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Extra > Imunto > Flashcards

Imunto Flashcards

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
Q

why before

A

Lymphocytes that recognise self antigens are eliminated (deletion) or made harmless in the generative organs as part of the maturation process.

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26
Q

AIRE

A

AutoImmune REgulator

27
Q

not all eptide made in thymus

A

yes

28
Q

How can a T cell developing in the thymus encounter MHC bearing peptides expressed in other parts of the body?

A

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
Q

mutations in aire results in

A

multi-organ autoimmunity

30
Q

Peripheral tolerance

A

destroy or control any self reactive T or B cells which do enter the circulation

31
Q

3 pathway if b

A

Antibody
Production
Memory
Affinity Maturation- self reactive b cell can be activated, recognise antigen change shape if antibody to bind on antigen

32
Q

somatic hypermutation

A

, B cells can change specificity after leaving the bone marrow

33
Q

good

A

as it improves antibody quality

34
Q

Exposure to environmental antigens or self antigens

A

can make them less tolerance

35
Q

how many Mechanisms of Peripheral tolerance

A 
Normal T cell
response 
Anergy  
Ignorance
 Deletion/ AICD  
Regulation
36
Q

Naive T cells needs in order to become activated

A

need co-stimulatory signals

37
Q

problem

A

Most cells lack co-stimulatory proteins and MHC class II

38
Q

what happens if n t cell see without co stimulatory protuen

A

If a naive T cell sees its MHC/peptide ligand without appropriate co stimulatory protein it becomes anergic

39
Q

whats anergic

A

unresposive, as actiavtion energy is too high

40
Q

what happens if it sees it in the future

A

less likley to become activated

slower to respond

41
Q

Conditions in anergic

A

+ Antigen

- Co-stimulation

42
Q

Ignorance Conditions

A
  • Antigen

- Co-stimulation

43
Q

what happens

A

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
Q

happens where

A

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
Q

Antigen Induced Cell Death (AICD) Conditions

A

+ Antigen

+ FasL

46
Q

how does it work

A

Activation through the T-cell receptor can result in apoptosis

47
Q

Treg (T regulatory cells) function

A

inhibit other T cells and other cells by cytokines

48
Q

what do they do

A

inhibit t cell activation
inhibit t cell effector function
Secretion of immune-suppressive cytokines
inactivation of dendritic cells or responding lymphocytes

49
Q

Treg express transcription factor

A

FoxP3

50
Q

Mutation in FoxP3 leads to

A

severe and fatal autoimmune disorder - Immune dysregulation, Polyendocrinopathy, Enteropathy X-linked (IPEX) syndrome.

51
Q

Treg main iL is what

A

IL-10 (master regulator) cytokine

52
Q

features and functions

A 
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
Q

“Natural” regulatory T cells (nTreg) develop where

A

in thymus

54
Q

function

A

Development (in thymus) requires recognition of self antigen during T cell maturation
prevent harmful reactions against self

55
Q

Inducible regulatory T cells (iTreg)

develop from

A

Develop from mature CD4 T cells

56
Q

function

A

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
Q

Cytokines prgms

A

immune response

58
Q

function

A

They can be inflammatory (increase the response)

Or anti-inflammatory (decrease the response)

59
Q

Chemokines function

A

Chemokines drive movement around the body

60
Q

Chemokine receptor profiles

A

change with activation state of the cells

61
Q

how do cell follow

A

moves up chemokine gradient

62
Q

T helper type defined by

A

transcription factors

63
Q

Different antibody classes have different

A

constant regions.

64
Q

T cells shape the antibody response

A

T cells cytokine drive Ig class switch

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