Adaptive Immunity

Question 1

What is SCID?

Answer 1

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

Question 2

what are 4 features of adaptive/specific immunity?

Answer 2

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

Question 3

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

Answer 3

antigen recognition

Question 4

what is an antigen?

Answer 4

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

Question 5

how long does it take for adaptive immunity to develop?

Answer 5

5-7 days roughly

Question 6

what is adaptive immunity mediated by?

Answer 6

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

Question 7

what are b-lymphocytes?

Answer 7

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

Question 8

where are b-lymphocytes produced and mature?

Answer 8

in the bone marrow – this is antigen independent

Question 9

where are b-lymphocytes activated?

Answer 9

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

this is antigen dependant (reacts and activates to antigens)

Question 10

where are b-lymphocytes differentiated?

Answer 10

• 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

Question 11

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

Answer 11

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

Question 12

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

Answer 12

they have the same:

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

Question 13

which two antigens does b-cell activation dependent on?

Answer 13

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

Question 14

cytokines

Answer 14

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

Question 15

class switching

Answer 15

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

Question 16

what are the two regions of the antibody?

Answer 16

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)

Question 17

5 functions of antibodies

Answer 17

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

Question 18

How do antibodies preform opsonization?

Answer 18

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

Question 19

how do antibodies activate the complement pathway?

Answer 19

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

Question 20

how do antibodies cause agglutination?

Answer 20

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

Question 21

How do antibodies cause neutralization?

Answer 21

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

Question 22

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

Answer 22

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

Question 23

what is serum?

Answer 23

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

Question 24

what is plasma?

Answer 24

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

Question 25

What are the 5 types of antibodies?

Answer 25

1. IgG 2. IgM 3. IgA 4. IgE 5. IgD

Question 26

IgG (immunoglobulin G)

Answer 26

- 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

Question 27

IgM (Immunoglobulin M)

Answer 27

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

Question 28

IgA (immunoglobulin A)

Answer 28

- 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)

Question 29

IgE (Immunoglobulin E)

Answer 29

- 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

Question 30

IgD (Immunoglobulin D)

Answer 30

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

Question 31

What is Cluster of Differentiation [CDs]?

Answer 31

- different proteins on surface of cells used to characterize different cell types in the body

Question 32

What are the 3 types of T-Lymphocytes?

Answer 32

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

Question 33

Cytotoxic T-Lymphocytes (CTLs)

Answer 33

CD8+ - target and directly kill virus-infected cells, tumour cells, or cells from a tissue graft [can kill cancer cells]

Question 34

Helper T-Lymphocytes

Answer 34

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)

Question 35

Regulatory T-Lymphocytes

Answer 35

can suppress other immune cells

Question 36

How do t-cells develop and where?

Answer 36

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

Question 37

how do t-cells activate?

Answer 37

- in peripheral lymphoid organs (i.e. glands) | - MHC and antigen-dependent

Question 38

How do t-cells differentiate?

Answer 38

- become effector cells (Th or Tc) or memory cells

Question 39

Cytotoxic T Lymphocyte Activation (Tc)

Answer 39

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

Question 40

what are perforin and granzyme?

Answer 40

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

Question 41

How do Cytotoxic T-Lymphocytes (Tc) differentiate?

Answer 41

- 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

Question 42

How are helper t-cells (Th) activated?

Answer 42

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

Question 43

How are helper t-cells differentiated?

Answer 43

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

Question 44

4 types of immunodeficiency caused by T-lymphocytes?

Answer 44

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

Question 45

How do immune cells kill infected cells?

Answer 45

apoptosis or necrosis

Question 46

what is apoptosis?

Answer 46

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

Question 47

what is necrosis?

Answer 47

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

Question 48

what is humeral immunity

Answer 48

B-cells and antibodies

Question 49

what is cell mediated immunity

Answer 49

cytotoxic t-cells and t-helper cells

Question 50

how do humeral and cell mediated immunity interact?

Answer 50

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