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POM 4: Immunity and Infection > 6: Immune Response to Infection > Flashcards

6: Immune Response to Infection Flashcards

1
Q

6 receptors for immune response

A

MHCI
MHCII
TCR
BCR
B7
CD40

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2
Q

MHCI receptor

A

on all nucleated cells
endogenous peptides = face of the cell, tell immune cell they are own cell

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3
Q

MHCII receptor

A

on all antigen presenting cells(DC, macrophages and B cells),
have exogenous peptides

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4
Q

TCR receptor

A

T-cell receptor
antigen-specific
self-reactive potential

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5
Q

BCR receptor

A

B cell receptor
IgM cell surface receptor
antigen-specific
self-reactive potential

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6
Q

B7 receptor

A

on antigen presenting cells
co-stimulation CD28
T cell activation

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7
Q

CD40 receptor

A

B cell receptor
co-stimulation CD40L
B cell activation

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8
Q

Roles of complement system

A

Anaphylatoxins
Chemokines
Opsonisation
Membrane Attack Complex

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9
Q

Lectins

A

neutralise and opsonise pathogens

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10
Q

What cells have complement receptors

A

innate immune cells

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11
Q

Interferons are

A

cytokines produced by both immune and infected cells in response to viruses and Gram -ve bacteria

produce antiviral proteins in response

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12
Q

Type I and III interferons promote

A

antiviral response

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13
Q

Type II interferons promote

A

antibacterial response

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14
Q

Opsonisation

A

Antibodies, complement factors and lectins bind to pathogenic surface
Recognised by innate immune cells
aid phagocytosis
neutralise pathogenic cell surface
activation of complement cascade (classical pathway)

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15
Q

What is the difference between MHCI and MHCII

A

MHCI shows peptides from inside the cell (endogenous)
MHCII shows peptides from outside the cell (extrinsic)

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16
Q

Detection of tissue damage

A

damage associated molecular patterns DAMPS initiated

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17
Q

Detection of pathogenic structures

A

pathogen associated molecular pattern PAMPs initiated

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18
Q

Activation of innate immune system is a

A

non-specific response

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19
Q

DAMPS and PAMPS cause

A

activation of innate immune system
attack pathogens and liaise with adaptive immune cells
cause non-immune cells to produce anti-microbial peptides (interferons)

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20
Q

Innate immune system

A

pre-determined, present at birth
Pattern recognition receptors - same cell types recognise same pathogens using same receptors

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21
Q

Receptors involved in innate immune system

A

TLRs, Fc receptors, complement receptors, scavenger receptors

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22
Q

What kind of immunity does the liver produce

A

innate humoral immunity:
-lectins - neutralise and opsonise
-complement factors -opsonisation, chemotaxis, MAC

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23
Q

Cellular innate immune cells

A

Granulocytes : neutrophils, basophils, eosinophils, mast cells, monocytes, macrophages
natural killer cells
dendritic cells

24
Q

First responders in immune response

A

Neutrophils - short lived ~6h

25
Naive/inactive cells become activated by
pathogens start secreting cytokines and chemokines
26
Where do macrophages reside
Tissues or circulationMs
27
Macrophage activation
expresses new genes for infection
28
Do NKC have MHCI
no
29
How can Viruses and cancer cells evade detection
by MHCI downregulation
30
NK cells, kill :
nucleated cells without MHCI opsonised cells or pathogens via antibodies and complement
31
Adaptive immune system
takes time correct specific cell found 2 receptors: TCR and IgM receptors (BCR) all lymphocytes have different receptors Clonal lineage in infection has same receptor Memory cells with same receptors enable quick immunity if reinfected
32
2 receptors of adaptive immune system
TCR IgM receptors (BCR)
33
Humoral response of antibodies is produced by
B plasma cells
34
Initiation of adaptive immune system
Activated macrophages and DCs present antigens in combination with MHCI or MHCII to T-cells - cytokines produced by antigen presenting cells; activate T cells -T cells provide cytokines that activate and stimulate phagocytes
35
T-cells are activated by
MHC and foreign peptide recognition from APC
36
T cells interact with B cells to
activate specific B cells to produce antibodies - B cells licensed for antibody production
37
Four functions of T cells
Activate phagocytes Activate B cells Directly kill infected cells Regulate immune response
38
Two functions of B cells
Present soluble antigen to T-cells produce antibodies
39
Sequence of immune response
1. Innate immune cells recognise pathogen and become activated 2. Start secreting cytokines and phagocytose pathogens 3. Antigen presenting cells move to lymph nodes to find specific lymphocytes 4. T helper cells proliferate and differentiate into specific type 5. Cytotoxic CD8+ T cells attack pathogens directly, B cells become activated 6. Activated B cells differentiate into plasma B cells and start antibody production 7. Phagocytes and complement cascade attack antibody-opsonised cell 8. Response of antibody production peaks 2 weeks after infection
40
After pathogen clearance
immune cells undergo apoptosis supressed production of inflammatory cytokines cell population contracts, some form memory cells tissue repair and remodelling
41
Inflammatory diseases are
Positive feedback loops
42
Effect of damage to tissues on immune response
stronger immune response
43
Immunity occurs due to 2 mechanisms
1.Formation of memory B and T cells 2. In re-exposure, antibody response is greater, more plasma cells keep producing protective serum antibodies both involved during vaccination
44
Memory cells in lymphoid tissues are in
lymph nodes spleen gastrointestinal mucosa (e.g Peyer's patches) Mucosal epithelia Bone marrow
45
Memory cells in circulation
Memory T cells - constantly migrate from and to lymphoid tissues Memory B cells can differentiate into plasma cells, secreting antibodies
46
Memory cells after immune response
do not contract
47
Thymic involution
Thymus shrinks in size stops producing new naive T cells over time, more T cells become activated and change from naive T cells to memory cells, so no. naive cells goes down and memory T cell no. goes up
48
A 1 year old is exposed to Staphylococcus aureus by a cut to his finger, what is the order of immune cell activation in response to this infection
Neutrophil > macrophage > DC > T cell > B cell -neutrophils are first to encounter pathogen in tissues -macrophages first to encounter pathogen in blood -macrophages then signal dendritic cells which activate Th cells via MHC II antigen presentation -T-helper cells migrate to lymphoid tissues and activate B cells with complementary receptor to pathogen
49
A baby is born with Severe Combined Immunodeficiency SCID but doesn't develop an illness from a virus, what could explain this?
Child has IgG antibodies against the virus - obtained from mother via placenta, providing acquired immunity
50
What does immunoglobulin gene arrangement allow for
large variety of B cell receptors in body, without need for equally large gene repertoire during reshuffling process, VDJ or VJ recombinase enzyme used to cut any unneeded genes, leaving new gene sequence that can produce a randomly unique B cell
51
SCID (severe combined immunodeficiency)
caused by : deficiency in Rag1 and Rag2 - essential proteins in VDJ or VJ recombinase immune system deficiency as patient can barely do immunoglobulin gene rearrangement, so don't have wide range of B cells
52
What is seen to be elevated in a blood sample soon (2 days) after initial infection
Mannose-binding lectin ; acute phase protein found in incr. conc. in blood in the first few days of infection
53
Acute-phase responses happen alongside
inflammatory response - happen to continue to fight infection - aim to produce more components (acute phase proteins) to continue fighting infection
54
Examples of acute-phase proteins
C reactive protein mannose-binding lectin fibrinogen complement proteins
55
Mannose-binding lectin
acts as an opsonin of innate immune system by activating lectin pathway of complement system to aid fight against infection Allows foreign substances to be efficiently identified for phagocytosis
56
In the case of immunosupression, how can an immune response still be carried out
Complement system can fight infection - alternate pathway of complement system which doesn't require antibodies or mannose binding lectin - triggered by surface-activation via presence of bacterial endotoxins
57

POM 4: Immunity and Infection (9 decks)

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