Innate Immune System SG

Immunity

ability to resist infection + disease

Leukocyte

white blood cell

Erythrocyte

red blood cell

White blood cell

A blood cell that fights disease.

Why do we need an Immune System?

-Keep out pathogens

-Environmental substances that challenge the lymphatic system

What do environmental substances include?

-Environmental pathogens (poison ivy, etc.)

-Toxins

-Abnormal body cells (cancers)

What is our immune system coupled with?

The lymphatic system

Lymphatic system

includes + connects your lymph nodes

Two branches of the immune system

Innate and adaptive

Innate Immune System

-present at birth

-Non-Specific Diseases

What can the Innate Immune System involve?

epithelium on body surface. in connective tissue, in the GI system (digestive), or cellular response

Does the Innate Immune System require exposure to a foreign substance?

No

1st Line of Defense for Innate

Physical barriers; Skin + mucosal barriers to keep hazardous materials outside the body

Physical Barriers

-Outer layer of skin

-Secretions (glands, mucus, urine, stomach acid)

-Direction of secretion (can prevent movement of pathogens)

Where are all white blood cells formed

bone marrow

2nd Line of Defense for Innate

-Phagocytes

-Immunological Survelience: Natural Killer cells (NK Cells)

-Interferons

-Complements

-Inflammation

-Fever

Phagocytes

type of white blood cell that engulfs pathogens + cell debris, release toxic chemicals, and present antigens

Why do phagocytes "display" the antigens?

So the rest of the immune system is aware + can signal for there to be an adaptive immune response

What two components mix inside of phagocyte?

-Lysosome: has lytic enzymes to break things down

-Phagosome: bubble that is created when phagocyte engulfs the pathogen

What is created from the lysosome and phagosome?

A Phagolysosome which destroys the infectious agent

What are types of phagocytes?

-Neutrophils

-Macrophages

-Eosinophils

Neutrophil

-developed in bone marrow

-most abundant white blood cells

-respond the quickest to infections + invasions

Eosinophil

involved with parasitic infections + antigen-antibody complexes

What do eosinophils secrete?

cytotoxic chemicals that are toxic to cells on a parasite; uses phagocytosis to kill

Macrophage

derived from monocytes; come in after neutrophils; recognize + phagocytose pathogens

Basophil + mast cell

Proinflammatory chemical-secreting cells

Arteriole

small branches from the artery; distribute blood to capillaries; above capillaries

Capillary

small blood vessel where oxygen rich veins and oxygen poor veins meet; where nutrients + oxygen can be transported; middle

Venule

small veins that connect the veins to the capillaries; carries blood that lacks oxygen; bottom

Basophil

Opens up vessels and increase blood flow; releases histamine, heparin, and eicosanoids

Mast cell

Cells that release chemicals (such as histamine) that promote inflammation.

Histamine

causes vasodilation (increase in diamter of blood vessels) + capillary permeability to increase; gets blood to locations faster

Heparin

anticoagulant; prevents + treats blood clots

Eicosanoids

vasodilation + vasoconstriction

Process of phagocytes invading the area of infection/injury

1. Release of inflammatory + chemotactic factors

2. Vascular changes

3. Recruitment of immune cells

4. Delivery of plasma proteins

1. Release of inflammatory + chemotactic factors

Basophils + Mast cells release chemicals

2. Vasuclar changes include:

-Vasodilation

-CAMs displayed

Vasodilation

increase size of blood vessels; capillary permeability

CAMs

Chemical Adhesion Molecules that allow diapedesis; stick to sides of capillaries to increase permeability; act as a flag for WBCs to know where a "gap" is to get somewhere more quickly

3. Recruit of immune cells

-Margination

-Diapedesis

-Chemotaxis

Margination

WBCs slow down + align on the blood vessel wall to find where CAMs are

Diapedesis

blood cells leave vessels + squeeze through gap

Chemotaxis

WBCs follow a chemical gradient towards infection

chemotactic

chemical factor that tells the cells where to go

Pus

exudate; occurs due to cluster of neutrophils (mostly dead) + other WBCs

What does the lymphatic capillaries do during swelling?

It increases fluid uptake to resolve swelling

Simple Steps for Inflammation

1. Chemical/chemotactic factors released

2. Response in blood vessels

3. Response in leukocytes

NK Cells (natural-killer)

-apoptosis-initiating cell

-less selective (respond to variety of abnormal cell antigens)

-highly versatile

-respond quickly

-does not release lyzosomaal components so other cells not damaged

2 Ways for NK Cells to kill cell

-Lyze (damage cell in surrounding area)

-Apoptosis

Apoptosis process

-release perforin (protein) and granzyme (enzyme)

-perforin beds in cell plasomembrane, creates pore for granzymes to enter

-granzymes cause apoptosis

Interferons (IFN)

signaling molecule (cytokine) released by viral-infected cells

cytokine

signaling proteins that help control inflammations, act as messengers to "signal" immune system to respond

What happens after the IFNs are released?

-Causes neighboring cell to produce enzymes that prevents viral replication

-can either cause macrophages to phagocytose OR activate NK cells

Complement Proteins

"complement" functions of antibodies + have many functions to defend against pathogens

-Opsonization

-Inflammation

-Cytolysis

-Elimination of Immune Complexes

Opsonization

-complement will stick on pathogen to maake it look different (acts as opsonin)

Inflammation

-activates WBCs to help inflammation

Cytolysis

-causes cell lysis (Big MAC attack)

-Complement sticks to pathogen, becoming MAC protein

-MAC will then lyse cell

Elimination of immune complexes

-The complement binds to an antibody that is attached to an antigen (antigen-antibody), links with a erythrocyte, takes to spleen to kill it

Symptoms of inflammation

-Redness (blood flow)

-Heat (blood low + metabolic activity)

-Swelling (increased permability)

-Pain

-Loss of function (severe cases)

Fever

-abnormal elevation of body temperature (1 C from normal 37C)

-Requires increased fluid intake to prevent hydration due to excess fluid loss

Why do fevers happen?

-Release of pyrogens

-Toxins

Pyrogens

-cytokines that cause fever

-target hypothalamus + release prostaglandin

Prostaglandin

hormone that raises temperature set point of hypothalamus

Benefits of fever

-slows reproduction of bacteria/viruses

-promotes IFN activity

-increases activity of adaptive immunity

-tissue repair

-Increasein CAMs

Risks of high fever

-above 103* is very dangerous

-change in metabolic pathways + detanturation of proteins

-death above 109