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Immune system Flashcards

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1
Q

outline the defense mechanism of the immune system (5steps)

A
  1. the pathogen encounters barriers –> the innate immune system–> if barriers are breached, cellular components are next –> cell-mediated and humoral response –> elimination of bacterial cells and generation of immunological memory
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2
Q

properties of the innate immune response

A

is non-specific
is rapid
has no memory

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3
Q

properties of the specific immune response

A

is specific
takes time to develop (first exposure)
shows memory (faster response on next exposure)

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4
Q

what does the immune system do and what is an infection

A

immune system defends body against pathogens and an infection is the process where a pathogen invades and multiplies in a host causing disease

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5
Q

what are pathogens

A

organisms that cause disease by invading and multiplying in the host
e.g bacteria fungi viruses worms and protozoa
can be intra or extracellular
have antigens on their surfaces

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6
Q

what are antigens

A

basically binding sites
trigger immune response when epitopes are recognised by receptors on immune cells or antigen binding sites of antibodies

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7
Q

what are epitopes

A

parts of a single antigen
each have a specific conformation which is complementary in shape and charge to a specific antigen-binding site of an antibody or T/B cell receptor

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8
Q

what are cells of the immune system and where are they found (exclude T and B)

A

Phagocytes –> engulf pathogens by phagocytosis
macrophages –> APC found in tissues
dendritic cells –> APC found in tissues
neutrophils –> found in blood

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9
Q

what are T cells capable of and originate from

A

originate from the haematopoietic stem cells in bone marrow but differentiate in the thymus to form naive T cells.
each T cell has a specific TCR on its surface
A TCR can only recognise and bind to a specific, complementary processed peptide of a peptide-MHC complex on an APC
when a specific naive T cell is activated by a specific APC, it undergoes clonal expansion and differentiation to form effector T cells and memory T cells

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10
Q

whats helper cytotoxic and memory T cell functions

A

Helper T cells: activates naive B cells so that it can undergo clonal expansion and differentiation
cytotoxic T cells: involved in cell-mediated response and hence protects against intracellular pathogens by killing cells that contain pathogens
memory T cell: when re-exposed to the same pathogen, memory T cells will recognise it and undergo faster clonal expansion and differentiation into effector T cells, mounting a faster and stronger secondary immune response. memory cells confer long term immunity to a specific pathogen

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11
Q

where are B cells originating from and what do they do

A

originate from haematopoietic stem cells in the bone marrow and differentiate in the bone marrow to form Naive B cells
each B cell has a specific BCR on its surface
a BCR can recognise and bind to a specific complementary unprocessed antigen of a pathogen.
when a specific naive B cell is activated by a specific helper T cell, it undergoes clonal expansion and differentiation to form effector B cells and memory B cells.

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12
Q

what are plasma cells and memory B cells

A

plasma cells produce antibodies which are involved in the humoral response and protect against extracellular pathogens and toxins excreted by pathogens.
memory B cells: when re-exposed to the same pathogen, memory B cells will recognise it and undergo faster clonal expansion and differentiation into antibody-secreting plasma cells, mounting a faster and stronger secondary immune response. memory cells also confers long term immunity to a specific pathogen.

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13
Q

5 steps of immune response

A
  1. pathogen encounter
  2. innate immune response
  3. phagocytosis + inflammation + antigen presentation
  4. adaptive immune response
  5. elimination of pathogen and generation of immunological memory
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14
Q

steps 1-2 in detail

A
  1. physical and chemical barriers of the innate immune system prevent entry of pathogens; when the barriers are breached –> the pathogen enters the body tissues
  2. this will cause phagocytes such as macrophages in the body tissues to engulf the pathogens by phagocytosis and induce inflammation to recruit more phagocytes.
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15
Q

step 3a in detail

A

a) phagocytosis by macrophage: bacterial membrane evaginations called pseudopodia surround and engulf pathogen
when the ends of the pseudopodia fuse, a vesicle containing the pathogen known as a phagosome forms
the phagosome fuses with a lysosome then forming a phagolysosome; hydrolytic enzymes from the lysosome digest the pathogen

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16
Q

step 3b in detail

A

inflammation: macrophages at site of infection release cytokines and chemokines which increase vasopermeability of blood capillaries so neutrophils can go to site of infection and cause vasodilation so that more phagocytes can be carried to the site of infection

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17
Q

How are naive cells activated and how does immunological memory arise

A
  1. an antigen presenting cell (APC) engulfs pathogen with phagocytosis
  2. the pathogen is processed
  3. a peptide of the antigen binds to a MHC protein to form a peptide-MHC complex which is transported to the cell surface of the APC for presentation to a specific naive T cell
  4. A specific naive T cell with a specific TCR binds to the complementary peptide-MHC complex on the APC
  5. the APC secretes cytokines that activate the naive T cells
    6.the specific activated naive T cell undergoes clonal expansion and differentiation into many cytotoxic T cells, helper T cells and memory T Cells.
  6. the helper T cells secrete cytokines which activate specific naive B cells which from plasma cells and stimulate macrophages to attack infected cells
  7. the cytotoxic cells kills cells infected with intracellular pathogens like viruses by producing perforins and granzymes.
  8. If the body is re-exposed to the same antigen, memory T cells undergo more rapid clonal expansion and differentiation into many helper T cells and cytotoxic T cells.
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18
Q

what is clonal selection and clonal expansion and differentiation

A

clonal selection is a process whereby a single B or T cell that recognises an antigen that enters the body is selected from the pre-existing cell pool of differing antigen specificities and then reproduced to generate a clonal cell population that eliminates the antigen.
clonal expansion and differentiation refers to the repeated division of cells by mitosis and specialisation of cells due to differential switching on of genes respectively.

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19
Q

B cell activation pathway

A
  1. a B cell receptor (BCR) on a specific naive B cell with an antigen binding site that is complementary in shape to an antigen of the pathogen binds to the antigen.. via receptor mediated endocytosis, the pathogen is processed and a peptide of the antigen binds to a MHC protein to form a peptide-MHC complex which is transported to the cell surface membrane of the naive B cell for presentation to a specific helper T cell
  2. a specific helper T cell with a specific TCR binds to the complementary peptide-MHC complex on a specific naive B cell
  3. the helper T cell secretes cytokines that activates the specific B cell
  4. the specific naive B cell undergoes clonal expansion and differentiation into many antibody-secreting plasma cells and memory B cells
  5. the antibodies then destroy and clear the extracellular pathogen by neutralisation, opsonisation and agglutination
  6. if the body is re-exposed to the same antigen, the memory B cells, undergo more rapid clonal expansion and differentiation into many plasma cells that can rapidly manufacture large quantities of antigen specific antibodies.
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20
Q

how does neutralisation occur

A

binding of antigen binding site of antibody to pathogen/toxin prevents binding of pathogen to host cell receptor and hence prevents entry into host cell.

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21
Q

how does opsonisation occur

A

after binding of antigen binding site of antibody to pathogen, the binding of Fc portion of antibody to Fc receptors on phagocyte
signals from the hc receptors on the phagocyte promotes phagocytosis of the pathogen

22
Q

how does agglutination occur

A

binding of an antibody to 2 pathogens simultaneously as each antibody has 2 antigen binding sites resulting in the clumping or aggregation of pathogens, promoting phagocytosis of the pathogen

23
Q

what is cell-mediated response

A

TCR on cytotoxic T cells recognise infected target cells which display short peptides from antigen of pathogen presented on a MHC
they release perforins and granzymes
(protection against intracellular pathogens by killing cells that contain pathogens

24
Q

what are antibodies

A
  1. immunoglobulins
  2. globular proteins secreted by plasma cells
  3. soluble and transported in blood
  4. made up of 4 ppt chains –> 2 identical light and heavy chains, has a quaternary structure held tgt by the 4 bonds
    5.antigen binding sites are in the Fab region
  5. Fc region determines the class and function of the antibody
25
Q

antibody structure and matching function

A

antigen binding site of a specific antibody is complementary in shape to a specific epitope of an antigen due to the precise folding of the variable heavy and light chains that gives rise to its unique 3D structure –> can carry out neutralisation
Fc region of antibody region of has a conformation that is complementary in shape to Fc receptors on phagocytes –> carry out opsonisation
disulfide bridges between heavy and light chains –> gives stability to the quaternary structure
each antibody has a hinge region to give the antibody flexibility when binding to epitopes tht are variable distances apart
ig G has two antigen binding sites –> allow for agglutination
constant region of heavy chains determine the class of antibody and thus different functions

26
Q

how does antibody diversity arise

A

involves 3 genes: 2 genes coding for light chains and 1 gene coding for heavy chains
due to a: somatic recombination b: hypermutation c: class switching d: combinatorial pairing of heavy and light chains.
occurs during b cell development

27
Q

what is the heavy chain gene

A

has many variable (V) diversity (D) joining (J) and constant (C) gene segments; the VDJ gene segments contribute towards the variable region of the heavy chains
the C segments contribute to the constant region of the heavy chain

28
Q

what is the light chain gene

A

has V J and C segments
the V and J segments contribute toward the variable region of the heavy chains and the C segments contribute to the constant region of the light chain

29
Q

process of somatic recombination

A

there are multiple gene segments at heavy and light chain genes
somatic recombination is a form of DNA rearrangement where various gene segments are joined together randomly, and some intervening segments are enzymatically removed followed by rejoining of remaining sequences.
at the IG heavy chain gene locus, one small V segment, one D segment and one J segment are randomly joined to form a single VDJ exon
at the lg light chain gene locus, one V segment and one J segment are randomly joined to form a single VJ exon

30
Q

somatic recombination in heavy chain gene

A

VDJ recombination occurs at the heavy chain gene during the B cell maturation in the bone marrow
1. During D and J rearrangement, one D segment and one J segment are joined, and the intervening sequences are enzymatically removed
2.during V and DJ rearrangement, one V segment is joined to the DJ segment and the intervening sequences are enzymatically removed.
3. the DNA segment then undegoes transcription
4. the resulting pre-mRNA undergoes RNA splicing during which the introns are excised and the VDJ exon and C exon are joined
5. the mature mRNA with the VDJC exons joined enters the cytoplasm where it undergoes translation to form the specific heavy chain protein with the specific VDJC domains

31
Q

somatic recombination in light chain gene

A

VJ recombination occurs at the light chain gene and during B cell maturation in the bone marrow
1. during V and J rearrangement, one V segment and one J segment are joined, and the intervening sequences are enzymatically removed
2. the segment then undergoes transcription
3. the resulting pre-mRNA undergoes RNA splicing during which the introns are excised and the VJ exon and C exon are joined
4. the mature mRNA with the VJC exons joined enters the cytoplasm where it undergoes translation to form the specific light chain protein with the specific VJC domains

32
Q

process of somatic hypermutation
7 step process

A
  1. somatic hyper-mutations are random point mutations that occur in the rearranged VDJ regions of the DNA in activated B cells
  2. they are called hypermutations as they occur at a higher rate than normal mutations
  3. this further diversifies the variable regions of antibody for antigen binding
  4. it occurs during clonal expansion of the activated B cells
  5. some point mutations result in the B cells expressing low affinity ig chains on their CSM and vice versa
  6. B cells that express higher affinity BCR are selected for clonal expansion and differentiation; this is called affinity maturation
  7. the resulting plasma cells and memory B cells will have BCRs with higher affinity antigen binding sites for a specific antigen. the plasma cells will also produce antibodies with higher affinity antigen binding sites for a specific antigen.
33
Q

process of class switching

A

class switching is DNA rearrangement at the constant gene segment of the heavy chain gene locus in activated B cells
it allows for the production of antibodies with the same antigen binding site but different function

34
Q

differences between active and passive immunity:
immune response
antibody production
duration

A

yes vs no
produced by own immune system vs transferred to recipient
long term immunity vs short term

35
Q

immunological memory; how does it work and whats the difference between primary and 2ndary immune response

A

when naive B cells are activated, clonal expansion and differentiation will produce plasma cells and memory B cells. memory B cells can remain in the body for years; immunological memory is established to ensure rapid re-induction of antigen-specific antibodies on subsequent encounters with the same pathogen, thus providing long-lasting protection against it.
primary vs secondary:
slower vs faster
response:
weaker vs stronger
no memory vs has memory

36
Q

vaccination: what does it do

A

the intentional administration of an antigen, a harmless form of a pathogen to induce a specific adaptive immune response that protects the individual against later exposure to the same pathogen by the production of memory cells. the individual should not develop disease symptoms
it is a form of artificial active immunity (initiates primary immune response so that immunological memory is attained for long lasting protection.

37
Q

how does vaccination work

A

the vaccine may contain a live attenuated or heat killed inactivated form of pathogen or made up of DNA/RNA
the vaccine will not cause disease but it still retains its immunogenic effect because characteristic surface antigens of the pathogen are retained and can be recognised by APCs –> adaptive immune response etc etc

38
Q

comparison of how variation is generated during somatic recombination and meiosis

A

somatic recom vs meiosis:
alters the heavy and light chain gene loci vs alters any gene locus
involves removing and joining of gene segments vs crossing over in meiosis involved exchange of equivalent segments
occurs on a single chromosome vs involves non-sister chromatids on a pair of homologous chromosomes

39
Q

how do vaccines protect from the actual pathogen

A

faster and stronger secondary immune response; memory B and T cells rapidly undergo clonal expansion and differentiation

40
Q

benefits of vaccines

A

protect individuals against disease and hence death etc etc
increase herd immunity –> if many individuals in a population are vaccinated and hence immune to the infectious agent, fewer susceptible individuals will contract the disease; hence transmission of the disease in a community is less likely.
can also completely eradicate some disease e.g smallpox

41
Q

risks of vaccines

A

risk of reversion to virulence to cause disease in live attenuated vaccines
allergy
may not be as effective as natural immunity
mutation rate of pathogens are very high and new vaccines are constantly needed
excessive vaccination may reduce effectiveness of immune system to respond to new infections

42
Q

how to treat bacterial infections with antibiotics

A

Disrupt cell wall synthesis
disrupt protein synthesis
disrupt nucleic acid synthesis
administration of antibiotics

43
Q

how do antibiotics disrupt cell wall synthesis

A

targets bacterial cell wall
e.g penicillin :
1. it is bactericidal and only effective when bacteria are growing and making new cellw all as it disrupts peptidoglycan cell wall synthesis
2. penicillin acts as a competitive inhibitor and binds to active site of transpeptidase
inhibits the formation of cross-links between tetrapeptides of adjacent chains of peptidoglycans; weakining the cell wall. high osmotic pressure causes lysis

44
Q

how do bacteria develop antibiotic resistance

A

failure to complete course of antibiotics –> some bacteria survive –> spontaneous mutation in bacterial population produces antibiotic-resistant strains –> transfer of antibiotic resistance genes from bacterium to bacterium via the 3 methods
when an antibiotic is given, it acts as a selection pressure -> those with antibiotic resistance gene survive, reproduce and pass the allele to daughter cells whereas those that are susceptible die -> over a few gens, microevolution occurs -> increased frequency of antibiotic resistant allele in population

45
Q

how do antibiotics disrupt protein synthesis

A

streptomycin: binds to small subunit of bacterial ribosome such that initiator tRNA cannot bind to small subunit
tetracycline: blocks aminoacyl-tRNA from attaching to the A site of bacterial ribosome

46
Q

how are drugs designed to treat viral infections

A

attachment : drug that binds to specific host cell plasma membrane receptor –> prevents virus from binding and entering via receptor mediated endocytosis
replication: drugs that carry antisense RNA to bind to viral RNA to form ds RNA; ribosomes cant bind and translation cannot occur
nucleoside analogs also impair virus’ ability to extend its RNA during replication
important virus specific enzymes/proteins: inhibit RNA-dependent RNA polymerase; reverse transcriptase/ integrase/ protease/viral polyproteins

47
Q

treatment of bacterial infections using bacteriophages

A

phage is very specific and will only attack a particular bacterial strain
as bacteria evolve resistance, viruses also evolve to overcome resistance; small qty of virus needed + stop reproducing once target bacteria are destroyed

48
Q

how do antibiotics disrupt nucleic acid synthesis

A

rifampin : inhibits RNA synthesis by binding to bacterial RNA polymerase, preventing transcription

49
Q

tuberculosis (how does it work what does it do how to treat etc etc)
pathogen name
target cells
transmission
pathogenicity
treatment
prevention

A

mycobacterium tuberculosis; obligate aerobe; requires oxygen
primary infection: lungs
airborne transmission : transmitted in fine aerosol droplets when an infected person with active TB sneezes/coughs and an uninfected person inhales the droplets
pathogenicity:
once bacteria is inside lungs, alveolar macrophages phagocytose the bacteria
in the phagosome, bacteria inhibit fusion of phagosome with lysosome-> no phagolysosome formed
bacteria survive and continue to multiply inside macrophages that phagocytosed them
more macrophages, dendritic cells and lymphocytes form a granuloma to wall off and isolate the infected macrophages. this eventually forms a tubercle. at the centre of the tubercle, cell death by necrosis occurs
disease may be arrested at this stage and remain latent for years, persons who have TB infection, but not TB disease, do not spread the disease to to others.
when the Tubercle ruptures, the bacteria spill into bronchioles and spread throughout the lungs -> cough that facilitates aerosol spread of bacteria
rupturing of tubercles -> formation of cavities in lungs -> lungs progressively destroyed
opportunistic infection to strike immunocompromised HIV positive ppl
6 months of daily treatment and combination of at least 2 antibiotics
BCG vaccine prepared from live, attenuated mycobacterium bovis.

50
Q

AIDS (how does it work what does it do how to treat etc etc)
pathogen name
target cells
transmission
pathogenicity
treatment
prevention

A

HIV
T helper cells or macrophages of immune system; gp120 binds to CD4 receptor
transmits primarily through unprotected sexual contact/ exposure to infected blood
once the virus enters the bloodstream, it targets T helper cells and macrophages.
virus infects T helper cells; infected T helper cells destroyed -> T helper cell levels fall
–> impaired immune responses –> susceptible to opportunistic diseases
(can also cause karposi sarcoma due to integration of viral dsDNA into host genome)
3 agents are administered in combination : reverse transcriptase inhibitors, protease inhibitors and integrase inhibitors, and entry inhibitors. sustained treatment is required.

51
Q

influenza (how does it work what does it do how to treat etc etc)
pathogen name
target cells
transmission
pathogenicity
treatment
prevention

A

influenze virus
epithelial cells of respiratory tract
droplets of moisture from lungs of infected person
virus settles on mucous membrane lining the nose –> yadda yadda yadda leads to runny nose + weakining of epithelial layer
no treatment for most ppl, usually bed rest and aspirin/paracetamol; antiviral drugs such as tamiflu that are neuraminidase inhibitors stop the virus
antibiotics to stop secondary bacterial infections like penumonia
vaccine

Bio (16 decks)

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