Innate Immune System Flashcards

1
Q

What are physical barriers

A
Saliva - IgA, IgG, lysozyme
Secretions
Mucociliary escalator
Skin + epithelium 
Alkaline pH small intestine
Acidic pH in stomach
Normal bacteria flora
Flushing of urinary tract
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2
Q

What are primary lymphatic organs

A

Bone marrow

Thymus

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3
Q

What are secondary lymphatic organs

A
Spleen
LN + lymphatics 
Mucosal associated lymphoid tissue (MALT) 
- Tonsil
- Adenoids
- Appendix
- Peye's patches
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4
Q

What is HLA and what do they code for and what chromosome is it on

A

Co-dominant alleles which determine what
Major histocompatibility complex (MHC) will be on cell surface that presents to antigen
Chromosome 6

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5
Q

How do you inherit MHC and what is it

A

MHC is a molecule that sits on surface of cell that cell can use to present antigen to T cells

One HLA allele from each present 
Express both on cell surface 
1/2 identical to parent
1in4 sibling will have same HLA 
50% match in twins
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6
Q

What do some HLA molecules increase likelihood of

A

Autoimmune disease

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7
Q

HLA-B27

HLA - DR4/DR1

A

AS / sero-ve arthritis

RA

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8
Q

What is histocompatibility

A

Likelihood of having similar HLA alleles and MHC

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9
Q

What express MHC 1 and what does this do

A

All nucleated cells + platelets

Self markers of healthy cell

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10
Q

What does MHC1 cells present and to who

A

Intracellular antigens to CD8 Tc

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11
Q

What does MHC 2 cells present and to who

A

Extracellular antigens to Cd4 Th

Most important in transplant rejection as extracellular

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12
Q

What expresses MHC 2

A
Antigen presenting cells
Macrophage
Monocytes 
Dendritic cells
B-lymphocyte (also have MHC1 as nucleus)
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13
Q

What are atypical APC

A

Basophil
Eosinophil
Mast cells
Limited to specific environments and active naive CD4 T cells

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14
Q

What is the innate immune system

A
Rapid 
Present from birth
No memory - get same response each time 
Detects alteration from haemostasis
Helps activate adaptive
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15
Q

What cells make up innate

A
Mast cell and NK cells
Basohpils
Eosinophils
Neutrophils
Dendiritc and macrophages
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16
Q

What is the mechanism of innate immunity

A
Recognition
Inflammation
Recruitment of immune cell
Complement activation
Opsonisation
Phagocytosis 
NK cell cytotoxicity
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17
Q

What recognises antigen

A

Pattern recognition receptors on
- Macrophages
- Monocytes
- Dendritic cells e.g. Toll like receptor
Induce inflammatory response by releasing cytokines
Also start phagocytosis

18
Q

What do PRR’s recognise (macrophages / monocytes)

A

Pattern associated molecular pattern
Damage associated molecular pattern
These are generic to pathogens which are not found on human cells
Not specific just general pattern of abnormal cell

19
Q

What causes inflammation and what are they released by

A

Macrophages and Th release
Cytokines which cause inflammation and activate immune
- Interleukins
- TNF
- CSF
Complement triggers degranulation of mast cells / basophils / eosinophils which release cytokines

20
Q

What are pro-inflammatory cytokines and what do they do

A

TNF-a, TNF-Y, IL
Fever
Increased glucocorticoids - hyperglycaemia
Vasodilation
Increased vascular permeability
Increased cell adhesion molecules
Chemotaxis - CXCL6
Increased sensitivity to pain - bradykinin (mast cell)
Recruit other immune cells - eosinophils and mast cells, T and B cells, neutrophils
More macrophage release
NK cells recruited and activated
Growth factor act on bone marrow to increase WCC production

21
Q

What are anti-inflammation cytokines

A

GM-CSF, TGF-B

22
Q

What is always released in inflammation

A

IL-2

23
Q

What are cardinal signs of inflammation

A

Pain due to bradykinin and histamine release

Heat / redness / swelling due to vasodilator and increased permeability

24
Q

Wha releases bradykinin and histamine

A

Mast cells

25
Q

What causes vasodilation

A

NO
Bradykinin
Prostaglandin
TNF-A

26
Q

What causes increased vessel permeability

A

NO
Leukotrienes
Histamine

27
Q

What are cell adhesion molecules and what causes

A

P selection + ICAM-1

Rleleased by TNF-A and IL-1

28
Q

What causes macrophage release

A
TNF-A
IL-1
CXCL-8
NO
Histamine
Prostaglandins
Leukotrienes
29
Q

What causes immunodeficiency

A

Any breach in innate, adaptive or physical barriers to inflammation

30
Q

What are 3 different pathways for activating complement

A
Classical = Ab binding to foreign antigen
Lectin = lectin protein attached to pathogen 
Alternative = direct by pathogen
31
Q

What do pathways act on

A

C3

32
Q

What happens

A

C3 splits into C3A + C3B

C3B acts as opsonin and activates C5 which activates membrane attack complex

33
Q

What does C3A and C5A

A

Inflammation

Chemotaxis to attract neutrophils, monocytes and eosinophils

34
Q

What is membrane attack complex

A

Cytolytic pore that forms and punches hole within cell membrane of target pathogens
Extracellular fluid flows into pathogen
Osmotic rupture and death

35
Q

What is opsonisation

A

Binding of opsonin to antigen to enhance phagocytosis

Reduces -ve charge so phagocyte can come clsoer

36
Q

What are main opsonins

A

C3b and C4b
Ab
Plasma protein

37
Q

What are main phagocytes and what do they do

A

Macrophages = main as always present in tissue
Neutrophils once inflammatory response started
Eosinophils to a lesser extent
Dendritic cells - APC which pick up antigen and go to adaptive

38
Q

What is released to attract phagocyte

A

IFN-y

Endotoxins

39
Q

What activates NK cells

A

Reduced MHC-1 in abnormal cell

Stimulated by interleukin

40
Q

What do NK cells do

A
Release perforin and granzyme
Perforin creates pore
Granzyme enters and destroys cells 
Release IFN-y to activate MO and other sentinel cells + complement 
INFLAMMATION
41
Q

What else can activate NK cells

A

IFN-y and IL-2

Ab opsonised antigen binds to Fc receptor on NK cell membrane

42
Q

What is always released in inflammation

A

IL-2