Defence Against disease 2 Flashcards

(34 cards)

1
Q

How do B lymphocytes defend the body ( vague)

A

Create humeral immunity

Dispatches antibodies in the bodies humours, fluids, blood and lymph

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2
Q

Stages of B lymphocytes defending an attack

A

1) identify antigen from pathogen : bacterium, fungus, toxin or virus
2) pathogens bumps into complimentary B cell, the one with the correct antibodies and binds to it (clonal selection)
3) B cell is then activated by t helper causing the b cell to proliferate clone rapidly, forming many cells with the exact same antibodies.
4) effector cells mass produce antibodies (2k per sec) for 4/5 days
5) antigens move round the body binding to as many antigens as they can, neutralisation or agglutination stops damage until pathogens engulf
humoral immunity

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3
Q

B lymphocytes maturing process

A

Mature fully in the bone marrow
Once mature they have unique antibodies on the membrane of each cell, up to 10k
Helper T cells help mature naive effector B cells by binding to them and releasing cytokines

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4
Q

How do t lymphocytes defend the body ( vague)

A

Cellular immune response

Cause immflamuation, activate macrophages, regulate immune response, fire up other T cells

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5
Q

Stages of how T cells defend the body, cell mediated immunity

A

1) in the non specific defence system macrophages engulf and digest pathogens and display their antigens on their cell surface (APC’s )
2) receptors on some of the 2 cells fit these antigens, they bind and release interleukin stimulating more 2 cells to divide by mitosis. they form clones of the activated t helper cell that all carry the right antigen to bind to a particular pathogen
3) cloned t cells may: differentiate into t memory cells, produce interleukins that stimulate phagocytosis produce interleukins that cause b cells to divide, stimulate the development of a clone of T killer cells that are specific for the presented antigen

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6
Q

What are professional antigen presenting cells

A

Macrophages that engulf pathogens and display pathogens antigens on their cell surface

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7
Q

What to regulatory T cells do

A

Release anti cytokines

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8
Q

Clonal selection

A

Correct\complimentary helper T cell binds to antigen presenting cell
Interleukin is released

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9
Q

Clonal expansion

A

Interleukin produced by helper T cells after binding to correct APC
This activates the B cells
Stimulates T cell replication, memory, killer, helper
The activated B cells divide by mitosis to give clones of plasma cells and b memory cells

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10
Q

Simple immune response

A

Nature of Antigen encountered, colonial selection , colonial expansion, differentiation, action

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11
Q

T helper cells

A

Bind to the surface antigens on APC’s

Produce interlinking , which as a type of cytokines

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12
Q

Interleukins

A

Stimulate the acuity of B cells, which increases antibody production , stimulates production or other types of T cells, and attracts and stimulates macrophages to enter the area

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13
Q

General Antibodies structure

A

Large proteins known as immunoglobulins
Specific shape that is complementary to a specific antigen
4 polypeptide chains held together with disulphides bridges
2 long identical chains called heavy chains
2 shorter identical chains called light chains

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14
Q

Antibody structure relating to function

A

Variable region - area of specificity, to an antigen, due to amino acid sequence. Located at the top of the Y
Hinge region- found between the long chains and short chains, allows flexibility for attachment to more than 1 antigen. Joining point of the Y
Constant region- same on all antigens ( main part of the Y) allows attachment to phagocytes

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15
Q

Ways in which antibodies defend the body

A

Antibody of antibody-antigen complex acts as an opison so complex is easily engulfed
Pathogens are neutralised, so they can no longer invade host cell
Antibodies act as agglutinins causing pathogens carrying antibody-antigen complexes clumped together
Antibodies can act as antitoxins

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16
Q

Active immunity

A

Already exposed to the pathogen, so body already has memory cells.
Antibody production is quick
Vaccination = artificial active

17
Q

Passive immunity

A

Artificial passive - injection of antibodies
Natural passive, mother giving baby chloesterin full of antibodies
Offers protection for a month

18
Q

Autoimmune diseases

A

Disease where the immune system mistakenly identifies your own cells as “foreign” rather than “self”
There are no cures: treatments are, immunosuppressants that slow down the immune system

19
Q

What factors increase the risk of autoimmune diseases

A

Genetics
Obesity
Sex - women

20
Q

Types of autoimmune diseases

A

Diabetes type 1 - destruction of pancreatic cells
Rheumatoid arthritis- damage to joints
Lupus - inflammation to lining of organs

21
Q

What vaccines contain

A

Killed or inactivated bacteria and viruses
Attenuated (weakened) strains of live bacteria or viruses
Toxin molecules that have been altered or detoxified
Isolated antigens extracted from the pathogen
Genetically engineered antigens

22
Q

Process of vaccination

A

Small amounts of save antigen, known as the vaccine, are injected into the blood
Primary immune response is triggered by foreign antigens, body produces antibodies and memory cells as if you were infected with the live pathogen
If you come into contact with the real pathogen the secondary immune response is triggered

23
Q

How vaccination changes due to pandemics or epidemics

A

Mass vaccination to to the spread

Herd immunity once enough of the population is vaccinated

24
Q

Sources of medicine

A
Penicillin- mould and fungus (melons)
Docetaxel - yew trees
Aspirin - willow bark 
Prialt- snake venom 
Vancomycin- soil fungus 
Digoxin- fox gloves
25
Synthetic biology
Use of genetic engineering Uses bacteria as a biological factory Populations of bacteria are modified to produce much needed drugs in larger quantities than we would ordinarily have access to
26
Development of antibiotic resistance
Random mutation occurs that makes some bacteria slightly more resistant, bacteria pass this mutation on to daughter cells Farmers in the US routinely adding antibiotics to animal feed. this accelerates natural selection. Over prescription/ not fishing prescribed course of antibiotics leads to antibiotic resistance Means some antibiotics may become useless
27
Use of antibiotics in 20th century
Large number of death were due to communicable diseases | Antibiotics interfere with the metabolism of bacteria without affecting human cells - selective toxicity
28
How do cytokines stimulate B lymphocytes
Cytokines has specific shape, complemnartyu to receptor Cytokines binds to receptor on cell surface membrane This activates clonal expansion
29
How does HIV take over the host cell
Viral DNA inserted into host nucleus Viral RNA and mRNA transcribed To code for viral proteins
30
Humoral immunity
Body responds to antigens found outside cells e.g free floating pathogens
31
Purpose of the constant reigon
Allows binding to phagocytes | Speed of production
32
Role of memory cells
Memory cells recognise display complimentary antigens to the pathgoen, binding to it (clonal selection) Memory cells undergo clonal expansion dividing by mitosis to produce clones which then differentiate into plasma cells that produce antibodies Help destroy viruses before symptoms appear
33
How HIV takes over host cell
Revrse transcriptase inserted into host nucleus which converts the RNA which has also been inserted to DNA The viral DNA is transcribed to produce viral RNA which is then translated to produce viral proteins
34
how phagocytes are able to pass into the tissue fluid
they have a : narrow nucleus, a flexible cell structure | histamines make capillary walls leaky allowing phagocytes to squeeze through more easily