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POM 3 G: IMMUNOLOGY AND INFECTION > 3.5 Immue Tolerance > Flashcards

3.5 Immue Tolerance Flashcards

1
Q

Immune regulation

A

Control of immune response to prevent inappropriate reactions

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2
Q

Immune regulation required to

A

Avoid excessive lymphocyte activation and tissue damage

Prevent inappropriate reactions against self antigens

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3
Q

Autoimmunity

A

Immune response against self antigen (pathologic)

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4
Q

Example 1 of failure of immune regulation

A

Auto immunity

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5
Q

Examples of auto immune disease

A

Rheumatoid arthritis (joint)

Psoriasis (skin)

Lupus (inflammation)

Graves’ disease (eyes)

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6
Q

Is autoimmunity more common in men or women

A

Women

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7
Q

Why do autoimmune diseases occur

A

Imbalance between immune activation and control where failure of control mechanisms is the underlying cause due to susceptible genes and environmental influences

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8
Q

What can an autoimmune response be against

A

Self antigens or microbial agents (crohns disease)

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9
Q

Second example of failure of immune regulation

A

Allergy

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10
Q

What is allergy

A

Harmful immune response to non infectious antigens causing tissue damage and disease

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11
Q

What is allergy mediated by

A

IgE antibodies and mast cells in anaphylactic shock

T cells in delayed hypersensitivity

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12
Q

Third example of immune regulation

A

Hypercytokinemia and sepsis

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13
Q

What triggers hypercytokinemia and sepsis

A

Pathogens entering the wrong compartment (sepsis) or failure to regulate response to the correct levels (too much immune response)

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14
Q

What does cell mediated include

A

T cells

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15
Q

3 phases of cell mediated immunity

A

Induction

Effector

Memory

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16
Q

If autoimmunity is occurring which step of immunity doesn’t occur

A

Effector cell sees MHC:peptide complex on infected cell and performs function,, always more antibody

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17
Q

Steps of cell mediated long version

A

Induction - cell infected and dendritic cell collects material,, MHC!peptide tcr interaction

Effector - naive T cell becomes effector,, sees MHC:peptide on infected cell and performs function

Memory- effector pool contracts to memory

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18
Q

What is a cardinal feature of immune responses (essential)

A

Self limitation

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19
Q

Self limitations of immune responses

A

Manifested by decline of immune responses mainly by eliminating antigen than initiated the response

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20
Q

Licensing a response (the 3 signal model)

A
  1. Antigen recognition (MHC1:peptide/antigen)
  2. Co-stimulation
  3. Cytokines release
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21
Q

3 possible outcomes to immune responses in the body

A

Resolution

Repair

Chronic inflammation

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22
Q

Resolution as an outcome to immunity

A

No tissue damage, returns to normal

Phagocytosis of debris by macrophages

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23
Q

Repair as an outcome to immune response

A

Healing with scar tissue and regeneration

Fibroblasts and collagen synthesis

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24
Q

Chronic inflammation as an outcome to immune response

A

Active inflammation and attempts to repair damage are ongoing

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25
Q

Immunological tolerance

A

Specific unresponsiveness to an antigen (induced by exposure of lymphocytes to that antigen)

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26
Q

Break down of self tolrwnce results in

A

Autoimmunity

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27
Q

Types of tolerance

A

Central and peripheral

Central- befo t and b cells enter circulation

Peripheral- once t or b cells in the circulation

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28
Q

Central tolerance

A

Destroy (deletion) self reactive t or b cells before they enter circulation in generative lymphoid organs (thymus and bone marrow)

29
Q

B cell selection in central tolerance

A

If immature b cell in bone marrow encounters antigen in a form which can cross link their IgM antibodies apoptosis is triggered

30
Q

T cell selection in central tolerance

A

Occurs in the thymus

Need to select for T cell receptors capable of binding self MHC/ self peptide

Positive, negative,, as well as death by neglect (apoptosis) where doesn’t bind and self MHC at all

31
Q

Why is T cell selection more complex than b cells

A

Because of the MHC:TCR interactions

Need to select for tcr which are capable of binding self MHC/ self peptide

32
Q

AIRE

A

Autoimmune regulator

33
Q

Mutations in AIRE result in

A

Multi organ autoimmunity

34
Q

How can T cells 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 pro,toed by AIRW

35
Q

Peripheral tolerance

A

Destroy or control self reactive b and T cells which enter the circulation (escapees or ones that have changed)

36
Q

B cell decisions after antigen exposure

A

Antibody production

Memory

Affinity maturation

37
Q

Antibody production in b cells

A

Naive b cell activated to antigen stimulated cell by cd4 T cells to perifollicular b cells

38
Q

Affinity maturation

A

With every re-exposure makes a better copy of an antibody

39
Q

Can lymphocytes change specificity

A

B cells can after leaving the bone marrow by somatic hypermutation

40
Q

Somatic hypermutation

A

Where b cells change specificity after leaving the bone marrow - usually good as improves antibody quality

41
Q

Mechanisms of peripheral tolerance

A

Normal T cell response

Anergy

Ignorance

Deletion (AICD)

Regulatjon

42
Q

Anergy (tolerance)

A

Naive T cells need co stimulatory signals to become activated

Lack of this causes it to become anergic (unresponsive)

43
Q

Ignorance (tolerance)

A

Antigen present in too low a concentration to reach threshold for T cell receptor triggering

Common in immunologically privileged sites e.g. the ye or brain

44
Q

Antigen induced cell death (AICD) tolerance

A

Activation through T cell receptor results on apopotosis (often caused by the death ligand cd95 or FasL)

45
Q

T cell mediated regulation

A

T regulatory (Treg) cells inhibit other T cells and other cells

46
Q

Treg phenotype

A

CD4, high IL2receptor
Foxp3 transcription factor

47
Q

Which transcription factor do Treg cells express

A

Foxp3

48
Q

Mutation in foxp3 in Treg

A

Severe and fatal autoimmune disorder - IPEX syndrome

49
Q

IL-10

A

Anti-inflammatory cytokines acting on a range of pro-inflammatory cytokine synthesis (TNF, IL6, IL8, IFNY)

Downregulates ,acrophage function

Multi fucntional

50
Q

What normal physiological process is regulation critical in

A

Pregnancy

51
Q

Types of Treg cells

A

Natural (nTreg)

Inducible (iTreg)

52
Q

Cytokines

A

Program immune response

Can be inflammatory to Inc response or anti inflammatory to decrease response

Examples: IL2, IL10

53
Q

Chemokines

A

Drive movement around the body

54
Q

The different constant region on antibodies gives rise to

A

Different functions reflecting the response required to clear pathogens

55
Q

How diverse are bacteria

A

Display genetic diversity,
Morphological diversity,
Metabolic diversity,
Habitat diversity
Functional diversity

56
Q

Immune responses have evolved mechanisms to detect diverse range of bacteria by

A

Recognising common features of bacteria

We.g. LPS in gram negative, LTA in gram positive, flagellum in some bacteria

57
Q

How are bacteria detected by the immune system

A

Complement system (opsonise or lose)

Antibodies (opsonise)

Phagocytes (detect and kill- macrophages and neutrophils)

58
Q

Complement opsonisation

A

Group of proteins which react with one another to opsonise (c3b) or Lysenko bacteria by formation of MAC

59
Q

Steps of complement cascade

A

Initiation

Generation of c3 convertase (bacterial killing by phagocytosis)

Generation of c5 convertase

MAC formation (bacterial killing by lysis)

60
Q

Complement pathways

A

Classic, lectin and alternative

61
Q

Classic complement pathway

A

Triggered by binding of specific antibodies (IgM or IgG) to surface of a pathogen or other target

Antibodies then interact with complement proteins initiating cascaded of enzymatic reactions resulting in activation of complement system

Forms c3 convertase by c4bc2a, then cleaves c3 to form c5 convertase (c4bc2ac3b)

62
Q

Lectin pathway

A

Triggered by lectin to carbohydrate patterns on microbial surfaces

Lectins bound to target then interact with complement proteins initiating cascade of enzymatic reactions intilamtely activating complement system by forming c3 and 5 convertase the same way as classical pathway

63
Q

Alternative pathway

A

Activated spontaneously or continuously at low level in absence of specific antibodies or lectin recognition of pathogens

C3 spontaneously activates and interact with other complement proteins initiating cascade of enzymatic reactions activating complement system

Here c3 convertase is c3bBb

64
Q

Why is the MAC important

A

Responsible in creating pores in pathogen membranes to disrupt osmotic integrity causing influx of liquid, cell lysis and ultimately destruction of the pathogen

65
Q

How is MAC produced

A

C5b recruits c6,7,8 and lots of 9

66
Q

What is the role of antibodies

A

Opsonise bacteria to make them more recognisable and easier to engulf by phagocytosis cells

67
Q

What are phagocytes

A

Leukocytes responsible for phagocytosis (engulfing and digesting pathogens, debris and foreign materials)

68
Q

How are pathogens opsonised to make more recognisable

A

Via complement receptors (c3b) or Fc receptors (antibodies- IgG)

POM 3 G: IMMUNOLOGY AND INFECTION (10 decks)

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