L28 Immune System Influence on Homeostasis Flashcards

1
Q

where do most immune cells originate?

A

bone marrow

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2
Q

what is the fate of b-cells?

A

stay in bone marrow and later form plasma cells that are capable of making antibodies

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3
Q

how does the lymphatic system help immune system?

A

gather and present foreign antigens to immune cells - increased adaptative responses to disease/ decreased suceptibility

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4
Q

what immune cells are part of the innate immune system?

A

dendritic, macrophage, natural killer cell NKC

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5
Q

what immune cells are part of the adaptive immune system?

A

B and T cells

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6
Q

what are innate immune cells?

A

rapidly expressed immune cells - recognise continuously recurring surface materials of pathogens

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7
Q

what are adaptive immune cells?

A

cells that are expressed only when present with antigens by innate cells

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8
Q

which immune system is slower forming and why?

A

adaptive immune system because it is specialised

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9
Q

what is a balanced immune system?

A

this is when immune cells have optimum effectiveness - they defeat pathogen as best they can without harming body cells

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10
Q

what happens in an immune under-reaction?

A

disease (cancer) and infection (bacteria) can override the system and take over body cells

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11
Q

what happens in an immune over-reaction to an internal threat?

A

auto immune problem example IBD, Type 1 diabetes

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12
Q

what happens in an immune response over reaction to an external threat?

A

an allergic reaction example eczema, food sensitivities

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13
Q

how does the body maintain a balanced immune system?

A

monitoring via homeostasis

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14
Q

what cells trigger and regulate immune responses?

A

cytokines

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15
Q

what happens if pathoegns override immune system?

A

progressive inflammation of cells

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16
Q

what are exogensis antigens?

A

antigens that enter from outside the body such as bacteria and fungi - not all are bad

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17
Q

apart from fighting infection, what role does the immune system play in the body?

A

maintaining homeostasis

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18
Q

how are viruses recognised?

A

nucleic acid detection

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19
Q

what are interferons?

A

protein signals that are induced when RNA viruses enter cell - they interfere with viral infection cycle

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20
Q

where are interferons released?

A

from infected cells to local cells

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21
Q

what is the purpose of interferon induction?

A

to signal the infection to neighbouring cells and initiate an immune response

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22
Q

describe the pathway of RNA virus detection

A

1) RNA Virus enters cell
2) infected cells induce interferons
3) local cells turn on signalling pathways to produce STAT proteins
4) Different genes are turned on to prevent adsorption of virus onto cell surface and prevent mRNA transcription

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23
Q

how do viruses block attacks from IFNs?

A

mutation and evolution

24
Q

what is the virus cycle?

A

1) adsorption
2) entry
3) uncoating
4) mRNA transcription
5) translation
6) genome replication
7) packaging

25
what happens if virus outcompetes interferons?
the innate immune system stimulates a chemotaxis response
26
what is chemotaxis?
Cells detect the direction and intensity of an extracellular chemical gradient, and migrate toward the source of stimulus - in this case it is towards infectious agent
27
what happens when there is an immune/ chemotaxic response in lung tissue?
inflammation - impaired breathing can lead to hypoxia, no oxygen to brain leads to tissue death and damage
28
what is hypoxia?
failure of delivering oxygen to tissues causes them to die - low oxygen levels in body
29
what are 4 examples of where immune system is involved in homeostasis?
invasion of viruses, cancer growth, fat interactions and brain health
30
how do NKC fight cancer cells?
secrete granzyme into tumour pore - digesting the tumour
31
how do t-cells become activated in repsonse to cancer?
1) APC presents specific antigen to naive T-cell 2) APC uses MHC to present antigen protein to T-cell receptor 3) Naive T-cell is partially activated 4) B7 protein on APC binds with CD28 of T-cell 5) cytokines are released - fully activated
32
How are T-cells fully activated in response to cancer?
1) APC'S MHC receptor presents protein to T-cell receptor (TCR) 2) B7 on APC binds with CD28 of T-cell 3) cytokine production
33
what is MHC?
major histocompatibility complex (MHC), group of genes that code for proteins found on the surfaces of cells that help the immune system recognize foreign substances
34
what is APC?
antigen presenting cells
35
what is pro-inflammatory?
cytokines promote inflammation of cells
36
what prevents B7(APC) and CD28(T-Cell) interactions?
CTLA4 and PD1
37
what happens CTL4 and PD1 prevent B7 and CD28 interactions?
T-cell population is suppressed - cancer cells grow uncontrollably
38
how are cells less likely to bind with CTL4 over CD28?
antibody introduction, CTL4 binds with antibody instead
39
What 2 checkpoints are important in recognising and destroying tumour cells?
1) ipilimumab antibiotic targets CTLA4 | 2) nivolumab antibiotic targers PD1
40
What does nivolumab target?
PD1
41
what does ipilimumab target?
CTLA4
42
What advantages do CTLA4 and PD1 have?
they prevent excessive responses of the immune system - somewhat regulation
43
where is the immune system unexpectedly active?
brain and adipose tissue
44
what happens adipose immune population when fat globules form?
they die - this is due to obesity
45
An immune response in tissue causes inflammation what can this cause?
insulin resistance leading to diabetes type 2
46
what happens NKT cells during obesity?
they deplete
47
what do NKT produce?
anti-inflammatory cytokine IL10
48
What happens as a result from NKT depletion?
pro-inflammatory state and obesity
49
what molecule does NKT depend on?
CD1d to present antigens
50
what are NKT cells regulators of?
adipocyte and lipid metabolism, insulin sensitivity
51
what immune cells are found in brain?
microglia macrophages
52
when do microglia macrophages become activated?
plaque deposition during Alzheimer's
53
what helps the removal of amyloid plaques?
proteins in meningeal membranes
54
why is the brain bad at detecting antigens?
we do not know
55
2 hit hypothesis
vulernable to a second stimulus after first stimulus - infection and brian injury