adaptive immunity Flashcards

(48 cards)

1
Q

reference between innate and adaptive

A
  1. slower
  2. long lived- memory cells
  3. non repetitive
  4. interact with innate and other cells of the adaptive immune systems
  5. non reactive to the host
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2
Q

hallmarks of the adaptive immune system

A
  1. called specific or acquired immunity
  2. adapts to the present of microbial invaders
  3. conceits of lymphocytes and there products, antibodies
  4. when they respond, it requires expansion and differentiation of lymphocytes in response to microbes.
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3
Q

wha tells are necessary for adaptive immunity

A

effector cells
memory cells
these are also what are vaccines are based on

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4
Q

types of lymphocytes

A

B cells
T cells

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5
Q

explain what B cells are

A

B because they are first discovered in the bursa of fabricious. they develop in the bone marrow. they are humeral immunity

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6
Q

explain T cells

A

the develop in the thymus. they do begin as hematopoeitetic stem cells in the bone marrow but develop in the thymus. T cells are the only immune cells that have their own organ to develop in.

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7
Q

how do cells develop

A

the yup regulate whatever receptors they need which makes them into that type of cell. once they have developed they will move to the secondary lymphoid organs.

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7
Q

what makes cells naive or mature

A

when else have not encountered anything, they are called naive

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8
Q

what makes B and T cells special

A

innate can recognise about 1000 molecular patterns with 100-200 molecular patterns. adaptive can recognise up to 10 trillion different things. the adaptive immune cells utilise diverse antigen specific receptors

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9
Q

why is it important to have adaptive immune cells

A

they develop polysaccharide coat to hide their antigens, develop protease break down NETs and develop things to inactivate phagolysosome, adaptive will keep us safe.

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10
Q

how do we code for antigen receptors

A

we don’t have specific genes for each antigen however cellular machinery amens it possible to alter these genes and rearrange them, this is what gives diversity. this is important for us to also be safe evolutionary while other organisms also evolve.

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11
Q

explain the concept of diverse antigen receptors

A

it is wrong to say that when we encounter smth new, the immunes cells alter themselves to protect us from these antigens. instead this diversity occurs during development. during he coarse of our lifetime, we hope that we have a few cells that are able to recognise it.

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12
Q

explain antigen

A

its a general term for a substance that generates an immune response against it.

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13
Q

explain the receptors of B cells and T cells

A

both are membrane bound receptors. they have constant regions which are like the stem but also variable regions where differentiation occurs. T cells have one antigen binding site while B cells have two. all receptors on a single cells are identical.
B cell receptor: it produces anti bodies that are Y shaped so its receptors are also Y shaped. it’s an antibody that is stuck on a cell surface (immunoglobulin or surface bound antibody.

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14
Q

how many B cells do we need to create an immune response and how does this become an issue.

A

we need millions. we have Lower frequency of cells with receptors of the same specificity.

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15
Q

what is low precursor frequency

A

lower frequency of cells with receptors of the same specificity.

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15
Q

what is the trade off in adaptive system and what does this Mean.

A

we have a lot of cells (variety) but that means not a lot of each of these cells. when it sees an antigen that it responds to, it proliferates (clonal expression). this takes a long time and thus why the adaptive response is a lot slower.

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16
Q

explain what b cells do

A

they are mediators of humeral immunity -bodily fluids like plasma. It secretes antibodies but also have complement proteins and antimicrobial peptides. they are the only cells that can make antibodies which hare secreted once the vesicles are ready to go

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17
Q

what do B cells do

A

they neutralise and eliminate extracellular microbes- cancer before infecting a cell and microbial toxins. they can’t enter cells so intracellular cells and so therefore readies the need for cell mediated immunity .

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18
Q

stages of B cells

A

the b cell receptor attaches to the antigen of the microbe. it undergoes proliferation, and differentiate into plasma cells (make the antibodies), this will be lymphocytes soon however and some will turn into a T cell.

19
Q

parts of a B cell

A

variable domain- antigen binding
constant domain: constant for each isotope of a species. there are 5 different classes of isotypes.
1. single Monomerthat will form pentamer
2. IGa will be in a dimer

20
Q

what doe we have different types of antibodies

A

they have different affecter functions.

21
Q

IgM

A

isotype of be cells in naive stage.it is produced first - when B cells put they receptors up, it will be IGM. this is because where the genes are. if be cells re activated and there are no other interactions ,it will develop a pentamer.

22
Q

IGD

A

on the surface of naive cells

23
IgG
most abundant antibody. useuful for fighting bacteria and virus. gives kids passive immunity as it crosses in the plasma
24
IgE
an immune response against a parasite. involved in allergy.
25
IgA
most abundant in the mucosal tissue. plasma cells secrete IgA in your gut and the antibody crosses over in the lumen of your gut and ready to neutralise pathogens.
26
what is isotope switching
T cells help B cells switch isotypes. the T cell talks to the about B cell and can start producing cytokines and molecules.
27
explain T cells.
28
explain the process of alerting adaptive cells from innate
because the innate needs to alert the adaptive immune response, the dendritic cell captures the pathogen. the proteases and molecules it has will break down the pathogen into peptides (processing). the dendritic cells will now MIGRATE to the T cells- secondary lymphoid organs). it will then present it to the T cell- break a part of it and attach it to the T cell. it will get activated if the T cell has a receptor it has.
29
how exactly do T cells see antigens
unlike B cells, T cell receptor cannot bind to antigen alone. it therefore needs denctiric cells to present the antigens to it. the molecule that does this is the MHC (major histocompatibility) molecule
30
what does the the major histocompatibility molecule do
this is the molecules that presents the antigen to the T cells. T cells are therefore known as major histocompatibility restricted
31
how do MHC influence transplant
the HLA or MCA must match
32
what happens to the T cells when they get activated.
they are cell mediated immunity. there are many kinds but the main two are helper T cells and killer T cells
33
Wha are helper T cells
they direct what other cells should to. they do this by cell interaction and type so cytokines they produce. eg. direct B cells to make a certain type of antibody create cytokine or neutrophils or activate macrophages- though can phagocyte by themselves, T cells can make them more efficient and potent.
34
what are cytotoxic T cells
they directly kill infected cells like intracellular viruses and bacteria. they don't kill the bacteria BUT instead kill the cell with the bacteria attached to it. they are activated by dendritic cells, it will come back and find cells that release DAMPs and the T cells will release their cytotoxic granules for the cell to undergo apoptosis.
34
what makes B and T cells even more special
1. memory: as some turn into effector cells, some turn into memory cells.
35
what are the benefits of memory response
allows for faster response because of higher precursor frequency and some stay in tissues that have been previously infected. they are more potent and are antigen specific.
36
explain autoimmunity
it is not the result of a broad non specific malfunction of the immune system but rather a highly specific immune attack against one cell type or molecule in the body.
37
how do autoimmune disease occur
during the process in development where the body alters gene segments to produce an array of diverse antigen receptors, we are also making self reactive cells. we do have the mechanism to deal with this known as the immune tolerance mechanism
37
what is the mechanism we use to deal with self tolerant cells and how does it work
immune tolerance mechanism. central tolerance: they delete or suppress highly reactive cells. they get checked in the bone marrow and the thymus. this doesn't delete minor auto reactivity. peripheral tolerance: suppress activation of auto reactive cells (mainly by regulatory cells)
38
what contributes to the development of autoimmune disease.
it's a combination of generic and environmental factors.
39
how do genetic factors play a role in autoimmune disease
despite having similar genes, variations vary (susceptibility). many genes responsible for autoimmune disease involve: - T cell activation -maintaining immunological tolerance (finding and destroying self reactive lymphocytes and activity of regulatory cells varients of these genes are inherited.
40
how do environmental factors play a role in autoimmune disease
environmental factors enviromental factor scan tip them over. it can be: - preceded by an infection - tissue damage. it basically loses homesostasis and cause auto reactive cell to be even more reactive and become unregulated. - inflammatory reaction that may release previously hidden antigens that our immune system responds to
41
why are females more susceptible to autoimmune disease
because of estrogen receptor in immune cells or X and Y chromosome differences .
42
targets of immunotherapy
autoimmune disease involves all aspects of the adaptive immune system. the mechanisms differ between them all. knowledge of this allows us to target them and create immunotherapy. eg. targeting cytokines can assist with psoriasis, integrals can help with cronhs disease and T cells with type 1 diabetes.
43
how does immune system play a role in cancer
its found that patients with tumours that have been infiltrated by lymphocytes that better prognosis, enlarged tumour- draining lymph nodes= better prognosis. also, immunodeficient patient have a higher susceptibility to tumour growth. this includes transplant patient with acquired immunodeficincies and people with acquired immunodeficiencies. they lose the ability to look out for damage cells
43
therapies for cancer in terms of stimulating killer T cell
Killer T cells are 'licensed'. therapies include re- engineered T cells through CAR T dells and antibodies to remove the immunologica; brakes and apply the immunological accelerator. this will block the molecules that would stop the T cells from killing cancer. when we found out that continual T cells will lead to tissue damage, we also discovered that blocking the molecules that cause this can be beneficial in treating cancer.