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Immunology year 3 > Lecture 1 Inflammation and adhesion > Flashcards

Lecture 1 Inflammation and adhesion Flashcards

1
Q

Inflammation:

What is it?
5 Cardinal Signs

A

Inflammation is a complex, multifactorial response to infection, damage and trauma.

Can be beneficial
Can be sterile
5 Cardinal signs: 
Calor (heat)
Dolar (pain)
Rubar (redness)
Tumor  (swelling) 
loss of function
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2
Q 
Acute Inflammation: 
Definition?
What is it?
Major cells involved? 
Purpose?
A

Acute inflammation is a quick onset local reaction to an immune challenge.

Movement of proteins and cells from blood and tissue.

Predominately neutrophils.

To aid in clearance of the immune challenge and achieve resolution.

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3
Q

Cardinal signs of inflammation

A 
Heat
Redness
Swelling
Pain
Loss of function
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4
Q

Chronic Inflammation

A

Chronic inflammation is a prolonged response in the body.

Non-resolving and leads to loss of function within tissue.

Persistent inflammatory cells, mediators & cytokines in tissue and circulation.

e.g. Rheumatoid arthritis
Can lead to further disease.

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5
Q

Regulators of inflammation:
Pro-regulators proteins. cytokines chemokines?
Anti-regulators proteins. cytokines chemokines?

A

Pro: Histamine, bradykinin, prostaglandins, leukotrienes, complement (C3a, C5a) cGMP, E-selectins, P-selectins, ICAM1, VCAM1, TNF, IL-1B, IL-6, CCL8, GRO,/KC, CCL3, CCL2.

Anti: Adrenaline, noradrenaline, prostaglandins, C1q receptor, cAMP, avB3 intergins, TSP receptor, PS receptor, TGF-B1, IL-10, glucocorticoids.

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6
Q

Receptors that recognise pathogens:

  • pattern recognition receptors
  • Classes of receptor
A

Pattern recognition receptors recognize pathogen associated molecular patterns.

  • Lectins recognize sugars.
  • Scavenger receptors.
  • Complement receptors and Fc receptors - recognize opsonized bacteria.

Toll like receptors.

All allow for the uptake of pathogens by phagocytosis.

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7
Q

Infection triggers an inflammatory response:

3 main Reponses (simplified)

A

Bacteria trigger macrophages to release cytokines and chemokines.

Vasodilation and increased vascular permeability causes redness and swelling.

Inflammatory cells migrate to tissue, release inflammatory mediators that cause pain.

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8
Q

Toll like Receptors:
What are they?
How many in humans?
Examples of TLR and what they bind?

A

Toll like receptors are pattern recognition receptors that recognize a wide range of PAMPs, and recognition at different cellular locations.

There are 10 known TLR in humans.

TLR 2: TLR 6 (Dimer) on cell surface recognizes lipoproteins.

TLR 1: TLR 2 (Dimer) cell surface.

TLR 5: cell surface recognizes flagellum

TLR 4 + (MD-2+CD14) cell surface recognizes LPS

TLR 3: endosome recognizes dsRNA

TLR 7 endosome recognizes ssRNA

TLR 8 endosome recognizes ssRNA

TLR 9 endosome recognizes capped G DNA.

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9
Q

Examples of how TLR can invoke an immune response:

TLR 4 + MD-2 + CD14

A

A complex of TLR 4 MD-2 and CD14 binds to lipopolysaccharide (LPS) and assembles on the surface of macrophages.

intracellular MyD88 binds complex and activates IRAK6 to phosphorylate TRAF6 which phosphorylates IKK

IKK phosphorylates IKB leading to degradation in IKB and releases NFKb which enters nucleus.

NFKb activates transcriptions of genes for inflammatory cytokines which are synthesized in the cytoplasm and secreted via ER.

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10
Q

Complement can cause inflammation

A
  1. Alternative pathway - pathogen surface

2 Lectin pathway pathogen surface

  1. Antibody: antigen (classical pathway)

All lead to opsonization, killing of pathogens and recruitment of inflammatory and immunocompetent cells.

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11
Q

Complement receptors cause inflammation:

6 receptors and their function:

A

CR-1 (CD-35): binds C3b, C4b promotes C3b & C4b decay and simulates phagocytosis and transport of immune complexes.

CR2: binds C3d and C3b part of the co-receptor of B-cells.

CR3 (MAC1/CD11b/CD18): Binds iC3b stimulates phagocytosis.

CR4 (GP150,CD11c/C18): Stimulates phagocytosis.

C5a receptor: Binds C5a activates G proteins.

C3a receptor Binds C3a activates G proteins.

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12
Q

Small components of complement:

Role in inflammation

A

C3a, C5a, C4a (small components of complement) act on local blood vessels to increase vascular permeability and increase cell adhesion molecules.

This causes vascular endothelial changes allowing for extravasation: fluid, complement and Ig Antibodies and migration of macrophages and lymphocytes.

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13
Q 
Mast cells: 
Where are they located? 
What activates it and they collective name? 
Releases?
Enables?
A

Resident in the tissue and sub mucosa.

C3a and C5a activates mast cells and are called anaphylatoxins. Mast degranulation causes anaphylaxis.

Releases: 
Vasoactive amines
Cytokines e.g. TNFa
Enables extravasation of 
-Fluid
-proteins
-cells
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14
Q

Inflammatory mediators:
5 Mediations and examples
Explain lipid mediators

A

Cytokines: IL, TNFa, INFy, granulocyte-macrophage stimulating factor (GM_CSF)

Chemokines: CXCL4, CCL5, CXCL5, CXCL8 (IL8)

Complement: C3a, C5a

Amines: Histamine, serotonin and bradykinin.

Lipid mediators:
- Eicosanoids (20 C chains)
Different subfamilies: Prostaglandins, Thromboxane’s, prostacyclin’s, Leukotrienes, Lipoxins, resolvins, maresins.

Produced from fatty acids (e.g arachidonic acid) by enzymes Cycloxygenase 1 (COX1) or lipoxygenase (LOX).

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15
Q

Inflammatory cells:
when are they present?
What are they?
What they do?

A

Present during the initial phase of inflammation.
Macrophages
Neutrophils

Lead to induced innate response.

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16
Q

The innate induced response:
Activated Macrophages secrete what?
5 mediators
What each do?

A

IL-1b activates vascular endothelial. Activates lymphocytes. Causes local tissue destruction. increase access of effector cells. Causes fever.

TNF-a: activates vascular endothelial and increases permeability. - Causes fever.

IL-6 Lymphocyte activation, increase antibody production - causes fever.

CXCL8 (IL8) Chemoattractant for neutrophils, basophils and T-cells.

IL-12 Activates natural killer cells and induces differentiation of CD4 T cells to Th1 Cells.

17
Q

Cell recruitment:

Adhesion molecules and examples + binding partners.

A

Selectins bind sugars and glycoproteins:

  • L-selectin
  • P-Selectin
  • E- Selectin

Sugars and glycoproteins:

  • SLe x
  • CD34
  • PSGL-1
  • MadCAM-1
Intergrins bind Ig superfamily:
-a4b1
-a4b7
-a6b1
-aLb2 (LFA-1)
-amb2 (monocytes (MAC1)
axb2

Ig superfamily:

  • ICAM 1, 2, 3.
  • VCAM -1
  • LFA- 2
  • LFA -3
18
Q 
Problems with adhesion: 
LAD 1
LAD 2
LAD 3
Causes?
Effects?
A

In LAD 1 - litle or no CD18 (b2) an integrin chain.

In LAD 2 - Poor glycosylation - No SLe x

In LAD 3 - possible defects in all b integrin chains - mutation in kindlin 3 protein gene (FERMT3)

Causes: Neutrophillia, Neurocytosis (high levels in blood)

Effects: Recurrent infections, necrotic in nature.

Immunology year 3 (3 decks)

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