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M1 Immuno > Immunology > Flashcards

Immunology Flashcards

1
Q

Name the 9 components of innate immunity.

A
  1. skin barriers
  2. mucous membranes
  3. phagocytes
  4. NK cells
  5. fever
  6. defensins
  7. type 1 interferons (alpha and beta)
  8. TNF-alpha
  9. complement system
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2
Q

Describe the various immuno protective components of mucous membranes.

A

• mucus traps pathogens and foreign material to be killed by mucins and immune cells
• cilia forms part of mucociliary escalator to move material up the airways and expel it via coughing, sneezing or digestion
• commensal bacteria prevent colonisation by pathogenic bacteria
• acidic environment kills pathogens

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3
Q

Describe the immune mechanisms of phagocytes.

A

• neutrophils and macrophages target bacteria
• defensins found in epithelial cells and phagocytes (mainly neutrophils) form pores in bacteria and fungal membranes
• IFN alpha and beta are produced by phagocytes (DCs and macrophages) when encountering virus, to inhibit viral replication and activate phagocytes and NK cells
• TNF alpha is released by macrophages to activate signalling cascades, binding to TNF receptors on target cells to activate caspaces and induce apoptosis

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4
Q

Describe the immune control of fever.

A

Fever is mediated by IL-1, TNF-alpha and IL-6

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5
Q

Describe the innate immune mechanisms of the complement system.

A

The complement system targets bacteria, fungi and enveloped viruses, releasing Membrane Attack Complex (MAC) to punch holes in the membrane.

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6
Q

Describe the relationship between TNF-alpha and TGF-B

A

TGF-B is the opposite of TNF-alpha. TGF-B is an immunosuppressive cytokine that downregulates T-cell responses, however it does cause IgA expression at mucosal sites.

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7
Q

How are extracellular bacteria neutralized by the immune system?

A

They are presented on MHC II, activating neutrophils, complement system, CD4+ T-cells, B cells and their antibodies to eliminate the extracellular bacteria and toxins.

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8
Q

How are viruses and tumour cells neutralized by the immune system?

A

Their antigens are presented on MHC I, activating NK cells, IgG activating ADCC and cytotoxic CD8 T-cells, resulting in cell death.

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9
Q

How are fungi neutralized by the immune system?

A

Via the complement system.

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10
Q

How are parasites neutralized by the immune system?

A

They cause IgE secretion and mast cell degranulation, class switching activated by cytokine IL-4, IL-13 and IL-5 stimulate eosinophils

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11
Q

What are the signals required to activate Th-cells?

A
  1. MHC-TCR binding
  2. costimulation: B7 on APCs (upregulated by immune signals) + CD28 on TCRs OR CD40 on B cells + CD40L on T-h cells
  3. increased T-cell clonal expansion with IL-2 cytokine secretion (increased B-cell clonal expansion with IL-4 cytokine secretion)
    if only signal 1 is present, T-cells enter unresponsive state of anergy.
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12
Q

What are the 7 types of myeloid white blood cells?

A

• Basophils (allergy)
• Eosinophils (parasite, allergy, cancer)
• Neutrophils (bacteria, fungal infections)
• Monocyte –> macrophages (phagocyte to remove debris and pathogens, professional APC)
• Monocyte –> dendritic cells (sentinel professional APC)
• Erythrocyte (produce RBCs)
• Megakaryocyte (produce platelets)

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13
Q

What are the 3 types of lymphoid white blood cells?

A

• B cells
• T cells
• NK cells

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14
Q

Define immune tolerance.

A

Immune tolerance is the prevention of adaptive immune responses to self antigens.

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15
Q

Define central tolerance.

A

Central tolerance is the selection process of immature lymphocytes in primary lymphoid organs.

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16
Q

Describe T cell positive selection in the thymus

A

• part of central tolerance
• T cells with some ability to bind to self-peptide - selfMHCs will have growth and survival signals
• T cells that cannot will undergo apoptosis by neglect
• MHC restriction: T cells positively selected are restricted to recognising the respective MHCs required for their function

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17
Q

Describe T cell negative selection in the thymus

A

• part of central tolerance
• T-cells that have high affinity to bind to self-peptide - selfMHCs will undergo apoptosis
• autoimmune regulator (AIRE) switches on expression of extra-thymic tissue specific antigens in the thymus
• T-cells that bind strongly to AIRE antigens will be negatively selected to prevent autoimmunity
• mutations in AIRE lead to autoimmune disease

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18
Q

Define peripheral tolerance.

A

Peripheral tolerance is mechanisms that act on mature lymphocytes in the periphery

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19
Q

Describe the 4 mechanisms of peripheral tolerance of T-cells.

A
  1. Ignorance: TCR - self-peptide MHC interactions are too weak to activate the mature T-cell
  2. Anergy: cognate TCR - self-peptide MHC interactions without costimulation, leading to unresponsive anergised cells (seen in immature DCs with low expression of B7)
  3. Deletion: mature T-cells that recognise self-peptide MHC are deleted from T-cell repertoire via apoptosis
  4. **Treg cells: act on self-reactive immune cells to suppress their activity (express foxp3, constitutively express CTLA-4)
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20
Q

What are immune checkpoints?

A

Receptors in T-cells that regulate and decrease T-cell responses (e.g. CTLA-4, PD-1)

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21
Q

Describe the function of CTLA-4 receptors in immune checkpoints.

A

• competitive inhibitor of CD28 by binding to B7 with higher affinity
• expressed on T-cells after a few days of T-cell activation
• constitutively expressed on Tregs
• expressed more on CD4 than CD8 T-cells
• sequesters B7 and reduces B7 expression on APCs to inhibit T-cell activation

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22
Q

Describe the function of PD-1 in immune checkpoints.

A

• signalling receptor of CD28 and TCR, to decrease T-cell activity –> reduce T-cell mediated tissue damage and autoreactive T-cells
• expressed on T-cells only, not Tregs
• expressed more on CD8 than CD4 T-cells
• PD-L1 is expressed by cancer cells and APCs that express selfMHCs
• PD-1 is strongly expressed on chronically activated T-cells

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23
Q

How do tumours evade anti-tumour T-cell responses?

A
  1. expressing PD-L1 ligands on their cells
  2. upregulating CTLA-4 or PD-1 receptors on tumour infiltrating lymphocytes
  3. recruiting Tregs to block T-cell activity
24
Q

In the first step of adaptive immunity, _____ activate _____, causing _______.

A

pathogens at infected sites
resident immune cells at local tissues (DCs, macrophages, mast cells)
phagocytosis

25
Q

Describe the process of acute inflammation

A

• vasodilation: via activated mast cells releasing histamine + mast cells and macrophages release prostaglandins
• neutrophil migration to site if action: via leukotrienes
• neutrophil rolling and accumulation: via e-selectins and integrins
• transmigration of neutrophils into vascular space: via histamines increasing vascular permeability
• fever: via macrophages releasing cytokines to augment local responses, upregulate integrin and selectin expression, increase COX activity in the brain and hence increase PGE2 synthesis

26
Q

Describe the process of DC maturation during adaptive immune response.

A

• DCs mature from phagocytosing pathogens at peripheral tissues to upregulating expression of B7 on their cell membranes
• Chemotaxis of mature DCs to draining lymph nodes (expressing CCL19 and CCL21 chemoattractants)

27
Q

Describe the activation of naive T-cells during adaptive immune response.

A

• naive T-cells have CCR7 receptor and L-selectin molecules
• these two + CCL19 and CCL21 expressed in lymph nodes stimulate T-cells to migrate to draining lymph nodes
• DCs act as APC with MHC class II to activate naive Th-cells (3 signals needed)
• viral infected cells or DCs present intracellular pathogenic virus antigens with MHC class I to naive CD8 Tc-cells (1 signal needed)
• selected naive T-cells undergo differentiation into mature effector Tc-cells or Th-cells
• mature effector T-cell chemotaxis out of lymph nodes to the site of infection, with the help of leukotrienes

28
Q

Describe the process of CD8 Tc-cell mediated killing of infected cells in adaptive immunity.

A

• release perforins, forming pores in cell membranes
• release granzymes and granulysins, enter via perforin pores
• in the cell, granzymes and granulysins increase pro-apoptotic BAX expression, binding and pulling bcl2 from mitochondrial membranes
• egress of cytochrome C from mitochondrial membranes activates caspases
• CD8 Tc-cells also have FAS-L, binding to FAS on target cells to activate caspases
• caspases activate proteases that break down cytoskeleton and endonucleases that break down DNA, leading to apoptosis

29
Q

Describe the general functions of Th-cells in adaptive immune response.

A

• can migrate to periphery or remain in lymph node to activate naive B-cells in germinal centres
• all T-cells release IL-2 to promote T-cell proliferation

30
Q

Describe the specific functions of Th1 Th-cells in adaptive immunity.

A

• release TNF-alpha and IFN-gamma to activate classical M1 macrophages
• classical M1 macrophages are pro-inflammatory and microbicidal, promoting phagocytosis
• TNF-alpha also binds to TNF-R on target cells to activate caspases and induce apoptosis

31
Q

Describe the specific functions of Th2 Th-cells in adaptive immunity.

A

• release IL-4 and IL-13 to activate alternative M2 macrophages
• M2 macrophages are anti-inflammatory and promote tissue healing and repair
• IL-4 released also promotes B-cell proliferation, Ab production, and class switching to IgE (used in allergies and parasitic infections)
• IL-5 released also develops and activates eosinophils
• IL-13 released acts as a regulator of IgE production and eosinophilic inflammation

32
Q

What do Treg Th-cells do?

A

inhibit effector T-cell function (mainly of Th1 Th-cells)

33
Q

Describe the activation of B cells in medulla of the lymph nodes during adaptive immunity.

A

• neutrophils release free antigens into the bloodstream which enter lymph nodes
• clonal selection: naive B-cells with a complementary BCR phagocytose pathogen and present on MHC II
• clonal expansion: effector T-cells will release IL-4 cytokines, leading to multiplication of these B cells
• B-cells then move into dark zone of germinal centres

34
Q

Describe the activation of B cells in dark zone of germinal centres of the lymph nodes during adaptive immunity.

A

• somatic hypermutation: the original B-cell which underwent clonal expansion hypermutates to generate BCRs with different Fab regions
• this creates antibody diversity

35
Q

Describe the activation of B cells in light zone of germinal centre of the lymph nodes during adaptive immunity.

A

• hypermutated B cells compete to bind to iccosomes presented by follicular dendritic cells
• B-cells with higher affinity receptors can outcompete other B-cells to rip the iccosomes of the DC, and are conferred survival signals
• unsuccessful B-cells undergo apoptosis due to neglect
• this process is affinity maturation
• successful B-cells move into the mantle zone of the germinal centre

36
Q

Describe the activation of B cells in mantle zone of germinal centre of the lymph nodes during adaptive immunity.

A

• B-cells present the antigens on MHC II (provided by neutrophils at the start of B-cell activation) to T-cells
• B-cells require 3 signals for activation
1. MHC II bind to Th2 TCR
2. costimulation: B-cell CD40 bind to Th2 cell CD40-L
3. release of IL-4, IL-5, IL-13 from Th2 cells promotes B-cell differentiation and expansion + class switching to become either plasma or memory B-cells
• plasma B-cells then release immunoglobins targeting pathogen

37
Q

Where are memory cells located?

A

• Central memory T-cells remain in lymphoid tissues
• Peripheral effector memory T-cells and B-cells reside in peripheral tissues

38
Q

Why are memory cells formed in adaptive immunity?

A

Activated Th cells promotes memory B-cell and T-cell formation, which enables faster and stronger adaptive immune response to future infections of similar pathogens, leading to long term immunologic memory

39
Q

Define specificity.

A

Ability to distinguish small differences in 3D structure of ligands/antigens

40
Q

Define epitope.

A

specific part of antigen that antibody binds

41
Q

Contrast affinity and avidity.

A

Affinity is the strength of monovalent antibody binding, while avidity is total binding strength of antibody after accounting for all binding sites

42
Q

What is valency?

A

The number of binding sites on an antibody

43
Q

Where do B-cells develop?

A

Initial B cells development takes place in the bone marrow. Later stages of maturation and differentiation take place in secondary lymphoid organs such as lymph nodes and spleen.

44
Q

What are the parts of an antibody?

A

• 2 heavy chains and 2 light chains
• Fab variable region formed by heavy and light chains to bind antigens
• Fc constant region formed by only heavy chain to interact with cell surface receptors of other immune cells

45
Q

When and why does somatic recombination of B-cells take place?

A

When: during initial B-cell development in the bone marrow
Why: to generate primary antibody repetoire

46
Q

Distinguish combinatorial diversity and junctional diversity in B-cell somatic recombination.

A

Combinatorial diversity: random selection and ligation of V and J segments to form light chain and V, D and J segments to form heavy chain
Junctional diversity: insertion of random nucleotides at joining sites between gene fragments
Both processes generate different Fab regions to increase primary antibody repetoire.

47
Q

When does positive and negative selection of B-cells take place?

A

Before antigen exposure during B-cell initial development in the bone marrow

48
Q

What is B-cell positive selection?

A

• successful expression of pre-BCR (functional heavy chain) confers growth and survival signals to B-cell
• B-cells which fail to express pre-BCRs undergo apoptosis by neglect
• Positively selected B-cells will go on to express IgM

49
Q

What is B-cell negative selection?

A

• B-cells with IgM that bind to self-antigens will undergo apoptosis or anergy
• This prevents autoreactivity
• B-cells that don’t bind self-antigens can exit the bone marrow into blood

50
Q

Describe the process of B-cell class switching.

A

• activated Th2 cells release IL-4, IL-5 and IL-13 to induce IgG and IgE class switch response
• this induces heterochromatin DNA to open up, allowing switch recombinase complex to access the DNA
• genes are deleted, hence class switching is non-reversible
• class switching changes the antibody produced by mature B-cell from initial IgM to other classes

51
Q

What are the 6 functions of antibodies?

A
  1. neutralisation: bind and block pathogens and toxins from binding to host cell receptors
  2. opsonization: Fc region recruits macrophages and neutrophils and enhances phagocytosis of pathogens
  3. agglutination and formation of immune complexes: use multi-valebt binding sites to bind and trap pathogens into large complexes which are phagocytosed
  4. activation of complement system: classical pathway where Fc region binds to complement proteins, induce MAC which leads to osmotic lysis
  5. antibody dependent cellular cytotoxicity: antibodies bind to tumour cells and virus infected cells, recruiting NK cells to kill pathogens with perforins and granzymes
  6. mast cell degranulation: IgE uses Fc region to bind to Fc€RI on mast cells, causing mast cells to release toxic granules with histamines, lipid mediators and prostaglandins (allergies, type I hypersensitivity, parasites)
52
Q

What are the functions of the IgM antibody class?

A

• agglutination and formation of immune complex
• activate complement system C1q classical pathway (for MAC)
• important in bacterial infections

53
Q

What are the functions of the IgG antibody class?

A

• neutralisation
• ADCC, which is important for cancers and virus
• opsonization
• agglutination and forming of immune complex

54
Q

What are the functions of the IgE antibody class?

A

• mast cell degranulation
• important for parasitic infections and allergens

55
Q

What are the functions of the IgA antibody class?

A

neutralisation at mucosal sites only

M1 Immuno (5 decks)

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