Year 1; Phase 1; Core Concepts; Immunology 1, 2 And 3

Front 1

Name 6 cells involved in innate immune responses

Back 1

NK cells

neutrophils

eosinophils

basophils

mast cells

monocytes

Front 2

Give 9 examples of innate immunity, and briefly describe how they offer protection

Back 2

mucous membrane (traps foreign bodies)

epidermis (barrier)

tears (washes things away and contains lysosymes)

excretion/urination/vomiting (removal/prevents colonisation)

vaginal secretions (removal/prevents colonisation, plus slightly acidic so prevents bacterial growth)

sebum (keeps skin pH at 3-5; inhibits growth of microorganisms)

perspiration (prevents colonisation and contains lysosomes)

- antimicrobial substances (interferons, complement, iron-binding proteins and antimicrobial proteins)

Front 3

Briefly describe the function of each of the antimicrobial substances (4)

Back 3

interferons: inhibit viral replication

complememt system: enhances immune responses (e.g. cytolysis, phagocytosis and inflammation)

iron-binding proteins: inhibit bacterial growth by reducing available iron

antimicrobial proteins: short pepides with antimicrobial activity; also recruit mast and denritic cells

Front 4

Briefly describe the function of NK cells and how they may kill microbes

Back 4

they recognise cells with abnormal or unusual membrane proteins

release perforin (cause lysis by making holes in membranes) and granzymes (initiate apoptosis by digesting intracellular proteins)

Front 5

Describe the 5 stages of phagocytosis

Back 5

chemotaxis: chemically stimulated recruitment of phagocytes

adherence: attachment of phagocyte

ingestion: extensions (psuedopods) engulf microbes, forming a phagosome

digestion: phagosome merges with lysosome - forming a phagolysosome

killing: microbe is destroyed. Substance unable to be digested remain in residual bodies.

Front 6

What are the three stages of inflammation

Back 6

vasodilation

emigration of phagocytes

tissue repair

Front 7

Where do B and T cells originate and mature respectively?

Back 7

both are formed in the red bone marrow

B cells mature in the bone marrow

T cells move to the thymus and mature there

Front 8

What are the two types of adaptive immunity?

Back 8

cell-mediated and antibody-mediated

Front 9

Briefly describe what is meant by clonal selection

Back 9

occurs in secondary lymphatic tissue and organs

involves proliferation and differentiation of lymphocytes with specificity towards a specific antigen

gives rise to effector cells which target the antigen, and memory cells remain in the circulation to respond to future infections

Front 10

Name the 5 different classes of antibody

Back 10

IgA

IgG

IgM

IgD

IgE

Front 11

What are the 5 functions of antibodies

Back 11

neutralizing antigens (e.g. blocking)

immobilizing (e.g. binding to cilia or flagella)

agglutination and precipitation of antigen

complement activation

enhance phagocytosis

Front 12

Which antibody classes are most abundant in the primary response?

Back 12

IgM and IgG

Front 13

Phagocytes bind to what three types of receptor on cells?

Back 13

scavenger receptors

carbohydrate receptors

toll-like receptors

Front 14

Name the cells of the adaptive immune system (4)

Back 14

plasma cells

memory B cells

T helper cells

Cytotoxic T cells

Front 15

In order from most to least abundant, name all the WBCs

Back 15

Neutrophils

Lymphocytes

Monocytes

Eosinophils

Basophils

Front 16

Illustrate the complement system

Back 16

Front 17

Describe what happens in complement system after C3 has been activated

Back 17

- inactivated C3 splits into activated C3a and C3b

- C3b binds to the surface microbes, and on the surface of phagocytes, increasing opsonisation

- C3b splits C5 which, in conjunction with C6-C9, leads to the formation of the membrane attack complex. The membrane attack complex inserts into the plasma membrane of microbes, causing cytolysis

C3a and C5a bind to mast cells, causing the release of histamine - increasing vessel permeability and inflammation. C5a also recruits phagocytes (chemotaxis)

Front 18

Describe the classical pathway of the complement system

Back 18

- antibody binds to antigen

- antigen-antibody complex activates C1. Classical pathway therefore links adaptive and innate immune systems.

- C1 can also bind directly to pathogens, and therefore trigger complement without antibodies

- pathway converges with the production of C3 convertase

- C3 becomes activated and the fragments initiate phagocytosis, cytolysis and inflammation

Front 19

Describe the mannose-binding pathway of he complement system

Back 19

- macrophages that digest microbes release chemicals that cause the liver to produce proteins called lectins

- lectins bind to mannose and other carbohydrates on the surface of microbes, leading to the production of activation of C3 convertase and activation of C3

Front 20

Describe the alternative pathway of he complement system

Back 20

- does not involve antibodies

- initiated by the spontaneous hydrolysis of C3

- involves interaction between lipid-carbohydrate complexes on the surface of microbes, and complement protein factors B, D and P.

Front 21

Draw and label standard antibody

Back 21

Front 22

Which cell links the innate and adaptive immune systems and why?

Back 22

Dendritic cells. Take up and internalise antigens in the periphery and then present them to T cells

Front 23

Name the primary lymphoid organs and give 3 examples of secondary lymphoid organs

Back 23

Primary: bone marrow and thymus

Secondary: spleen, lymph nodes andlymphatic nodules

Front 24

Draw and label a lymph node

Back 24

Front 25

What is the function of a lymph node?

Back 25

Sites of immune responses

Receive antigen from the periphery and act as immunological filters

Front 26

What three signals do APCs deliver to T cells

Back 26

activation

survival

differentiation

Front 27

Draw a diagram summarising the activity of T cells

Back 27

Front 28

Draw a diagram summarising the activation of B cells

Back 28

Front 29

What are the stages of leukocyte trafficking?

Back 29

margination and rolling adhesion

tight binding

diapedesis

chemotaxis/migration

Front 30

Describe the pathology of type I hypersensitivity with examples

Back 30

- IgE binds mast cells and basophils via Fc portion

- cross-linking of IgE induces degranulation, causing histamine release

- histamine and other mediators - such as prostaglandins, cytokines and leukotrienes - have various affects, including vascular permeability, bronchodilation and VSMC contraction

- common examples of type 1 hypersensitivities are asthma, allergic rhinitis and anaphylaxis

Front 31

Describe the pathology of type II, III, and IV hypersensitivities with examples

Back 31

Front 32

Give 5 examples of organ-specific autoimmune disorders

Back 32

organ-specific;

type 1 DM (pancreas)

Goodpasture's syndrome (basement membrane in lungs and kidneys)

Multiple sclerosis (brain and/or spinal cord)

Grave's disease (thyroid gland)

Vitiligo (skin)

Front 33

Give 5 examples of systemic autoimmune disorders

Back 33

vasculitides (Churg Strauss)

Rheumatoid arthritis

Scleroderma

Systemic Lupus Erythromatosus

Polymyositis

Front 34

Briefly describe the pathology of the following;

psoriasis

RA

Grave's disease

Hashimoto's thyroiditis

SLE

Sjorgens syndrome

Crohn's disease

MS

Type 1DM

Back 34

Front 35

What is the difference a primary and secondary immunodeficiency?

Back 35

primary: typically congenital. Caused by a genetic defect affecting the function of the immune system

Secondary: acquired due to other diseases or conditions e.g. infections or immunosupression

Front 36

Give three examples of a primary immunodeficiency

Back 36

Severe Compromised Immunodeficiency (SCID)

Wiskott-Aldrich Syndrome

DiGeorge syndrome

Front 37

Give three examples of a secondary immunodeficiency

Back 37

Acquired Immunodeficiency Syndrome

Leukaemia

Malnutrition

Aging

Front 38

Defects in which cell type are likely to have the biggest impact on immunodeficiency? Why?

Back 38

phagocytes

three levels of deficiency: cell prodution, phagocyte interacton (linking adaptive responses) and kiling

Front 39

Explain the life cycle of HIV

Back 39

Front 40

Explain the pathogenesis HIV

Back 40

Oninfection, the HIV virus migrates into T-cells from its mucosal siteof inoculation, viamacrophages and/or dendritic cells.

The virus then disseminatesthroughout the systemic circulatory system before replicating(predominantly) in CD4+ T-cell reservoirs and sanctuary sites - suchas the lymph nodes, spleen, liver, gastrointestinal submucosa, andbone marrow.

Throughout the course of infection, HIV reduces memoryand naïve CD4-cell populations, with the subsequent loss of CD4T-cell populations, and immunodeficiency.

Four mechanisms regardinghow HIV reduces CD4-populations, have been postulated: lysis, immunedestruction, apoptosis, and impaired lymphocyte regeneration.