second line of defence

Question 1

when is second line of defence activated?

Answer 1

when first line of defence is passed

Question 2

how are extracellular pathogens attacked?

Answer 2

by phagocytes

Question 3

define: phagocyte

Answer 3

type of white blood cell that engulfs a pathogen by phagocytosis and uses intracellular digestion to destroy it.

Question 4

3 types of phagocytes?

Answer 4

neutrophils, monocytes and macrophages

Question 5

describe neutrophils

Answer 5

Found in circulation but migrate into sites of infection in tissues.
First cells to arrive at infection site in response to signals from other cells.
3 lobed nucleus
Short lived

Question 6

describe monocytes

Answer 6

Found in circulation. When they move into tissues, they differentiate into macrophages.
Long lived

Question 7

describe macrophages

Answer 7

From differentiated monocytes in tissues.
In addition to phagocytosis, they eliminate dead cells and cell debris, and initiate inflammatory response by secreting cytokines, play a role as antigen presenting cells.

Question 8

describe how phagocytosis works

Answer 8

• Macrophage ‘s pattern recognition receptors on pm bind to molecular patterns, which recognise it as belonging to a group of pathogens
• Macrophage engulfs the pathogen via phagocytosis, forming a vesicble around it called a phagosome.
• Lysozymes containing digestive enzymes fuse with the phagosome, and release the enzymes into it, which digests the pathogen
o Indigestible material excreted by exocytosis.
o Some partially digested peptides are retained by macrophages and dendrites for the purpose of antigen presentation

Question 9

how are intracellular pathogens attacked

Answer 9

whole cell containing thme eliminated by natural killer cells by degranulation

Question 10

describe how NK cells decide whether to kill a cell

Answer 10

• Natural killer cells have killer activating and killer inhibitory receptors.
• All body cells carry ligands that bind to killer activating receptors – which signals to the NK cell to kill the cell.
• However, normal HLA markers bind to killer inhibitor receptors – which makes a signal which blocks the kill signal.
• HLA markers can be abnormal (on cancer cells) or missing (on virus infected cells, which suppress expression of Class I NHA markers); so there won’t be anything that can mind to the killer inhibitory receptors, and the cell will be killed.

Question 11

describe degranulation

Answer 11

• Granules (vesicles) contain protease enzyme granzyme and the cylindrical protein perforin.
• Granules undergo exocytosis.
• Perforin pierces the plasma membrane to form a pore, then the granzymes enter through them and induce apoptosis
o Important that apoptosis, not lysis, happens, as otherwise the virus would be released into the extracellular fluid and infect other cells.

Question 12

dendritic cells are the main type of…

Answer 12

antigen presenting cells

Question 13

define: antigen presenting cell

Answer 13

cells that move antigens to their surface and then display these antigens to other immune cells.

Question 14

where are dendritic cells typically found?

Answer 14

in tissues like skin, airway linings and gut

Question 15

how do dendritic cells work?

Answer 15

o Engulfs pathogens via phagocytosis and degrades them; but some peptide fragments are retained, forming antigens
o Antigens are then linked to class II MHC molecules in cytoplasm and then transferred to the cell surface.
o Then, the dendritic cells go to the nearest lymph nodes and present them to naïve helper T cells.

ALSO secrete antiviral cytokenes

Question 16

where are mast cells usually found?

Answer 16

in tissues near external environment

Question 17

what do mast cells do?

Answer 17

• IgE antibodies produced by plasma bodies bind to mast cells = primed.
• Mast cells’ antibodies bind to antigen, activating the mast cells and causing degranulation – chemicals like histamine are produced.
o Histamine and other chemicals attract other immune cells to the infection site
o Occurs in inflammation/allergies

Question 18

define: complementproteins

Answer 18

proteins dissolved in blood plasma

Question 19

how many types of complement proteins

Answer 19

about 20

Question 20

describe how inactive comp proteins are changed to active forms

Answer 20

• Exist in bloodstream as dissolved, inactive enzymes, but when they make direct contact with molecules on the surface of a pathogen they are activated (split). The activation of one leads to the activation of others in a cascade effect.

Question 21

3 effects of complement proteins

Answer 21

o Opsonising pathogens
 Opsonisation: complement proteins coat pathogens surface antigens.
 Phagocytes have receptors for complement proteins. The cp’s, along with the pathogen, bind do the phagocytes which digest the whole thing.
 This makes the pathogen more susceptible to phagocytosis.
o Small complement proteins can diffuse from surface of pathogens and chemically signal to attract immune cells involved in the inflammatory response to the site of infection
o Causes pathogens to lyse
 Multiple CP’s form a membrane attack complex, which pierces the cell membrane and enables entry of extracellular fluid, due to osmosis of cell it will swell and lyse.

Question 22

define: interferons

Answer 22

proteins secreted by some cells after a viral infection

Question 23

how do interferons work?

Answer 23

they bind to recepotrs on neighbouring cells to produce signals that:
• IgE antibodies produced by plasma bodies bind to mast cells = primed.
• Mast cells’ antibodies bind to antigen, activating the mast cells and causing degranulation – chemicals like histamine are produced.
o Histamine and other chemicals attract other immune cells to the infection site
o Occurs in inflammation/allergies

Question 24

first thing that happens in the inflammatory response after pathogens enter body?

Answer 24

damaged cells release histamine and cytokines

Question 25

what does the damaged cells releasing histamine cause?

Answer 25

o Arteriole, capillary bed and venule to dilate
 More blood flow causes redness and heat
 Increases the permeability of the capillaries; exudate (protein-rich fluid) leaks into infected region – causes swelling, increases pressure on surrounding tissues which activates pain receptors.
• Contains clotting agents which isolate the infection
 Immune cells can squeeze through capillary cells to enter infection site.

Question 26

what does the damaged cells releasing cytokines cause?

Answer 26

attract neutrophils. Following this, other cells are attracted: eg. mast cells and macrophages (which release histamine which amplifies these responses and attract more immune cells)

Question 27

what are the roles of phagocytes (neutrophils/macrophages?)

Answer 27

phagocytose bacteria/cell debris, resulting in pus formation

Question 28

deifn:E pus

Answer 28

substance containing dead immune cells (esp. phagocytes, some live cells and cell debris)

Question 29

what happens when the pathogen is eliminated?

Answer 29

above responses are reversed.