Chapter 21 1012

Immune system

• Function system, not organ

• Bodys defence mechanism

• Identifies foreign “non-self” (we didn't make) cells in the body.

• Protects against harmful invaders

• Promotes healing

How does invasion occur?

1. Pathogen (agent)

2. Where germs live (reservoir)

3. Way out (portal of exit)

4. Method of travel (mode of transmission)

• Contact (skin to skin or skin to surface)

• Droplets (6 feet)

• Airborne (travel long distance

• Carrier (vector)

5. Enter new invasion site (portal of entry)

6. Host of invasion (susceptible host)

Types of defense

1. Innate

2. Adaptive

Innate Defense

• Inborn

• Fast acting

• 1st and 2nd line of defence

Adaptive Defense

• Slower

• Strengthens over time

• Acquires tools and skills required to mount a more effective defence

• 3rd line of defence

Innate Defense - The first line

1. Skin

2. Mucous membranes:

- protective chemicals: acid, sebum, sweat

- enzymes: saliva, resp tract, tears

- mucin: digest, resp tract

- defensins: mucous membranes and skin (antimicrobial)

Innate defense - The second line

• White blood cells 

• Esinophil, basophil

• Phagocytes (neutrophils, eosinophils, basophils, macrophage, monocyte, dendritic cells

• NK cells

• Inflammation

• Fever

Toll-like receptors (TLR)

Detect or recognize invaders and sound the alarm that initiates immune response.

Phagocytes

White blood cells that ingest and digest (eat) foreign invaders.

What are the most abundant phagocytes?

Neutrophils. But they die fighting, they become phagocytic on exposure to infectious material and aren’t always successful.

Steps of Phagocytosis:

1. Phagocytes such as neutrophils and macrophages confront microorganisms that breach the external barriers.

2. Phagocytes use the receptors on their cell walls to be able to stick to and trap a pathogen before it can be engulfed.

3. Neutrophils and macrophages complete the destruction of the invading pathogen by swallowing them up and forming a capsule called a phagosome.

4. Phagosomes combine with lysosomes and become a phagolysosome.

Oponoization

• Immune system uses antibodies or complement proteins as opsonin’s that coat pathogens

• Act as handles for phagocytes to grab on to, enhancing phagocytosis

• Opsonization makes the pathogen “tasty” and speeds up the phagocytosis of the pathogen

• Happens when phagocyte is unsuccessful in destroying pathogen

Natural killer "(NK) cells

• white blood cells (lymphocytes)

• “police” blood and lymph

• can kill cancer and virus infected cells before asaptive immune system is activated

• attack cells that lack “self” cell-surface receptors

• kill by inducing apoptosis in cancer cells and virus-infected cells

• secrete potent chemicals that enhance inflammatory response

Inflammation

Triggered whenever body tissues are injured. Protects against spread/destruction

• trauma

• heat

• irritating chemicals

• infections by microorganisms (ex: inflammation of lungs in asthma attack)

5 cardinal signs of inflammation:

1. pain

2. heat

3. redness

4. swelling (edema)

5. loss of function

Purpose of inflammation:

• isolate injury/infection

• prevent spread of damaging agents

• disposes of cell debris and pathogens

• alerts adaptive immune system

• prepares for repair

Inflammatory chemical release

• chemicals are released into ECF by injured tissues or immune cells

• histamine released is key inflammatory chemical

• other inflammatory mediators:

  1. histamines (neutrophils/mast cells) - vasodialation

  2. Kinins, prostaglandins - pain and fever

  3. cytokines if pathogens are involved

  4. complement

• induce vasodilation of local arterioles to make the capillaries leaky and attract phagocytes to area

Antimicrobial properties

Enhance innate defenses by attacking microorganisms or by hindering their ability to reproduce.

Consist of interferons, and complement.

Interferons

• used to prevent replication of virus in body

• cause synthesis of proteins that interfere with viral replication

• small proteins produced by virally infected cells

• help protect surrounding healthy cells

Complement

Group of about 20 proteins that provide a major mechanism for destroying foreign pathogens in the body

Fever

abnormally high body temp, a systemic response to invading microorganisms.

the body’s thermostat is rest upwards in response to pyrogens.

Pyrogens

• substance released by bacterium which produces fever when introduced or released into the blood

• pyrogens produced by WBCs (leukocytes and macrophages) act on the hypothalamus, causing a rise in body temp

Adaptive defense - the 3rd line

• adaptive

• not born with it

• slower

• strengthens over time

• identifies and remembers threats (memory)

• acquires tools and skills required to mount a more effective defense

• kicks in when the invader is stronger than what the 2nd and 3rd line can handle

Septic

infection which travels throughout body

Types of Humoral (fluid) immunity

1. active, naturally acquired

2. active, artificially acquired

3. passive, naturally acquired

4. passive, artifically acquired

Active, naturally acquired humoral immunity

Infection; contact with pathogen

Active, artifically acquired humoral immunity

Vaccine; dead of attenuated pathogens

Passive, naturally acquired humoral immunity

Antibodies passed from mother to fetus via placenta, or to infant in milk (colostrum)

Passive, artificially acquired humoral immunity

injection of exogenous antibodies (gamma globulin). antibodies from people who had disease injected to another person.

ABO blood typing system:

• Type A has A antigen

• Type B has B antigen

• Type AB has A and B antigen

• Type O has neither A or B antigens

What happens when there is a mixing of blood between a Rh - mother and Rh + fetus?

• Antibodies are produced in mom

• Transfusion reaction occurs (immune response)

• Miscarriage can occur in next pregnancy of Rh+ fetus

Antigens

• large signalling molecules not normally found in the body

• their presence stimulates an immune system response

• invader from the outside world

• can be bacteria, fungus, virus, toxin, diseased cell

B cells mature in:

Red bone marrow

T cells mature in:

Thymus

Immunocompetence:

the ability to develop an immune response following exposure to an antigen.

Self tolerance:

the immune system can identify and not react against self produced antigens

Membrane bound antibodies

receptors for antigen on the surface of B cells

B cell immunity:

• Naive B cells colonize secondary lymphoid cells and float around the blood

• Virus enters blood

• The virus is encountered by a B cell that has antigens for the virus (from exposure/vaccine)

• B cell attaches to the antigen and activates the humoral immune response and is activated

• Once activated: cloning, effector cells (active fighters/antibody production), memory cells all occur to create a more effective response.

4 mechanisms of defense:

1. Neutralization

2. Agglutination

3. Precipiation

4. Complement

Neutralization:

Block specific sites on viruses or bacterial exotoxins so they cant attach

Agglutination:

Bind to the same antigen on more than one cell-bound antibody

Ex: clumping of mismatched blood cells

Precipitation:

the formation of insoluble complexes as a result of the specific interactions between antigen molecules and the corresponding antibody molecules

Complement

enhances (complements) the ability of antibodies and phagocytic cells to clear microbes and damaged cells from an organism, promote inflammation, and attack the pathogen's cell membrane.

Cellular immunity

The final stage of combat. occurs when all other defenses have failed.

T cells activate:

• inflammation

• macrophages

• other T cells

• regulate the immune response

Amature APCs:

• displayed by all body cells except RBCs

• displays fragments of endogenous antigens (proteins made inside the cell)

• infected cells undergo programming for cell death (apoptosis)

Prefessional APCs:

• displayed by APCs

• macrophages, dendrites, and B cells

• displays fragments of exogenous (outside the cell) pathogens that are engulfed and processed in the cells

• sends messages of dangerous abnormality and need to be destroyed

T cells

• lymphocytes that mature in the thymus

• attack cells that have lost their initial fight and have been invaded by bacteria, fungus, virus, or disease (cancer)

Helper T cells:

can’t kill but activate the cells that do and lead the process

Cytotoxic T cells:

the cells that actually do the damage

What are memory T cells and what do they do?

• produced by copying of activated helper T cells

• raise the alarm that there is a problem

• release cytokines to stimulate the production of more memory/effector T cells that increase the alarm signal, calling more cells to the area

What are cytotoxic T cells and what do they do?

• roam the blood and lymph looking for infected/diseased cells looking to be destroyed

• drills a hole in the membrane and releases perforin, a chemical, into the cell destroying it

Immunodeficiency:

immune system cant attack

Autoimmune deficiency:

immune system starts attacking itself