Immunity

Question 1

What is chemotaxis?

Answer 1

Using chemical signals to attract cells to a particular site.

Question 2

What is histocompatibility?

Answer 2

Literally, compatibility of tissue. Determined by human leukocyte antigens and used to determine whether a transplanted tissue or organ will be accepted by the recipient.

Question 3

What is the human leukocyte antigens (HLA)?

Answer 3

A group of identification molecules that are located on the surface of all cells in a combination that is almost unique for each person, thereby enabling the body to distinguish self from nonself. Also called the major histocompatibility complex.

Question 4

Name the 4 parts of a successful immune response.

Answer 4

Recognition, activation and mobilisation, regulation, resolution.

Question 5

What role do dendritic cells play?

Answer 5

Antigen presenting cell - Phagocytoses the invader, breaks it into antigen fragments which are presented on its surface with its HLA. Receptors on T lymphocyte plasma membrane bind to antigen fragments and activate immune response.
(Macrophages and B lymphocytes can also do this.)

Question 6

Which of CD4+ T cells and CD8+ T cells are cytotoxic and which are helper cells?

Answer 6

CD4+ = helper cells.
CD8+ = cytotoxic.

Question 7

What is humoral immunity?

Answer 7

Recognising pathogens before they infect cells. B cells function in this, it is antibody-mediated.

Question 8

What is cell-mediated immunity?

Answer 8

Destruction of antigens, infected cells, and cancerous cells by phagocytes and antigen-specific cytotoxic T cells (CD8+).

Question 9

What is a primary lymphatic organ?

Answer 9

An organ where stem cells divide and become immunocompetent (ready to mount an immune response).
i.e. red bone marrow (immunocompetent B cells and pre-T cells produced), and the thymus (pre-T cells become immunocompetent T cells).

Question 10

What are secondary lymphatic organs and tissues?

Answer 10

Sites where most immune responses occur.

i.e. spleen, lymph nodes, lymphatic nodules.

Question 11

What are the boundaries of the anterior cervical triangle?

Answer 11

Inferior: Jugular notch and manubrium.
Anterior: Midline of neck from chin to jugular notch.
Posterior: Anterior margin of sternocleidomastoid.
Superior: Inferior border of body of the mandible.

Question 12

What are the boundaries of the posterior cervical triangle?

Answer 12

Inferior: Middle 1/3 of clavicle.
Anterior: Posterior margin of sternocleidomastoid.
Posterior: Anterior margin of trapezius.
Superior: Union of sternocleidomastoid and trapezius at superior nuchal line on occipital bone.
Roof: Investing layer of deep cervical fascia.

Question 13

What is the pathway along which lymph travels through a lymph node?

Answer 13

Afferent lymph vessels => Subcapsular sinus => Trabecular sinus => Medullary sinus => Efferent lymph vessels.

Question 14

What is the difference between a primary lymphatic nodule in the outer cortex of a lymph node and a secondary lymphatic nodule?

Answer 14

Primary lymphatic nodules are made up of B lymphocytes. Secondary lymphatic nodules form in response to an antigen and are made up of plasma cells and memory B lymphocytes, with a germinal centre of B lymphocytes and macrophages and follicular dendritic cells.

Question 15

What is found in the inner cortex of a lymph node?

Answer 15

Dendritic cells and T cells that have migrated in from other tissues.

Question 16

What is found in the medulla of a lymph node?

Answer 16

B cells, plasma cells, and macrophages embedded in a network of reticular fibres and cells.

Question 17

What is common about the capsule of the thymus, spleen, and lymph node?

Answer 17

It is dense connective tissue and has trabeculae extending into the organ.

Question 18

What constitutes the stroma of the lymph node?

Answer 18

Capsule, trabeculae, reticular fibres, and fibroblasts.

Question 19

What constitutes the parenchyma of the lymph node?

Answer 19

Cortex and medulla (functional part).

Question 20

What constitutes the stroma of the spleen?

Answer 20

Capsule, trabeculae, reticular fibres, fibroblasts.

Question 21

What constitutes the parenchyma of the spleen?

Answer 21

Red pulp and white pulp.

Question 22

What is the white pulp in the spleen?

Answer 22

Lymphoid tissue (lymphocytes and macrophages) arranged around central arteries (branches of splenic artery).

Question 23

What is the red pulp in the spleen?

Answer 23

Blood filled venous sinuses, and splenic cords (Billroth’s cords).

Question 24

What are splenic cords?

Answer 24

Cords of splenic tissue containing red blood cells, macrophages, lymphocytes, plasma cells, granulocytes.

Question 25

What are the three functions of the spleen?

Answer 25

1) Removal of old and worn out red blood cells by macrophages.
2) Storage of platelets.
3) Haematopoiesis during foetal life.

Question 26

Where are lymphatic nodules found in mucous membranes?

Answer 26

In the submucosa.

Question 27

Name the four types of hypersensitivity (of which the first three are humoral).

Answer 27

Type I = Anaphalactic (immediate) (IgE antibodies).
Type II = Cytotoxic (IgG antibodies targeting blood cells).
Type III = Immune-complex (IgG antibodies and complement system).
Type IV = Delayed (cell-mediated) (TH1 cells activating macrophages, TH2 cells activating eosinophils, cytotoxic T cells).

Question 28

Describe Type I hypersensitivity.

Answer 28

On first exposure to the allergen, IgE antibodies are produced which then bind to mast cell and basophil membranes. On subsequent exposure to the allergen, the antigen binds to the IgE antibodies causing the mast cells and basophils to secrete histamine, kinins, prostaglandins, and leukotrienes.
This causes vasodilation, increased capillary permeability, increased contraction of smooth muscle of airways and lungs, increased mucus production, vomiting and diarrhoea.
Treat by infection with adrenaline to dilate airways and increase force of heartbeat.

Question 29

What is the difference between the immediate, early, and late response of the immune system?

Answer 29

Immediate and early are innate, late is adaptive.
Immediate response uses preformed agents, early requires protein synthesis. Innate immunity prevents early death during the expansion phase of the adaptive immune response (and instructs adaptive immune response).

Question 30

Name something really important in regulating the immune response.

Answer 30

Microbial flora.

Question 31

There are several different pathways to initiate the complement cascade, what do they all lead to?

Answer 31

C3 being broken down into C3a and C3b, to allow efflux of fluid and cells into tissue.

Question 32

What do C3a and C5a do in the complement cascade?

Answer 32

Trigger the release of histamine from mast cells and basophils, and cause inflammation.

Question 33

What does C3b do in the complement cascade?

Answer 33

Bind to membranes of pathogens and the complement receptors on phagocytes to cause chemotaxis and opsonisation and phagocytosis. This is a receptor-ligand interaction, with the mammalian cell protein being the receptor and the pathogen cell protein being the ligand.

Question 34

What’s the main difference between the TLR receptors of the innate and adaptive immune system for recognising pathogens?

Answer 34

Innate has to recognise them fast and not need to make any new proteins so has a limited number of flexible receptors for recognising the broad category of pathogen.
Adaptive has a higher number of more specific receptors because the response is slower and more directed.

Question 35

What are TLR receptors?

Answer 35

Toll-like receptors, highly expressed on innate immune cells like macrophages and dendritic cells, which recognise molecules derived from different classes of pathogens.

Question 36

What are the first and second responses of the complement system?

Answer 36

First response = inflammation.

second response = membrane-attack complex (C5-C9 form pores so cell dies due to osmotic lysis).

Question 37

How may a pathogen be killed once it is in a phagolysosome?

Answer 37

Acid, lysozyme, nitric oxide, NADPH oxidase producing free radicals superoxide (O2 -) ions that are converted to hydrogen peroxide ions and disrupt the cell membrane.

Question 38

When neutrophils can’t catch a pathogen, war do they do?

Answer 38

Explode to produce a NET (Neutrophil Extracellular Trap) which is formed from chromatin and granule proteins, and traps the pathogen so they can be degraded.

Question 39

Where do most tissue macrophages arise from?

Answer 39

Non-haematopoietic precursors, though they can arise from monocytes in the blood.

Question 40

What changes the endothelium during inflammation so they dilate and more adhesion molecules are expressed (so leukocytes move to the blood vessel periphery) and the wall becomes more permeable?

Answer 40

Cytokines, histamine, complement proteins.

Then chemokines cause leukocytes to move out into the tissues.

Question 41

What are cytokines and chemokines?

Answer 41

Small soluble protein molecules that allow immune cells to communicate with other cells, so the immune response is regulated. Chemokines are chemotactic cytokines, so they regulate function and movement, and cause chemotaxis.

Question 42

What prevents the cytokines becoming systemic and causing a cytokine storm or toxic shock syndrome?

Answer 42

The cytokines are short acting. They are released at the interfaces between cells (synapses) and only act locally. Receptor expression by cells is highly regulated so that the duration of the response and the target is controlled.

Question 43

What are natural killer cells and what do they do?

Answer 43

They are lymphocytes involved in the innate immune response. They kill pathogens and “altered self” cells (e.g tumour cells) by making pores in their membrane using perforins and then secreting toxic granzymes into the cells.
They produce the cytokine Interferon gamma (IFNgamma).

Question 44

How does a Natural Killer cell activate a resting macrophage when the macrophage recognises a pathogen?

Answer 44

The macrophage secretes two cytokines (IL-12 and IL-18) which bind to receptors on the NK cell (safeguard = both cytokines must bind to produce response), then the NK cell produces IFNgamma, which activates the macrophage so it kills the pathogens more effectively.

Question 45

If a cytokine pathway leads to disease, why can’t you just block the pathway?

Answer 45

The cytokine signalling network is so complex that blocking parti of the pathway may block another part that is related and essential, and result in a cytokine storm.

Question 46

Why are many steroids anti-inflammatory?

Answer 46

They target cytokines.

Question 47

Name three differences between IgG and IgM.

Answer 47

IgM is bigger because it is pentomeric and IgG is monomeric.
IgG lasts longer than IgM.
IgG is distributed throughout the body, but IgM is only found in blood and lymphatics.

Question 48

Which antibody is the main one released in a primary immune response?

Answer 48

IgM with a small amount of IgG.

Question 49

Which antibody is the main one released in a secondary immune response?

Answer 49

IgG with a small amount of IgM.

Question 50

Give three examples of atopic conditions which are examples of Type I hypersensitivity.

Answer 50

Anaphylaxis, hay fever, asthma.

Question 51

Give the test for Type I hypersensitivity reactions.

Answer 51

Blood test for IgE antibodies, skin test.

Question 52

Give four examples of Type II hypersensitivity reactions.

Answer 52

Myasthenia gravis, acute (not chronic)transplant rejection, rheumatic fever, Guillain-Barre, haemolytic anaemia (e.g penicillin allergy).

Question 53

Give the blood test for Type II hypersensitivity reactions.

Answer 53

Coombs test.

Question 54

Give three examples of Type III hypersensitivity reactions.

Answer 54

Rheumatoid arthritis, systemic lupus erythematosus, post-streptococcus glomerulonephritis, Farmer’s lung.

Question 55

Give four examples of Type IV hypersensitivity reactions.

Answer 55

Multiple sclerosis, contact dermatitis, type 1 diabetes mellitus, chronic transplant rejection.

Question 56

Where do T cells mature and where do B cells mature?

Answer 56

T cells mature in the thymus, B cells mature in the red bone marrow.

Question 57

Which enzyme does aspirin inhibit?

Answer 57

Cycloxygenase (COX).

Question 58

What are the two isozymes of COX?

Answer 58

COX-1 (constitutive) - found in stomach, platelets, endothelium, intestines
COX-2 (induced) - found in cells at inflammatory sites.

Question 59

How does aspirin block COX?

Answer 59

Aspirin irreversibly blocks the channel of access so arachidonic acid can’t move up the channel and bind to the catalytic site and be converted to prostaglandins and thromboxane.

Question 60

What are phospholipids converted to?

Answer 60

Arachidonic acid, then thromboxane and prostaglandins.