B + T lymph+ antibodies+diseases , immune system - biodiversity, evolution and disease

Question 1

Definition and examples of infectious diseases

Answer 1

-caused by pathogens
-transmissible
-examples include cholera, malaria, HIV, tuberculosis

Question 2

non infectious diseases

Answer 2

-long term degenerative diseases not caused by pathogens
-e.g lung cancer, sickle cell anaemia

Question 3

bacteria and diseases from it

Answer 3

-prokaryotic organisms
-M. tuberculosis causes tuberculosis (TB) in humans
The bacteria infect the lungs, causing a chronic cough and bloody mucus
-ring rot, bacteria infect the vascular tissue and prevent the transport of water, causing the plant to wilt and die

Question 4

viruses and diseases caused

Answer 4

-do not have a cellular structure
This means they can’t respire, produce ATP, replicate genetic material or synthesise protein
They infect host cells and hijack their machinery to replicate their own genetic material and proteins
-tobacco mosaic, influenza, HIV

Question 5

protoctista

Answer 5

unicellular eukaryotes
-malaria, potato blight

Question 6

fungi

Answer 6

heir eukaryotic cells have cell walls and large central vacuoles
However, instead of being made of separate cells, their bodies consist of filaments known as hyphae
These hyphae form a network and spread throughout a host/soil
-ringworm, athletes’ foot, black sigatoka

Question 7

2 types of lymphocytes

Answer 7

T lymphocytes, mature in thymus gland
B lymphocytes, mature in bone marrow

Question 8

maturation of T lymphocytes

Answer 8

-mature in thymus gland
-During the process of maturation:
T lymphocytes (T cells) gain specific cell surface receptors called T cell receptors (TCRs)
These receptors have a similar structure to antibodies and are each specific to one antigen
-T cells within each clone differentiate into different types of T cell: T helper cells, T killer cells and T regulator cells

Question 9

T helper cell activation (4 main)

Answer 9

antigen presentation, clonal selection, clonal expansion, antibody production

Question 10

antigen presentation

Answer 10

Macrophages and (phagocytes) engulf pathogens and present the pathogen antigens on their own cell surface membrane
They become antigen-presenting cells (APCs)

Question 11

clonal selection

Answer 11

T helper cells with T cell receptors complementary to the specific pathogenic antigen bind to the APC
They are the clones that have been selected for replication
The APC secretes molecules of the cytokine interleukin 1 (IL-1)
IL-1 stimulates the activation of selected T helper cells

Question 12

clonal expansion

Answer 12

Selected T helper cells divide by mitosis to produce larger clones
T helper cells release interleukin 2 (IL-2)
IL-2 stimulates:
B cells to divide and produce plasma cells
The T helper cells to become more active and release more cytokines, including interferon (IFN) that stimulates macrophage activity
The activation of T killer cells

Question 13

antibody production

Answer 13

Plasma cells secrete antibodies specific to the antigen (that belongs to the pathogen)

Question 14

activation of t killer cells

Answer 14

-when a t killer cell encounters a foreign antigen complementary to its t cell receptor it becomes activated (clonal selection)
-attatches to foreign antigen and secretes toxic substances that kill the body cells along with the pathogen
-perforins secreted which punch a hole in CSM to allow toxins to enter

Question 15

t regulator cells

Answer 15

T regulator cells down-regulate the host immune response by:
Preventing T cells from attacking and killing uninfected host cells
Shutting down the immune system once the body is cleared of the pathogen

Question 16

B lymphocyte response

Answer 16

-In bone marrow, immature b cells divide by mitosis and mature- production of antibody receptors + remain in csm.
-Part of each antibody molecule forms a glycoprotein receptor that can combine specifically with one type of antigen

Question 17

key things about antibodies

Answer 17

-globular glycoproteins called immunoglobins
-quarternary structure, two ‘heavy’ (long) polypeptide chains bonded by disulfide bonds to two ‘light’ (short) polypeptide chains
-Each polypeptide chain has a constant region and variable region. The constant region determines the mechanism used to destroy the antigens

Question 18

variable region on antibodies

Answer 18

• The variable region is where the antibody attaches to the antigen to form an antigen-antibody complex
  -end of varible region=antigen binding site, composed of many amino acids and has both light and heavy chains
  -The ‘hinge’ region (where the disulfide bonds join the heavy chains) gives flexibility to the antibody molecule which allows the antigen-binding site to be placed at different angles when binding to antigens

Question 19

Key differences between T and B lymphocytes

Answer 19

-B mature in bone marrow, T in thymus
-B manufacture antibodies, T do not
- both B and T undergo clonal selection, B - memory and plasma cells, T-helper and killer
-plasma cells secrete antibodies, helper release cytokines, killer attach to antigens and secrete toxins
-T can activate other lymphocytes by mitosis

Question 20

Memory cells are produced when a patient is vaccinated against influenza.
Describe the role of these memory cells when the influenza virus enters the body

Answer 20

recognise , virus / antigen / pathogen ;
produce a clone ;
can , change to / form , plasma cells (on infection) ;
make antibodies (against influenza , virus / antigen) ;
responsible for secondary response /
destroy virus before symptoms appear ;
can , change to / form , named T-cell ;

Question 21

State why a doctor would not prescribe antibiotics to treat influenza

Answer 21

(antibiotics) are, not effective against viruses / effective
(only) against bacteria (and fungi / protozoa )

Question 22

Neuraminidase is an enzyme which is present on the protein coat of the influenza virus.
This enzyme is used to break down the host cell membrane and allow the influenza
viruses to leave the infected cell. Tamiflu® is a neuraminidase inhibitor.
Suggest how Tamiflu® could inhibit neuraminidase

Answer 22

Tamiflu® is , competitive inhibitor which
binds to active site ;
prevents , substrate binding to active site /
formation of enzyme-substrate complex /

Question 23

Describe how cytokine molecules can stimulate specific groups of B lymphocytes to
divide.

Answer 23

-cytokine receptor has a specific shape which can bind to receptor on B lymphocyte as they have complementary shapes
-this stimulates clonal expansion