Imunto Flashcards

(64 cards)

1
Q

Regulation of lymphocyte responses prevents:

A

Responses against self (tolerance),
Tissue damage
Excessive lymphocyte activation during immune responses

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2
Q

Immune regulation is

A

control of the immune response to prevent inappropriate reactions

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3
Q

IR us required to

A

Avoid excessive lymphocyte activation and tissue damage during normal protective responses against infections;
Prevent inappropriate reactions against self antigens (“tolerance”).

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4
Q

autoimmunity

A

immune response against self (auto-) antigen = pathologic

Systemic or organ-specific

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5
Q

auto-immune diseases featires

A

Chronic diseases with prominent inflammation, often caused by failure of tolerance or regulation

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6
Q

Fundamental problem

A

imbalance between immune activation and control;

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7
Q

Failure of control mechanisms

A

is the underlying cause autoimmune diseases;

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8
Q

autoimmunity results from

A

May result from immune responses against self antigens (autoimmunity) or microbial antigens (Crohn’s disease);

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9
Q

causes

A

May be caused by T cells and antibodies;

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10
Q

chronic

A

because it is attacking self-antigen there is always more antigen to attack.

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11
Q

Allergy

chronic

A

Harmful immune responses to non-infectious antigens that cause tissue damage and disease

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12
Q

mediated by

1/2

A

Antibody (IgE) and mast cells – acute anaphylactic shock

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13
Q

2/2

A

Or T cells – delayed type hypersensitivity

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14
Q

Hypercytokinemia and Sepsis

causes

A

Too much immune response
Often in a positive feedback loop
Triggered by pathogens entering the wrong compartment (sepsis) or failure to regulate response to correct level

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15
Q

3 phases of Cell mediated immunity

A
Induction
Effector 
Memory 
 1. Cell infected
DC collects material 
2. MHC:peptide 
TCR interaction 
3. Naïve T becomes effector
4. Effector cell  sees MHC:Peptide on infected cell
Performs function
5. Effector pool contracts to memory
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16
Q

Principal mechanism:

A

immune response eliminates antigen that initiated the response

=> First signal for lymphocyte activation is eliminated

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17
Q

Licensing a response – the 3 signal model

A

Antigen Recognition
Co-stimulation- protien protien interactiom on cell surface
Cytokine Release

all 3 cause t or b cell activation

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18
Q

Antigen

A

Responses against pathogens decline as the infection is eliminated
Apoptosis of lymphocytes that lose their survival signals (antigen, etc)
Memory cells are the survivors

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19
Q

Three possible outcomes of infections

A

Resolution: no tissue damage, returns to normal. Phagocytosis of debris by macrophages.

Repair: healing with scar tissue and regeneration. Fibroblasts and collagen synthesis.

Chronic inflammation: active inflammation and attempts to repair damage ongoing.

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20
Q

Tolerance

A

specific unresponsiveness to an antigen that is induced by exposure of lymphocytes to that antigen (tolerogen vs immunogen)

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21
Q

Significance

A

All individuals are tolerant of their own antigens (self-tolerance); breakdown of self-tolerance results in autoimmunity


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22
Q

restoring tolerance may be exploited to prevent

A

treat autoimmune and allergic diseases

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23
Q

Types of tolerance

A

Tolerance occurs at two time points:

Before the T or B cells ever enter the circulation (central)

Or once in the circulation (peripheral)

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24
Q

Central tolerance

A

destroy self-reactive T or B cells before they enter the circulation

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25
why before
Lymphocytes that recognise self antigens are eliminated (deletion) or made harmless in the generative organs as part of the maturation process.
26
AIRE
AutoImmune REgulator
27
not all eptide made in thymus
yes
28
How can a T cell developing in the thymus encounter MHC bearing peptides expressed in other parts of the body?
A specialised transcription factor allows thymic expression of genes that are expressed in peripheral tissues AIRE promotes self tolerance by allowing the thymic expression of genes from other tissues
29
mutations in aire results in
multi-organ autoimmunity
30
Peripheral tolerance
destroy or control any self reactive T or B cells which do enter the circulation
31
3 pathway if b
Antibody Production Memory Affinity Maturation- self reactive b cell can be activated, recognise antigen change shape if antibody to bind on antigen
32
somatic hypermutation
, B cells can change specificity after leaving the bone marrow
33
good
as it improves antibody quality
34
Exposure to environmental antigens or self antigens
can make them less tolerance
35
how many Mechanisms of Peripheral tolerance
``` Normal T cell response Anergy Ignorance Deletion/ AICD Regulation ```
36
Naive T cells needs in order to become activated
need co-stimulatory signals
37
problem
Most cells lack co-stimulatory proteins and MHC class II
38
what happens if n t cell see without co stimulatory protuen
If a naive T cell sees its MHC/peptide ligand without appropriate co stimulatory protein it becomes anergic
39
whats anergic
unresposive, as actiavtion energy is too high
40
what happens if it sees it in the future
less likley to become activated | slower to respond
41
Conditions in anergic
+ Antigen | - Co-stimulation
42
Ignorance Conditions
- Antigen | - Co-stimulation
43
what happens
Antigen may be present in too low a concentration to reach the threshold for T cell receptor triggering not activating so can become anergic
44
happens where
Immunologically privileged sites e.g. eye, (brain) where t cells don't see the antigen Compartmentalisation of cells and antigen controls interactions if they never meet they can't become active
45
Antigen Induced Cell Death (AICD) Conditions
+ Antigen | + FasL
46
how does it work
Activation through the T-cell receptor can result in apoptosis
47
Treg (T regulatory cells) function
inhibit other T cells and other cells by cytokines
48
what do they do
inhibit t cell activation inhibit t cell effector function Secretion of immune-suppressive cytokines inactivation of dendritic cells or responding lymphocytes
49
Treg express transcription factor
FoxP3
50
Mutation in FoxP3 leads to
severe and fatal autoimmune disorder - Immune dysregulation, Polyendocrinopathy, Enteropathy X-linked (IPEX) syndrome.
51
Treg main iL is what
IL-10 (master regulator) cytokine
52
features and functions
``` Key anti-inflammatory cytokine Multi-functional (pleiotropic) Acts on a range of cells Blocks pro-inflammatory cytokine synthesis including TNF, IL-6, IL-8, IFNγ Downregulates Macrophage functions Viral mimics ```
53
“Natural” regulatory T cells (nTreg) develop where
in thymus
54
function
Development (in thymus) requires recognition of self antigen during T cell maturation prevent harmful reactions against self
55
Inducible regulatory T cells (iTreg) | develop from
Develop from mature CD4 T cells
56
function
Develop from mature CD4 T cells that are exposed to antigen in the periphery; no role for thymus May be generated in all immune responses, to limit collateral damage
57
Cytokines prgms
immune response
58
function
They can be inflammatory (increase the response) | Or anti-inflammatory (decrease the response)
59
Chemokines function
Chemokines drive movement around the body
60
Chemokine receptor profiles
change with activation state of the cells
61
how do cell follow
moves up chemokine gradient
62
T helper type defined by
transcription factors
63
Different antibody classes have different
constant regions.
64
T cells shape the antibody response
T cells cytokine drive Ig class switch