2.2 - Adaptive Immunity Flashcards

1
Q

Key Features of Adaptive Immunity

A
  • destruction of infectious microorganisms that evade the 1st and 2nd line of defence/ resistant to inflammation

Features
1) Inducible - activated in response to a specific pathogen

2) Specific - targets specific pathogens

3) Long-lived - provides immunity for a long time

4) Has memory - remembers previous pathogens to allows for faster response upon re-exposure

2 Elements if Adaptive Response
1) Antigens - molecules found on patthgens that trigger the immune response
2) Lymphocytes

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2
Q

Humoral Vs. Cellular Immunity

A

Humoral Immunity
- antibodies (produced by B cells) bind to antigens on pathogens
- marks cells for destruction

Cellular
- T cells either 1) directly kill cells or 2) stimulate leukocytes to enhance the response
- destroys infected cells

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3
Q

Active VS Passive Immunity

A

Active
- developed by exposure to antigens
- ex. Vaccine, Infection

Passive
- developed when antibodies are transferred from 1 person to another
ex. from mother to baby

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4
Q

Antigens and Immunogens

A

Antigens
- sit on the surface of the pathogen
- bind to antibodies

Immunogens
- type of antigen
- induce production of antibodies, T and B cells
- all immunogens are antigens (bind to receptors), but not all antigens are immunogens (some antigens bind but dint produce response)

Haptens
- small molecules that can not cause an immune response on their own
- only become immunogenic when combined with larger molecules

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5
Q

What are Immunoglobulins

A
  • antibodies produced by B cells
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6
Q

Immunoglobulin G: IgG

A
  • most abundant
    ** can cross placenta and provide immunity to fetus**
  • accounts for most protection against infections

Classes
1) IgG 1 - involved in parasitic infxns
2) IgG 2 - detects bacteria
3) IgG 3 - activates complement
4) IgG 4 - involved in allergic response

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7
Q

Immunoglobulin A: IgA

A

2 Types

1) IgA
- in blood
- targets pathogens that enter the bloodstream

2) IgA2 (secretory)
- found in bodily secretions: breastmilk, saliva, tears, mucous
- prevents pathogens from adhering to epithelial layers
- forms protective barrier on mucosal surfaces

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8
Q

Immunoglobulin M: IgM

A
  • largest antibody
  • 1st antibody produces in response to an antigen
  • synthesized in neonatal life (provides protection for newborns)
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9
Q

Immunoglobulin D: IgD

A
  • low concentration in blood
  • expressed on surface of immature B cells
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10
Q

Molecular Structure of Antibody

A

Y - shaped

Tip of Y = fab region
- where antigens bind

Arms of Y = 4 Polypeptide chain
- each chain has a Variable region and constant region
- variable region allows antibodies to recognize various antigens

Stem of Y - fragment crustibale
- rects with other immune cells

Hinge region - between stem and arms
- allows flexibility in shape to enable better binding

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11
Q

Epitope VS Paritope

A

Epitope - determinant
- part of the antigen that is RECOGNIZED by antibodies

Paratope - binding site
- binds to corresponding site on antigen (tip of Y)

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12
Q

Functions of Antibodies

A

Direct (NAP)
1) Neutralization
- neutralizes toxins: antibody binds to pathogen to prevent it from binding with other cells

2) Agglutination
- antibodies clump pathogens together
- makes it easier to be detected by immune system

3) Precipitation
- antibodies bind to antigens that form insoluble complexes
- the complexes can not join tissue so it gets removed

Indirect - antibody activates other components of immune response
1) Inflammation
- binding of antibody to antigen releases inflammatory mediators

2) Phagocytosis
- antibody binds to phagocyte receptors and stimulates them to engulf pathogens

3) Complement
- binding initiates cascade leading to more inflammation

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13
Q

Immunoglobulin E - IgE

A
  • defends against parasites (by attracting eosinophils)
  • binds to allergens: triggers allergy symptoms
  • binds to mast cells and cause degranulation
    • histamine gets released and attracts eosinophils and kills parasites
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14
Q

Secretory/Mucosal Immunity

A
  • lymphoid tissues protect against pathogens that enter through external surfaces
  • IgA 2 is the dominant immunoglobulin in mucosal secretions
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15
Q

Why is Clonal Diversity Needed?

A
  • our body can respond to all antigens with only 5 immunoglobulins bc of clonal diversity
  • immune system’s ability to produce clones of lymphocytes that can recognize unique antigens
    • lymphocytes develop their recognition capacity in thymus and bone marrow
  • develops in fetal life
    - naive cells remain in the body and are primed to become specific when they encounter an antigen
  • result in naive but immunocompetent cells
    -immunocompetent bc these cells can produce an immune response, but naive bc they have not encountered the antigen and produced specific receptors
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16
Q

B and T cell Development

A

B Cell
- produced in bone marrow
- each B cell only recognizes 1 type of antigen

T cells
- produced in the thymus
- develop antigen specific t cell receptors that allow them to recognize specific pathogens

B and T Cells
- once mature, leave bone marrow/thymus travel to lymphoid tissues where they become immunocompetent
- undergo central tolerance: to ensure they dont attack bodys own tissues

17
Q

Primary and Secondary Response

A

Primary
- occurs when 1st exposed to antigen
- IgM antibodies are detected 1st
- then IgG response

Secondary
- occurs after re-exposure to the same antigen
- response is more rapid bc memory cells have been previously sensitized (need less differentiation/activation)
- a lot of IgG is produced for longer-lasting immune response

18
Q

Antigen Processing and Presentation

A

1) B cells and T cells encounter an antigen and get processed by APC’s such as macrophages, B cells

2) APC’s catch the antigen, break it down into smaller fragments, and present these on the surface of a histocompatibility complex (MHC )

3) While B cells process antigens, they differentiate into plasma cells (which then produce antibodies)

T cells differentiate into effector cells:
T - helper - coordinate immune response
T cytotoxic - destroy cells

Result:
B cells - antibody producing plasma cells
T cells - contribute to immune response and kill pathogens

19
Q

Cell Interactions

A
  • intrecellular collaborations result in the production of effector and memory cells
  • requires 3 intracellular signalling events
    1. Antigen specific recognition
  • T cells identify and bind to antigens presented by APC’s
    2. Activation of adhesion molecules
    3. Response to specific cytokines
  • cytokines propagate response to other immune cells
20
Q

Function of T Helper Cells

A
  • help drive the maturation of T and B cells
  • amplify interactions bw APC’s and lymphocytes

2 Types
1) Th1
- develop cell-mediated immunity
- activate macrophages and cytotoxic cells (destroy pathogens)

2) Th2
- develop humoral immunity
- activate B cells to produce antibodies (mark antigens for destruction)

21
Q

What are Super Antigens

A
  • SAG binds to non-specific (variable) portion of T cell receptor
  • the non-specific binding activates a lot of T cells = overwhelming immune response
  • result is excessive cytokine production which causes fever, low BP, and shock
22
Q

B Cell Clonal Selection

A
  • when immunocompetent B cell encounter antigen for the 1st time, it is stimulated to differentiate and proliferate
  • it differentiates into a plasma cell
  • each plasma cell produces antibodies specific to antigens
  • B cells undergo class switch: they can produce different classes of antibodies which allow a more targeted immune response
23
Q

T Cell

A
  • T cells are activated when an antigen binds to a T cell receptor

T cells either
1) directly kill abnormal cells
2) assist activation of other immune cells

T-regulatory cells
- prevent the immune system from attacking bodys own tissues

Memory T Cells
- remember previous encounters with antigens and allow for quick response

24
Q

T Cytotoxic Cells

A
  • destroy infected cells

Role of perforin and granzymes
- Perforin: creates pores in infected membrane
- Granzyme: enters cell and triggers apoptosis

25
Q

Fetal Immunity

A
  • fetus has sufficient IgM (produced in neonatal life)
  • IgG passes from mother to fetus to provide immunity in 1st few months of life
  • newborns are immunologically immature
    • deficient antibody production,
      phagocytotic actvity
26
Q

Aging and Immune Function

A

1) Decreased T cell activity
- fewer T cells migrating to thymus (where they mature) = decreased function

2) Thymus Shrinks
- decreased production of thymic hormone which are required for T cell differentiation/maturation
- decreased T cell efficiency

3) Decreased ability for antibody to respond to antigens
- teeters: amt of antibodies in our system for certain illness
- teeters decrease overtime
- insufficient teeters can make us experience infection we were previously immue to