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POM 1a - Immunology And Infection > Immune Tolerance > Flashcards

Immune Tolerance Flashcards

1
Q

What is immune regulation?

A

Control of the immune response to prevent inappropriate reactions

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2
Q

What is immune regulation required to do?

A

Avoid excessive lymphocyte activation and tissue damage

Prevent inappropriate reactions against self antigens

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3
Q

What is autoimmunity?

A

Immune response against self antigens or microbial antigens

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4
Q

What causes autoimmunity?

A

Imbalance between immune activation and control —> failure of control mechanisms

Susceptibility genes + environmental influences

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5
Q

Why are many immunological diseases chronic and self-perpetuating?

A

Attacking self-antigen there is always more antigen to attack

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6
Q

What is allergy?

A

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

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7
Q

What can allergy be mediated by?

A

Antibody (IgE) and mast cells —> acute anaphylactic shock

T cells —> delayed type hypersensitivity

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8
Q

What is hypercytokinemia and sepsis?

A

Too much immune response

Often in a positive feedback loop

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9
Q

What is hypercytokinemia and sepsis triggered by?

A

Pathogens entering the wrong compartments (sepsis)

Failure to regulate response to correct level

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10
Q

What are the 3 phases of cell mediated immunity?

A

Induction

Effector

Memory

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11
Q

What happens in the induction stage in cell mediated immunity?

A

Cell infected

Dendritic cell (DC) collects material

Loads it onto MHC

Moves into lymph nodes

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12
Q

What happens in the effector stage of cell mediated immunity?

A

Present antigen through MHC to T cells —> recognise specific MHC complex

Get activated and expand clonally

Effector T cells return to site of infection —> elicit response

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13
Q

What happens in the memory stage of cell mediated immunity?

A

Infected cells cleared —> T cells move into contraction phase —> shut down immune response

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14
Q

How is the immune response self-limiting?

A

Decline of immune response due to the response of the eliminating agent that initiated the response

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15
Q

What 3 signals are required to license a response?

A

Antigen recognition

Co-stimulation

Cytokine release

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16
Q

How are the responses against pathogens declined as the infection is eliminated?

A

Apoptosis of lymphocytes that lose their survival signals

Memory cells are the survivors

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17
Q

How are responses to persistent antigens limited?

A

Active control mechanisms —> ‘tolerance’

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18
Q

What are the 3 possible end responses of an infection?

A

Resolution —> no tissue damage, return to normal, phagocytosis of debris my macrophages

Repair —> healing with scar tissue and regeneration

Chronic inflammation —> active inflammation and attempts to repair damage ongoing

19
Q

What is tolerance?

A

Specific unresponsiveness to an antigen that is induced by exposure of lymphocytes to that antigen

20
Q

What is the significance of immunological tolerance?

A

All individuals are tolerant of their own antigens —> breakdown results in autoimmunity

Therapeutic potential —> restoring tolerance may be exploited to prevent graft rejection, treat autoimmune and allergic diseases

21
Q

At what two times does tolerance occur?

A

Before T or B cells ever enter the circulation —> central

Once in the circulation —> peripheral

22
Q

What happens in central tolerance?

A

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

23
Q

Why delete cells before circulation?

A

Function of the way the immune restore is generated

24
Q

How are B cells centrally tolerated?

A

If immature B cells in borne marrow encounter antigen in a form which can cross link their IgM —> apoptosis is triggered

25
Q

How are T cells centrally tolerated?

A

T cell selection occurs in the thymus

Need to select for T cell receptor that’s capable of binding self MHC

T cell receptor don’t bind to any self-MHC —> death by apoptosis

T cell binds too strongly to self-MHC —> apoptosis triggered - negative selection

T cell bins=do weakly to self-MHC —> signal to survive - positive selection

26
Q

What is AIRE?

A

Autoimmune regulator

A specialised transcription factor that allows thymidine expression of genes tat are expressed in peripheral tissues

—> promotes elf tolerance by allowing the tunic expression of genes from other tissues

27
Q

What happens in peripheral tolerance?

A

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

28
Q

What are the 3 pathways activated B cells can undergo?

A

Antibody production

Memory

Affinity maturation —> recognise antigen and change shape of antibody to better bind to it

29
Q

How can affinity maturation cause autoimmunity?

A

Normally good but exposure to environmental antigens or self antigens in context of infections can alter the outcome

30
Q

Mechanism of peripheral tolerance - what is anergy?

A

Naive T cells need co-stimulatory signals in order to become activated

Most cells lack co-stimulatory proteins and MHC class II

If naive T cells sees firs MHC w/out appropriate costimulatory protein —> becomes anergic —> deactivated

Less likely to be stimulated in future

31
Q

Mechanism of peripheral tolerance - what is ignorance?

A

Antigen may be present in too low a conc. to reach the threshold for T cell receptor triggering

Happens in immunologically privileged sites —> T cells never sees antigen so can ‘ignore’ it

Also happens in compartmentalisation of cells and antigens —> T cell never encounters antigen so never becomes reactive

32
Q

Mechanisms of peripheral tolerance - antigen induced cell death

A

Activated through the T cell receptor can result in apoptosis

Influenced by the nature if the initial T cell activation events

In peripheral T cells —> often caused by induction of expression of the death ligand —> Fas ligand

33
Q

What are Treg cells?

A

Sunset of helper T cells that inhibit other T cells and other cells

34
Q

What are some of the defining features of Treg cells?

A

CD4

High IL-2 receptor (CD25)

Foxp3 transcription factors

35
Q

What are some mechanics of Treg cells?

A

Secretion of immune-suppressive cytokines

Inactivation of dendritic cells or responding lymphocytes

36
Q

What do mutations in FoxP3 lead to?

A

Severe and fatal autoimmune disorder -immune dysregulaton, Polyendocrinopathy, Enteropathy X linked (IPEX) syndrome

37
Q

What does the IL-10 cytokine do?

A

Key anti-inflammatory cytokine

Multi-functional —> acts on a range of cells

Block pro-inflammatory cytokine synthesis

Downregulates macrophage functions

Viral mimics

38
Q

Who do Tregs only exist in mammals?

A

Critical when mother is exposed to antigens often expressed in context of MHC I in baby —> half of baby’s from dad so foreign

39
Q

What is ‘natural’ regulatory T cells?

A

Development in thymus requires recognition of self antigen during T cell maturation

Residues in peripheral tissues to prevent armful rations against self

40
Q

What are inducing regulatory T cells?

A

Develop from mature CD4 T cells that are exposed to antigen in periphery —> no role for thymus

May be generated in all immune responses to limit collateral damage

41
Q

What are cytokines?

A

They program immune response —> focus it for the right kind of response

Can be inflammatory or anti-inflammatory

42
Q

What are chemokines?

A

Drive movement around the body

Act like address labels sending stuff to the right place

Receptor profile change with activation state of the cells

43
Q

What is cross regulation in regards to T cells?

A

T helper type is defined by transcription factors —> Cytokines shape transcription factor pathways

Cross regulation is where cytokine response from 1 type of Th cell will shutdown the response of other Th cell types

44
Q

How do T cells help[ improve the function of antibodies?

A

Different antibody classes have different constant regions which is important for their functions

Difference in function reflect the different types of response required to clear pathogens

There are a number of gene cassettes that can be swapped in and out

T cell produce cytokines which programme B cells to activate gene factors to switch Ig classes

POM 1a - Immunology And Infection (6 decks)

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