Chapter 21--The Immune System

Innate Defense System

first and second lines on defense

first line—external body membranes (skin and mucosa)
second line—antimicrobial proteins, phagocytes, other cells, cytokines, inflammation

Adaptive defense system

third line of defense—attacks foreign substances with T and B cells

very specific but takes longer to activate

the two arms of the adaptive system

humoral immunity—B cells

cellular immunity—T cells

how do the innate and addaptive systems work together?

they work independantly but together to provide immunity

the APCs from the innate activate the adaptive

antigens

substances that provoke an immune response

“non self”

innate immune responses

first and second lines of defense

always on and responds immediately

activates adaptive immunity

first line of defense and 2 examples

outward barriers: skin and mucous membranes, and their secretions

ex. stomach is a barrier to infection by digesting bacteria with gastric juice
ex. the windpipe/trachea is lined with cilia, which makes mucus to trap germs

second line of defnese

internal cells and chemicals

phagocytes, antibodies and complement, natural killer cells

phagocytes

adhere to pathogen and digestis it, sometimes uses exocytosis

neutrophils, macrophages, and dendrictic cells

neutrophils

first to respond

chemotaxis toward bacterial infection

macrophages and dendritic cells

serve as APCs, activate T-cells

antibodies and complement

help by opsonization

opsonization

to coat something with antibodies

helps the body to eat and digest the antigen

NK cells

nonphagocytic

can kill some cancer and virus infected cells

attack any cells that do not have MHC (which identifies self)

inflammatory response

macrophages, mast cells, WBCs, inflammatory chemicals

part of the body becomes red, hot, swollen, painful

protective mechanism

stages of inflammation

1. inflammatory chemical release

2. vasodilation and increase vascular permeability

3. phagocyte mobilization

inflammatory chemical release

histamine (increases vasodilation) and prostaglandins (causes neuro pain) released by damaged cells

NSAIDs shut down histamine and prostaglandins production

vasodilation and increase in vascular permeability

capillaries widen to promote more fluid and cells into inflamed area; edema

phagocyte mobilization

migrate to the area via chemotaxis

innate defenses/internal defenses

1. leukocytosis—neutrophils enter blood from bone marrow

2. margination—neutrophils cling to capillary wall

3. diapedesis—neutrophils flatten and squeeze out of capillaries

4. chemotaxis—neutrophils follow chemical trail

antimicrobial proteins

enhance innate defense by attacking microorganisms directly and hinder a microorganisms’ ability to reproduce

complement proteins

20 blood proteins that circulate in inactive form (called zymogen)

enhances inflammation, directly destroys bacteria

generates inflammation, opsonization, and kills pathogens

MAC

membrane attack complex

complement ‘stack’ tha tpokes holes in bacteria so that its eaten

cytokines

chemical messengers of the immune system

mediate cell development, differentiation, and responses

two classes: interferons and inter Leukin

adaptive immune response

specific, systemic, and memory

takes days, but activated by APCs

capable of recognizing different antigens in a very precise way

humoral and cellular

how do both wings of the system begin

an antigen enters the body, and the APC presents the antigen to the helper T cell

the helper T cell takes the antigen to B cells and cytotoxic T cells

humoral immunity

antibodies made by plasma cells

circulate freely in body fluids

5 different types

bind temporarily to target cells

B cells secrete antibodies

steps in humoral immunity

1. neutralization—antibodies block specific sites on cells, enhances phagocytic properties and can activate the complement system

2. precipitation—soluble molecules are cross-linked into complezes, precipitated complexes are easier for cells to engulf

cellular immunity

T cells activated by APCs

form memory cells and effector cells, responds to antigens on body’s own cells

clonal expansion

Directly—cytotoxic T cells (CD8) kills things and attack infected body cells
Indirectly—cytokines (CD4) release chemicals

APCs

dendritic cells and macrophages

the link between innate and acquired immunity

steps for APCs

1. engulf bacteria

2. present antibody to MHC (self) receptor

3. this and other signals activate the cells

4. specific to the antigen that was present

MCH 1 and MCH 2

both are on APCs

MCH 1—displays the antigen to cytotoxic cells

MCH 2—displays antigen to helper T cells

helper T cells

activate humeral and cellular immunities

AIDS affects this cell, without them there is no acquired response

cytotoxic T cells

directly attack and kill other cells

targets virus infected cells, cells with intracellular bacteria or parasites

targets cancer cells, foreign cells (transfusions or transplants)

regulatory T cells

dampen immune system response by direct contact or by secreting inhibitory cytokines

important in preventing autoimmune reactions

T cell selection/maturation

occurs in Thymus, where the cells learn self-tolerance

positive selection—taught to recognize self
negative selection—taught to recognize not self and destroy it

activation/differentiation of B cells

activated by 2 signals:
1. binding to antigen by cell surface receptors to display T helper cell
2. signals from a T helper cell activates the B cell

activates B cells proliferation, makes memory and effector cells

secrete specific antibodies for 4-5 days, then die
memory cells help with quicker responses in the future to the same antigen

antibody IgG

most abundant, activates phagocytosis,

in fetal circulation in pregnant women

antibody IgM

first one you produce in an immune response

antibody IgA

protects mucosae

secretions like saliva, milk, tears, sweat, and mucus

antibody IgE

destorys parasitic worms

allergic responses

natural vs artificial immunity

natural—you get sick, you develop the immunity

artificial—man made, like a vaccine

active vs passive immunity

active—your body produces its own T and B cells

passive—immune system components from another source

primary immune response

first time exposure

slow response, 3 to 6 day lag before antibody production

peak antibody levels reaches in 10 days

antibody levels decline quickly

secondary immune response

re-exposure to the same antigen

quicker response, within hours

higher peak within 2 to 3 days

stay in system for months

isograft

tissue graft with equal/the same or your twin; 0% chance of rejection

autograft

tissue graft within yourself; 0% chance of rejection

allograft

tissue grafts between the same species; high chance of rejection

we give immunosurpressant for decades

xenograft

tissue graph between different species; high chance of rejection

rejection

the body rejects the organ and begins attacking the rest of the body

classified in four stages

hypersensitivity and allergies

and overreaction of the immune system

reactions require a pre-sensitized state of the host

type 1 allergic reaction

simple histamine releases

in response to allergies like pollen

type 4 allergic response

T-cell response

mostly autoimmune

AIDS

cripples helper T cells, so the whole adaptive immune response never even begins