cells to the site of infection
  3. recruitment of monocytes from peripheral circulation
  4. differentiation of monocytes to macrophages and the activation of macrophages (predominated by the secretion of IFNy by Th1s…
  5. elimination of pathogen
45
Q

What happens as a result of a failed DTH response? (VIP)

A
46
Q

List some examples of in trace lunar pathogens that are cleared by CMI responses.

A

Mycobacteria spp. (Bacteria)
Herpes simplex virus (virus)
Cryptococcous neoformans (fungi)

47
Q

Outline the role of macrophages and their function in CMI.

A
  • Macrophages & Th cells stimulate each other.
  • TNF Alpha & IL-2 contribute to macrophage activation in the presence of IFNy.
  • Macrophages retained at DTH site by macrophage inhibition factor (MIF), secreted by Th cells.
48
Q

What is the principle mechanism of immunity in regards to extracellular pathogens(in blood and lymph)?

A

Protective immunity for extracellular microbes consist of Complement & Phagocytosis (which is part of the Innate Immune Response), as well as, antibodies (which is part of the Humoral Adaptive Immune Response).

49
Q

Outline the role of neutrophils in the immune system.

A

Neutrophils are important defences against extracellular infections. Neutrophils are short-lived immune cells and they’re weapons of mass destruction, they play a role in reconigzing bacteria and being able to response to bacteria by a range of mechanisms (e.g. response to extracellular pathogens is phagocytosis). As a result of phagocytosis, a signal illicits other immunological responses which results in degranulation of a range of products (includes ROS which is toxic for extracellular pathogens).

50
Q

What is the principle mechanism of immunity in regards to extracellular pathogens(epithelial surfaces)?

A

Epithelial associated extracellular bacteria, the protective immunity is defined by antimicrobial peptides and antibodies (especially IgA).

51
Q

Define and outline antibody response.

A

Major antigens of many bacteria are polysaccharides, and defense is mediated only by antibodies; these T-Cell-indepednant antibody responses may be short-lived and weak.

52
Q

What are the two types of intracellular pathogens that exist? (In terms for location) and how do they differ in illiciting an immune response?

A

Its imporatnt to note that intracellualr bacteria can reside, either in the cytoplasm or hidden in the vesicalles. with regards to vesicualr resident bacteria, the most known bacteria is mycobacterium tuberculosis. intracellualr bacteria escape humoral defenses by resideing with the cell so the infected host cell must be killed in order to destroy the pathogen, this is done through the protective immunity. In cytoplasmic intercellular bacteria immunity, NK cells and cytotoxic T-cells are used, while in vedicualr it is t-cell and nk-cell mediated macrophage activation(a sort of DTH repsonse). both repsonses to both types are a form of cell-mediated immunity.

53
Q

Outline CMI in more detail. (Note the cytokines)

A

Cell mediated immunity is what predominates when responding to intracellular bacteria. there are four mechanisms to CMI and they include how Th1 and the cytokines they produce drive a whole range of responses. TNF beta and alpha can activate neutrophils, IFNy can activate b-cells to produce opsonizing and complement-binding antibodies. BUT the two mechanisms that are at the forefront of CMI for intracellular bacteria is mechanisms 1(macrophage activation by IFNy produced by Th1, considered DTH response) and 2(Th1 mediated activation and differentiation of cytotoxic t-cells via IFNy and IL-2)

54
Q

How are viruses targeted by the immune system?

A

Viruses are typically very small and hence are mostly intracellular resident pathogens (targeted mainly by CMI). Cytoplasmic intercellular bacteria is all about where they reside within the cell and how the immune system response through innate and adaptive mechanisms.

55
Q

Explain the employment of cytotoxic t-cells.

A

Cytotoxic t-cells are activated by cytokines released by the Th1s. The IFNy and IL-2 produced by Th1s help activate and differentiate cytotoxic t-cells. The mechanisms that result in killing infected hots cells, is both soluble mediated and contact mediated.

56
Q

Explain the roles of antibodies and CTLs in adaptive immunity against viruses.

A
  • Antibodies neutralize viruses and prevent infection
    • Block infectious virus early in course of infection (before entering cells) or after release from infected cells (prevents cell-to-cell spread).
  • CTLs kill infected cells and eradicate reservoirs of established infection
    • In some latent viral infections (CMV), CTLs control but don’t eradicate the infection; defective t-cell immunity leads to reactivation of the virus (in HIV, immunosuppression caused by leukemias, treated for graft rejection).
57
Q

Define antigenic drift vs. shift.

A
  • Antigenic drift; involves the accumulation of a series of minor genetic mutations (Makes it difficult for the immune system to recognize).
  • Antigenic shift; involves “mixing” of genes from influenza viruses from different species (e.g. pigs, birds, and humans). (This results in a new combination = a new strain, humans don’t have the immunity to recognize this new strain).
58
Q

Identify 2 examples of immune reactions that cause disease.

A

Hypersensitivity

Autoimmune

59
Q

Define hypersensitivity.

A

Exaggerate or inappropriate, damaging immune responses following second challenge of antigen.

60
Q

List the categorizes of hypersensitivity reactions.

A

Type 1 - clinical allergy
Type 2 - antibody-dependent
Type 3 - complex-mediated
Type 4 - delayed type

61
Q

Provide brief notes on hypersensitivity type 1.

A

A hypersensitive reaction involves an exaggerated to inappropriate immune response.
Type 1 involves IgE Abs released in response to an allergen.
In atopic individuals mast cells and basophils become sensitized when IgE binds.
Further exposure causes degranulation and release of mediators (e.g. histamine).
Causes wide range of localized or systemic effects. Includes; hayfever, asthma, etc…

62
Q

Outline type 2 hypersensitivity.

A

An-dependent cell-mediated cytotoxicity (ADCC);

  • antibody on target cells is bound by other cells (e.g. cytotoxic cells via their Fc receptors).
  • release contents of intracellular storage granules which kill target cell.
63
Q

List examples of type 2 hypersensitivity.

A

Transfusion reactions, haemolytic anaemia, etc…

64
Q

How do viruses inhibit MHC I and what occurs as a result? Is there an immune mechanism to compensate for the evasion?

A

The activation of cytotoxic t-cells, viral proteins are presented in the context of MHC I, which is what helps with the activation of ctyo t-cells to kill the infected cell. there are some clever viruses that use that knowledge and actively engage in inhibiting that pathway. some viruses can effectively suppress the way in which the viral proteins are cut (proteasome) if this step is not the virus cannot be presented by the MHC I and hence will disable any further action.

additionally, more bacteria have found evasion strategies which block the transport of the protein. furthermore, some viruses can also block MHC synthesis (disabling presentation), they can also induce removal of class I from endoplasmic reticulum. finally, some viruses can produce decoys of their own version of viral class I molecules.

there is a safety net to these evasion strategies; Upon MHC I being down-regulated by viral infection, the immune system can use the cells of the innate immune system (NK CELLS). Missing self hypothesis is shown below where a comparison between a cell with the presenting MHC I molecules present whilst one without inducing a killing response.

BHCS1006 (2 decks)

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