Organisation of the Immune System Flashcards

1
Q

Name some physiological barriers?

A

fever - not favourable for MOs to replicate.
Low pH in stomach - kills many MOs.
Chemical mediators - interferons, lysozymes and complement.

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2
Q

Physiological barrier - epithelium?

A

skin and mucosa = first line of defense - physical mechanical barrier, acidic environment. Very large surface area - Mucous membranes - mucus secretions trap MOs, cilia expel MOs. mucosa single layer thick, easier to invade and therefore heavily defended by the immune system (MALT)

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3
Q

What is GALT?

A

villi ( have lymphatic vessels), specialised areas Peyers patches - large aggregates of lymphocytes. Draining that enters mesothelial lymphatic system. M cells can sample antigens in the gut and pass them to lymphocytes in Peyers patches.

Most lymphocytes are in the gut. Peyers patch has predominantly B cells that develop into germinal centres during immune response.

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4
Q

What else is present in the gut?

A

Commensal bacteria in the gut also present, don’t respond to unless have a disease (inflammatory bowel disease).

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5
Q

Physiological barrier - skin?

A

draining lymphatic vessels in skin, and venules of circulation. Lymphocytes in the skin layers, e.g. Epidermal Langerhans cells - these catch antigens in the skin, and migrate through the layers to present antigens to the lymph nodes.

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6
Q

What are neutrophils?

A

most abundant, involved in phagocytosis and killing microbes - multilobed nucleus. Polymorphonuclear cells + granulocytes. 40-75% of leukocytes. Short lived, circulate in blood and migrate to tissues, first cells to site of damage

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7
Q

How do neutrophils move into tissues?

A

Neutrophils move into tissues via chemokine release binding to surface of endothelium (near site of infection), neutrophils rolling past, detect chemokines and integrins on neutrophil surface increase affinty and stop neutrophil moving. Diapedesis - moving through endothelial layer.

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8
Q

Where do neutrophils bind to in tissues?

A

Once in tissue neutrophils bind to opsonins (molecules that coat antigen to faciliate phagocytosis - antibodies or complement).

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9
Q

How to neutrophils kill pathogens?

A

Neutrophil killing mechanisms can either be:
Oxgyen-dependent = radical burst - superoxide, hydrogen peroxide, hydroxyl radical, nitric oxide, reactive oxygen intermediates.
Oxygen-independent = enzymes, lysozymes, hydrolytic enzymes, antimicrobial peptides

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10
Q

What is a neutrophil extracellular traps?

A

traps pathogens in granule protein and chromatin net of extracellular fibres enhancing phagocytosis - neutrophils die as a result.

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11
Q

Describe Eosinophils

A

granulocytes, release granules that attack MOs, defence against parasitic infections and help B cell responses in teh GUT and production of IgA.

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12
Q

Basophils granulocytes?

A

can act as antigen presenting cells in type 2 immunity for IgE.

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13
Q

What are Macrophages and Monocytes?

A

phagocytosis, release cytokines when they take up and digest MOs to then present antigens on cell surface that T cells can find complementary ones.reside in tissues and signal infection through cytokine release

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14
Q

What are Mast Cells?

A

contain histamine and cytokines, producing pro-inflammatory response, found in mucosa and connecive tissue.
Good at recognising bacterial tissue and phagocytose when activated.
Activated by complement products, histamine release increases vasodilation and vascular permeability - slowing blood flow at infection site, - cells and fluid can leave infection site

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15
Q

What’s a dendritic cell?

A

antigen capture and presentation

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16
Q

What’s an NK cell?

A

lysis of infected cells - granulated large lymphocytes, secretes interferon gamma. 5-10% of peripheral blood lymphocytes.
No specific antigen receptor but express activating and inhibiting receptors.
Their receptors bind to antibody-coated cells (Antibody Dependent Cell-mediated Cytotoxicity) important in defence against tumor cells and viral infections.

17
Q

Why doesn’t an NK cell kill self cells?

A

If target cell has MHC class 1 molecules (self molecules) on cell surface, then NK cells leave it alone, by binding to MHC Class 1 with inhibitory receptors.

If the target cell is missing self molecules as they have been removed by pathogen, then activating receptor on NK cells bind to stress induced molecules on target cell.