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MMI > Adaptive Immunity > Flashcards

Adaptive Immunity Flashcards

1
Q

What is SCID?

A

severe combined immunodeficiency –> when you dont have an adaptive immune system

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2
Q

what are 4 features of adaptive/specific immunity?

A
  • specialized immune cells
  • specific responses
  • self/non-self recognition
  • memory generation (remembering the antigen)
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3
Q

what is the specificity of the adaptive immune system based on?

A

antigen recognition

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4
Q

what is an antigen?

A
  • most are proteins
  • foreign molecules recognized by adaptive immune cells
  • elicit an immune response
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5
Q

how long does it take for adaptive immunity to develop?

A

5-7 days roughly

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6
Q

what is adaptive immunity mediated by?

A 
B lymphocytes (humeral / blood)  --> humeral is body fluids, blood and lymph
T lymphocytes (cell-mediated)
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7
Q

what are b-lymphocytes?

A

b-lymphocytes produces antibodies in response to specific antigens to fight infection

they produce cytokines, chemical signals that change behaviour of other cells

act as APCs (antigen presenting cells) –> activates other immune cells to combat infection

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8
Q

where are b-lymphocytes produced and mature?

A

in the bone marrow – this is antigen independent

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9
Q

where are b-lymphocytes activated?

A

in the peripheral lymphoid organs (i.e. lymph nodes)

this is antigen dependant (reacts and activates to antigens)

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10
Q

where are b-lymphocytes differentiated?

A
  • differentiation occurs after they recognize antigen
  • they differentiate into plasma or memory B cells
    in the lymph nodes (peripheral lymphoid organs)

this is also antigen decedent because they produce specific antibodies to a specific antigen

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11
Q

what is the process of b-cell activation and differentiation in 4 steps?

A
  1. antigen binds to IBM antibody which causes signalling
  2. COLONIAL EXPANSION: clones of b-cell with same antibody get produced (rapid cell division and proliferation)
  3. a portion of those clones become Memory cells and are stored for second encounter of antigen
  4. the majority of the clones become plasma cells or effector cells which secrete antibodies
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12
Q

what are the two commonalities between the proliferating b-cells during colonial expansion?

A

they have the same:

  1. B cell receptor (BCR)
  2. specificity for antigen
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13
Q

which two antigens does b-cell activation dependent on?

A
  1. Thymus-dependent (TD) antigens –> proteins like bacterial cell wall components or parts of capsule [requires t-helper cell contact to help with memory]
  2. Thymus-independent (TI) antigens –> mostly other molecules like sugars and carbs
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14
Q

cytokines

A

cytokines are solvable proteins secreted by immune cells

they are chemical signals that can change the behaviour of other cells

can cause b-cell proliferation (clonal expansion) and class switching

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15
Q

class switching

A

changing ig (antibody) produced by B cell (i.e. IgM to gig) with no loss of antigen specificity

production of different antibodies depending on the cytokine environment around plasma cells and depends on infection

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16
Q

what are the two regions of the antibody?

A

Fab region –> where the antigen binds [Y shaped arms]
Fc region -> constant region which is recognized by other immune cells that have a Fc receptor (used by phagocytes to find the pathogen after the antibody binds to it)

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17
Q

5 functions of antibodies

A
  1. opsonization
  2. complement activation (activation of MAC)
  3. agglutination
  4. neutralization
  5. antibody-dependent cell-mediated cytotoxicity
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18
Q

How do antibodies preform opsonization?

A

antibodies recognize bacterial antigens and the FAB region binds them

then macrophages have Fc receptor that bind the antibody Fc stem which in turn eats the antigen-antibody complex

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19
Q

how do antibodies activate the complement pathway?

A

antibodies that attach to the antigen attract the C3b complement protein which is an opsonin –> then that activates the entire complement pathway forming MAC (membrane attack complex) and cell lysis

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20
Q

how do antibodies cause agglutination?

A

each Y shape arm of the antibody can bind to an antigen and then form a ring and clump together; this attracts the phagocytes and allows them to take up more pathogens at once

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21
Q

How do antibodies cause neutralization?

A

antibodies attach onto the virus and bacteria before it gets into the host, therefore blocking up all its receptors so it can attach onto the host cell

it also blocks toxins from attaching to host cells
i.e. tetanus vaccine has antibodies specifically for the toxin so it binds to it and takes up its availability so it cant bind

22
Q

How do antibodies cause antibody-dependent cell-mediated cytotoxicity?

A

used by NK cells which have FC receptors that bind to the antigen-antibody complex at the FC end and kill the infected cell

23
Q

what is serum?

A

serum is yellow liquid separated from coagulated blood after its centrifuged and the fibrin is removed

  • rich in proteins and used in lab testing
  • contains no active blood clotting proteins
24
Q

what is plasma?

A

plasma is the yellow fluid obtained by treating blood with an anticoagulant
- RBCs are removed by centrifugation (they sediment at the bottom)
- contains intact blood clotting proteins that have not been activated (has chemical to prevent clotting like sodium citrate)
used in blood donations

25
Q

What are the 5 types of antibodies?

A
  1. IgG
  2. IgM
  3. IgA
  4. IgE
  5. IgD
26
Q

IgG (immunoglobulin G)

A
  • 80% of serum antibodies produced
  • most abudnant class
  • long lasting
  • transferred from mom to unborn child via placenta and covers the fetus’s immunity for 6 months
  • highly efficient for activating complement
  • high affinity for Fc receptors on phagocytic cell membranes and can readily mediate opsonization
27
Q

IgM (Immunoglobulin M)

A

5-10% of serum antibody

  • 1st antibody produced by b-cell in primary response (first time contact with virus)
  • 1st antibody to be made by neonates (fetuses can make this in the uterus)
  • when in monomeric form (one antibody) it forms BCR (B-cell receptor)
  • plasma cells secrete soluble IgM as a pentamer (5 molecules connected by a joining chain) J chain
  • IgM is more efficient to activate complement
28
Q

IgA (immunoglobulin A)

A
  • 10 to 15% of antibody in serum
  • predominant antibody in external secretions like breast milk, saliva, tears, and mucus in bronchial, digestive and genitourinary systems
  • exists as a monomer, but dimers can form and are held by J-chains (joining chain) used for easy transport across mucosal surfaces
  • prevents the attachment of bacteria or viruses to mucosal surfaces and prevents colonization
  • IgA is secreted in breast milk and protects the newborn during first months of life (this is why breast feeding is important to protect fetus from respiratory infections)
29
Q

IgE (Immunoglobulin E)

A
  • extremely low concentrations in serum (0.0002%)
  • responsible for allergies
  • binds to Fc receptors mast cells and eosinophils (secrete histamine)
  • plays an important role in the neutralization of parasites
30
Q

IgD (Immunoglobulin D)

A
  • 0.2% of serum antibodies
  • expressed at the cell surface of mature B cells, along with IgM
  • unknown biological function
31
Q

What is Cluster of Differentiation [CDs]?

A
  • different proteins on surface of cells used to characterize different cell types in the body
32
Q

What are the 3 types of T-Lymphocytes?

A
  1. cytotoxic t-lymphocytes (CTLs) –> CD8+
  2. helper T-lymphocytes: CD4+
  3. Regulatory T-lymphocytes
33
Q

Cytotoxic T-Lymphocytes (CTLs)

A

CD8+

  • target and directly kill virus-infected cells, tumour cells, or cells from a tissue graft [can kill cancer cells]
34
Q

Helper T-Lymphocytes

A

CD4+

  • produce cytokines that support inflammation and activates other immune cells [bind to peptide on MHC 2 receptors)
  • activate B cells which leads to antibody production (produce cytokines to activate other immune cells)
35
Q

Regulatory T-Lymphocytes

A

can suppress other immune cells

36
Q

How do t-cells develop and where?

A

immature t-cells travel to the thymus from the bone marrow

in the thymus, development is dependent on self MHC molecules and antigen

  • cells are programmed so they dont auto react to self
37
Q

how do t-cells activate?

A
  • in peripheral lymphoid organs (i.e. glands)

- MHC and antigen-dependent

38
Q

How do t-cells differentiate?

A
  • become effector cells (Th or Tc) or memory cells
39
Q

Cytotoxic T Lymphocyte Activation (Tc)

A

a virally infected cell with an MHC 1 showing the viral protein on it, will bind to a CD8+ Tc cell and then the CD8+ cell will produce and secrete effector molecules to destroy target cells (perforin and granzyme) then the cell dies via apoptosis (neat and tiny way to die without evoking an immune response)

the t-cells can recognize foreign antigens via infection and cancer

40
Q

what are perforin and granzyme?

A

these are the two effector molecule secretions by cytotoxic t-lymphocytes (CD8+ cells)

perforin helps granzyme enter the cell and kill it by punching a hole

the cell death is apoptosis

41
Q

How do Cytotoxic T-Lymphocytes (Tc) differentiate?

A
  • they undergo clonal expansion
  • majority are killer cells
  • but a small % become memory cells that can quickly activate after a second encounter with same antigen and MHC 1
42
Q

How are helper t-cells (Th) activated?

A

helper t-cells are activated when an antigen is bound to MHC 2 receptor on a cell and then binds to the t-helper cell receptor on the CD4+ cell

it makes cytokines to activate immune cells and initiate CTLs (cytotoxic cells) or act as B-cell helpers to secrete more antibodies

43
Q

How are helper t-cells differentiated?

A

activated Th cells undergo clonal expansion

  • majority will remain as helper cells
  • small percentage will become memory helper cells that are readily activated by a second encounter with same antigen and MHC 2
44
Q

4 types of immunodeficiency caused by T-lymphocytes?

A
  1. partial immunodeficiency (highly prone to infections)
  2. auto-immunity (t-cells unable to differentiate from self and non-self) –> hyper-immune response
  3. severe immunodeficiency –> SCID, can be fatal if not treated by bone marrow tx
  4. acquired immune deficiency syndrome –> i.e. HIV jacking Th cells
45
Q

How do immune cells kill infected cells?

A

apoptosis or necrosis

46
Q

what is apoptosis?

A

cell death that occurs as a normal part of development or because of a targeted event

does not trigger inflammation because phagocytes clean up the compartmentalized parts that were released

47
Q

what is necrosis?

A

cell death that is triggered by extrinsic factors like an infection
- detrimental to host and accompanied by inflammatory response

48
Q

what is humeral immunity

A

B-cells and antibodies

49
Q

what is cell mediated immunity

A

cytotoxic t-cells and t-helper cells

50
Q

how do humeral and cell mediated immunity interact?

A

they interact by cross-talk and do not work independent of each other

MMI (18 decks)

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