Topic 6 Immune Response

Front 1

Physical barriers that prevent infection

Back 1

1) Skin > impermeable

2) Gut & Skin flora > competes with microbe > space & nutrients > limits no. of microbes

Front 2

Chemical barriers that prevent infection

Back 2

• stomach acid secreted by gastric glands > hydrochloric acid > destroys microbes

• mucosal surfaces (e.g. eyes, mouth, nose) > secrete lysozymes (e.g. in tears) > kills bacteria by damaging cell walls (& causing them to lyse)

( • gut flora > secrete chemicals, e.g. lactic acid, useful in defence against pathogens )

Front 3

Ways pathogens enter the body

Back 3

- cuts in skin (e.g. through blood)

- digestive system (e.g. contaminated food/drink)

- respiratory system (e.g. through inhaling)

- mucosal surfaces (e.g. in nose)

Front 4

What is the non specific immune response

Back 4

1) inflammation at site of infection

2) interferons

3) phagocytosis

4) lysosome

(LIIP)

Hint 4

LIIP

Front 5

Inflammation

Back 5

1. Bacteria enter due to break in physical barrier (skin) e.g. a cut

2. Immune system recognises foreign antigen on surface of pathogen

3. Damaged tissue (mast cells & damaged white blood cells) release histamines > triggers inflammation

4. ARTERIOLES dilate/ VASODILATION > ^ blood flow > ^ w.b.c at site of infection = REDNESS

5. ^ permeability of CAPILLARIES > immune cells move out of blood vessels & into infected tissue = SWELLING

(Immune system starts to destroy pathogen)

6. causes redness, swelling, pain

Front 6

Lysozyme action

Back 6

• Breaks down chemical bonds in the cell wall of bacterial cell

• lysozymes = digestive enzymes

• lysozyme action destroys pathogens

Front 7

What is a histamine

Back 7

Chemical that causes dilation of arterioles & increases the permeability of capillaries

Front 8

Interferon (Define)

Back 8

1) infected cell makes anti-viral protein called interferon

2) Inhibits viral replication inside cells/ prevents virus infecting other cells

Front 9

How does interferon prevent virus spreading

Back 9

1) prevent viral replication by inhibiting production of viral proteins

2) activate cells involved in specific immune response to kill infected cell

3) activate other mechanisms of non-specific immune response > e.g. promote inflammation at site of infection

Front 10

Phagocytosis

Back 10

1) macrophages check/scan for abnormality

2) recognises antigens on pathogen as foreign

3) engulfs it/ goes into cell vesicles by endocytosis

4) lysozymes (in lysosome) released which break down the pathogen

5) releases antigen by exocytosis which combines with the cell surface membrane

6) becomes an Antigen Presenting Cell (APC) to help other cells develop immunity to the specific pathogen

Front 11

How are T cells activated?

Back 11

1. APC presents antigen of pathogen

2. Receptors complementary to this binds (‘antigen receptor complex’)

3. T cell is activated > T killer, helper, memory cell (differentiates)

4. divides by mitosis (clonal expansion) to produce clones of itself

Front 12

How are B cells activated?

Back 12

1 ) APC presents antigen of pathogen

2) antibody of B cell is complementary & binds to form antigen-antibody complex

3) binding & cytokines (from T helper cells) activates the B cell > B effector, memory cells

3) B cell divides by mitosis so proliferates/ clonal expansion occurs where clone of B cell made

Front 13

Types of B cells

Back 13

B effector cells = differentiate to become plasma cells that release antibodies

B memory cells = remain in blood & remember pathogen > able to produce B effector cells

Front 14

Types of T cells

Back 14

T helper cells = release cytokines > activates B cells, T cells & macrophages

T killer cells = destroy cells with antigens detected as foreign/non-self - pathogens

T memory cells = remain in blood > proliferate & differentiate into T killer & helper cells

Front 15

What’s the difference between T and B cells

Back 15

T cells directly attack the pathogen whilst B cells release specific antibodies

Front 16

Antibody structure

Back 16

- Y shaped immunoglobulin (glycoprotein)

- 4 polypeptide chains (2 heavy & 2 light chains)

- variable region (complementary to specific antigen)

- constant region (allows binding to receptors or immune system cells)

- disulfide bridges (bond holding polypeptide chains together)

- hinge region (allows flexibility when the antibody binds to antigen)

Front 17

Role of antibodies

Back 17

1. Agglutination of pathogen > each antibody has 2 binding sites > binds to 2 pathogens at same time > ‘clumped together’ > phagocytosis of both (as held together by antibody)

2. Neutralising toxins > antibody bind to toxin > x effect human cells as neutralised/inactivated

(Toxin-antibody complex phagocytosed)

3. Preventing pathogen binding > antibody blocks cell surface > receptor needed for pathogen to bind to body cell is blocked > x attach/infect cell

Front 18

Clonal selection

Back 18

Activation of immune cell with complementary antibodies/ receptors to the antigen (of pathogen)

Front 19

Clonal expansion

Back 19

Replication (by division) of selected cells (B/T cells) by mitosis

Front 20

How & why are different antibodies made?

Back 20

1) B cells covered in antibodies

2) different antigen on pathogen’s surface = different antibody shape (complementary)

Front 21

Role of antigens

Back 21

1) antigens used to detect pathogen (^ specific shape)

2) needed to create APCs

>> these initiate/activate the primary immune response (non specific & specific)