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AFN Pathophysiology > Immunobiology > Flashcards

Immunobiology Flashcards

1
Q

Cytokines

A

INFy - Antiviral interferon
TNFα - ^ vascular permeability (pro-inflammatory)
Interleukins
IL-6 Fever
IL-6 Acute phase response
IL-8 PMN chemotaxis
IL-12 NKT, Th1
IL-10 Anti-inflammatory

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2
Q

Primary cytokines in fever?

A

TNFα and IL-1

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3
Q

Classical complement pathway

A

C1 binds Antigen/Antibody complex > c1 is activated > Eventually activates C4 > lysed into C4a and C4b

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4
Q

Complement molecules

A

proteins made by liver, float around in inactive state.

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5
Q

MBL Complement Pathway

A

Mannose binding lectin
binds pathogen oligosaccharides
happens in mucous membranes.
Eventually activates c4 which splits into C4a and C4b.
C4b activates C3 convertase
C3 convertase breaks C3 into C3a and C3b

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6
Q

What is important about c3 convertase step in complement cascade?

A

Where classical, alternative, and MBL pathways all converge

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7
Q

Alternative complement pathway

A

Random activation of C3 in serum > C3 convertase activated > C3 broken down into C3a and C3b > C3b activates C5 > C5 split into C5a and C5b > C5b recruits additional C proteins > membrane attack complex (MAC) is formed. This MAC creates a large pore in the pathogen’s membrane so water and ions can flow in.

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8
Q

Mainly C3a and C4a just a little bit

A

major pro inflammatory cytokines
chemoattractant for PMNs

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9
Q

Mainly C3b but also C46 to a lesser extend

A

increase rate of opsinization
increase phagocytosis
acts as C5 convertase
bind any loose Ag/Ab complexes > deliver to spleen (type III reaction if we don’t properly get rid of these Ag/Ab)

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10
Q

C5a

A

Vasodilation/^ capillary permeability
Chemokine for PMN

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11
Q

Phagocytes receptors

A

MBL receptors
Complement receptors
PAMP receptors

When phagocytes gobble up pathogens they then take antigens and put them on their membrane to also become antigen presenting cells

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12
Q

Complement pathway leads to?

A

Primarily inflammation
It can also cause activation of innate immune response

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13
Q

Inflammation

A

Every pathologic process in the body involves inflammation
*Hallmark of all disease processes

Purpose is to recruit and activate white blood cells to get rid of pathogen and eventually result in healing

Only occurs in vascularized tissues. First get vascular response, then get 2ndary cellular response, all mediated by cytokines.

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14
Q

5 Rs of inflammation

A

Recognition of PAMPs or DAMPS > innate immunity

Recruitment of WBCs, Acutely PMNs, chronically, monocytes and lymphocytes

Removal > activation of phagocytes, NKTs, and cytotoxic T cells (CTL). NKTs and CTLs cause apoptosis of infected host cells

Regulation: limit inflammation and initiate repair phase

Repair phase:

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15
Q

3 Types of Phagocytes

A

Macrophages
Dendritic cells
neutrophils

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16
Q

2 Hallmark Signs of Inflammation?

A

Redness (rubor) and warmth (calor)

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17
Q

Inflammation

A

Marcrophages/Mast cells > histamine, prostaglandin, and leukotrine release > vasodilation > ^ increased blood flow to bring more WBCs to location > causes rubor and calor

Histamine, prostaglandinds, leukotrines, and bradykinin also cause ^ sensitivity > pain (dalor)

Cytokines also cause endothelial cell contraction > ^ diameter of pores between cells > ^ vascular permeability so large things like WBCs and proteins can get out of blood and into tissue where the infection is. This causes increased oncotic pressure in interstitium, so water follows causing edema.

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18
Q

S/S of Inflammation

A

Always: redness and swelling
Sometimes warmth and increased pain

19
Q

IL-6 Release

A

At location of ^ vascular permeability where WBCs are extravating into interstitium IL-6 is released

IL6 > travels in blood stream to liver > acute phase response activation > coagulation

20
Q

Cellular Changes from Inflammation

A

Acutely: PMNs recruited to the area. Later on: monocytes and leukocytes

Resident macrophages in the tissue recognize microbes that have been opsonized and have either antibodies and complement on them > they phagocytize the microbes > cytokine release stimulate endothelial cell activation.

pathogens with C3a and C5a on them also activate mast cells > mast cell degranulation > cytokine release > endothelial cell activation

21
Q

Endothelial cell activation (within cellular response of inflammation)

A

Adhesion molecules on endothelial cells so that they can adhere the WBCs that are passing by. Cytokines act as chemokines and are also placed on endothelial cells to attract WBCs to the area.

Chemokines: typically sugars or proteins

22
Q

Endothelium Cells

A

Also have selectins (which are CD# molecules) on their membranes, (or if not, the cytokines will cause them to appear there).

Selectins/ICAMs are the arms that grab and hold the WBCs, so we need them to be exposed and active. Two kinds,

The cytokines cause the selectins to go from low affinity (closed) state to a high affinity (open) state.

23
Q

WBCs adhesion molecules

A

WBCs also have adhesion molecules on them to help them adhere to the slectins on the endothelium. They are held loosely though, and are passed down the endothelium to the location of ^ vascular permeability.

Two primary kinds: oligosaccharide and integrin (CD11) .

These must also be in a high affinity state.

As WBCs are pulled to the endothelium by the chemokines their adhesion molecules are activated as they move towards endothelium.

24
Q

Margination

A

WBCS being pulled to the endothelium surface

25
Q

WBC Process to get into tissues

A

Margination > rolling > diapedesis

26
Q

Diapedesis

A

WBCs are held tightly at site of ^ vas permeability, and WBC change morphology squeezing. flat to fit through the whole between endothelial cells.

27
Q

End of inflammation

A

When no more pathogens in the tissue for Monocytes, lymphocytes, and PMN to gobble up, so they start releasing IL-10 and TGFb switching from pro-inflammatory to anti-inflammatory.

28
Q

IL-6

A

Cytokine
released by monocytes/lymphocytes/PMN that get into the tissue,
Goes to liver and activate liver to release acute phase proteins,
Also goes to brain and causes stress response

29
Q

Systemic Acute Phase Response

A

Initiated by IL-6
Liver proteins secrete Acute Phase Response Peptides
Ferritn/Haptoglobin > bind and decrase [Fe]
CRP > bind pathogens > opsonization via classical pathway
Serum amyloid A > ^prostaglandin synthesis & functions as chemokine for WBCs
Fibrinogen > ^ coagulation (pool blood at site of increased permeability to increase
interation between pathogens and WBCs)
Complement > (CL1 & MBL)
Growth Factor > IGF1 (&glucagon) > ^ gluconeogenesis, ^ protein catabolism, ^ FA
metabolism, decreased insulin sensitivity
IL-6 also goes to brain > stress response > cortisol release > ^ glucagon
At the End of inflammation
Anti-coag factors, (R1-antitrypsin, PAI)

30
Q

Acute Phase Response Proteins (APRP)

A

Ferritin
CRP
Serum Amyloid A
Fibrinogen
Anti-Coag factors
Complement
IGF-1

31
Q

IL-6 Effects

A

Acute Phase Response in Liver
Stress response in Brain
Leukopoiesis left shift

32
Q

IL-6 Brain Pathway

A

IL-6>fever/stress response in brain > ACTH & GF > ^ Cortisol and glucocorticoids > mineral corticoids > ^ Na retention > water retention > ^ BP in acute phase of inflammation

33
Q

When unable to clear pathogens

A

Switch to chronic inflammation > activation of fibroblasts > secrete extracellular matrix proteins (mostly collagen)

Over time we can eat up this scar tissue.

34
Q

Types of repair Phases

A

Serous
fibrinous
Suppurative

35
Q

Serous repair phaes

A

transudative (low Protein) or exudative (high protein)

36
Q

Fibrinous repair

A

Fibroblasts release fiver in body cavities. Pericardial cavity, pleural cavity, etc. Can cause cross linking of visceral and parietal pleura.

37
Q

Suppuritive repair

A

big pustule with very high protein content Abscess/ulcers

38
Q

Innate Immune Response

A

Phagocyte activated by pathogen binding through PAMP or Opsonin on the pathogen

Also

NKT activated by pathogen or self infected cell

Both lead to cytokine mediated responses
1. Acute Phase Reaction Activation
2. Recruit WBCs (Chemokines)
3. ^ blood flow and vascular permeability
4. Micro coagulation (part of acute phase response)
5. Fever

Either cytokines activate adaptive response OR antigens presented on phagocytes/NKTs? activate adaptive response

39
Q

Adaptive Immune Response

A

Happens in Lymph Nodes
Takes time for this process to start
Initiated by antigen presenting cells with antigen on MHC1 or MHC2 or by secondary signals (cytokines from phagocytes NKTs etc)
2 requirements to start adaptive response
1. Must present antigen on MHC molecule. We need a specific attack
2. Need a second signal

Actual Process
T-helper cell activated, IL-2, IFN4, IL-4, IL-5 released and determine what kind of t cell the helper t cell will differentiate into.

Th2 cells > B cell activation via antigen presentation from Follicular dendritic cell (in follicule of lymph node) AND 2ndary signal of CD40 CD ligand interaction. B Cells > memory cells or plasma cells that secretes immunoglobulins.

40
Q

Immunoglobins (antibodies)

A

Secreted from plasma B cells
IgG Most abbundant,
IgM 1st secreted during infection, can also act as complement
IgD B cell receptor, mast cell and beta cell degranulation
IgE anti-parasitic and mast cell degranulation > Type 1 hypersensitivity reaction
IgA dimer, mucous secretions

41
Q

Immunoglobin Actions

A

Opsinization
fix complement
MAC lysis
Agglutinate/imobilize pathogens
neutralize bacterial toxins
prevent bacterial binding
promote inflammation

42
Q

Cytotoxic T cell activation

A

Th0 > Th1 > cytotoxic t cell activation

OR

CD8+ activation > with Th1 activation > cytotoxic t cell activation. Or CD8+ > memory t cell if no Th1 to co activate the cytoxic t cells.

43
Q

Cytoxic T Cell Actions

A

IFN gamma > mess up viral replication of virus
perforin release
granzymes and granulysin release go through perforins to cause apoptosis
Fas ligand > death complex > cell apoptosis

AFN Pathophysiology (6 decks)

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