Lymphatic System—Saladin, Ch. 21

Front 1

functions of Lymphatic System

Back 1

-collect excess fluid from tissues
-return it to blood
-circulate immune system components
-special function in intestine: lacteals absorb fat

Front 2

lymph

Back 2

fluid in lymph vessels; similar to plasma
-once the fluid enters the bloodstream, it is called plasma

Front 3

network of vessels throughout body

Back 3

start in tissues as lymph capillaries  lymph vessels  lymph trunks  collecting ducts (2)

Front 4

lymph nodes scattered along vessels

Back 4

-large numbers in neck, armpit, groin
-bring pathogens in contact with immune cells

Front 5

pathogen

Back 5

disease-causing organism or substance

Front 6

collecting ducts

Back 6

right lymphatic duct

thoracic duct

Front 7

right lymphatic duct

Back 7

-empties into right subclavian vein
-collects from right side of head, thorax, arm

Front 8

thoracic duct

Back 8

-empties into left subclavian vein

-collects from left head and arm & everything below diaphragm

Front 9

movement of lymph

Back 9

by muscle action

(one-way valves prevent backflow)

Front 10

structure/function

Back 10

-tonsils protect against inhaled and ingested pathogens
-thymus active in fetus & child for T lymphocyte development
-spleen acts like a big lymph node

Front 11

Three Lines of Defense against pathogens

Back 11

1st & 2nd are nonspecific)

1 external barriers

2 substance & mechanisms of the body

3 specific immunity

Front 12

1st line

Back 12

external barriers
-skin, mucous membranes

Front 13

2nd line

Back 13

substances and mechanisms of the body, such as:
-inflammation, fever, antimicrobial proteins

Front 14

3rd line

Back 14

specific immunity
-acts against specific pathogens
-leaves a “memory” to protect against future attacks

Front 15

Nonspecific Resistanc

Back 15

-nonspecific means guards against many different pathogens
-no previous exposure is needed
-includes 1st and 2nd lines of defense

Front 16

First Line of Defense

Back 16

-external barriers
-skin surface layers contains keratin (tough protein)
-mucous membranes
-at body entrances (nose, mouth, trachea, urinary, reproductive tracts)
-traps pathogens

Front 17

Second Line of Defense (cell types)

Back 17

neutrophil

eosinophils

basophilis

lymphocytes

Front 18

Leukocytes

Back 18

WBC

Front 19

neutrophils

Back 19

-found mostly in connective tissues
-kill bacteria by phagocytosis & by secreting toxic substances
-the secreted toxic substances partly responsible for damage caused in rheumatoid arthritis

Front 20

eosinophils

Back 20

-found mostly in resp., diges., unrinary tracts
-phagocytize allergens & inflammatory chemicals
-release enzymes against some parasitic worms (hookworms and tapeworms)

Front 21

basophils

Back 21

-secrete histamine (vasodilator) and heparin (anticoagulant)

-speeds other leukocytes reaching an area where needed

Front 22

lymphocytes

Back 22

T and B lymphocytes involved in specific immunity
-natural killer cells (NK cells)
-a non-specific type of lymphocyte
-circulate and lyse (seek and destroy):

-self-cells that are cancerous or infected with virus
-cells of transplanted tissue

Front 23

monocytes

Back 23

-migrate into tissues to become macrophages
-phagocytic cells
-some stationary, some migrate

Front 24

Antimicrobial Proteins

Back 24

interferons & compliment system

Front 25

interferons

Back 25

-proteins secreted by cells infected with virus
-stimulate neighboring cells to secrete antiviral proteins
-interfere with viral replication
-also activate NK (natural killer) cells & macrophages
-destroy other infected or abnormal cells
used in cancer treatment because they stimulate NK cells, which can destroy cancer cells

Front 26

complement system

Back 26

group of at least 20 proteins
-role in non-specific and specific immunity
-always present in plasma in inactive form
-must be activated by presence of pathogen

Front 27

complement system cascade reaction occours

Back 27

1. greater inflammation
2. opsonization
-coats bacteria to promote binding of macrophages so they can phagocytize the bacteria
3. cytolysis (rupture of target cells)

Front 28

Immune Surveillance

Back 28

NK cells patrol the body, looking for diseases or abnormal cells

Front 29

Fever

Back 29

-abnormal increase in body temperature
-inhibits bacteria and viruses

Front 30

inflammation (function)

Back 30

1) mobilization of defenses
-stimulation of many cells & substances
2) containment & destruction of pathogens
-slows and destroys pathogens; limits their spread
3) tissue cleanup & repair
-four cardinal signs: redness, swelling, pain, heat

Front 31

Steps in Inflammation

(know full process)

Back 31

1) mobilization of defenses

2) containment & destruction of pathogens

3) tissue cleanup & repair

Front 32

1) mobilization of defenses

Back 32

release of chemicals that promote vasodilation

damaged blood vessels secrete sticky substances

Front 33

2) containment & destruction of pathogens

Back 33

fibrinogen (a clotting factor) forms a sticky mesh at injury site

neutrophils attracted to site by bradykinin, leukotrienes
neutrophils secrete cytokines

macrophages & T lymphocytes secrete colony-stimulating factors

Front 34

3) tissue cleanup & repair

Back 34

-monocytes migrate from blood & become macophages
-macrophages then phagocytize bacteria, damaged cells

-cells & chemicals needed for repair attracted to site of injury
-pain helps keep injured area immobilized

Front 35

Specific Resistance (Third Line of Defense)

Back 35

natural active immunity

artificial active immunity

natural passive immunity

artificial passive immunity

Front 36

1) natural active immunity

Back 36

-acquired naturally
-body makes its own Abs
-ex: after having chicken pox, you have immunity

Front 37

2) artificial active immunity

Back 37

-obtained by medical intervention
-body makes its own Abs
-ex: vaccine: antigens of pathogen are given, body makes Ab

Front 38

3) natural passive immunity

Back 38

-acquired naturally
-body does not make its own Abs
-ex: Ab obtained by fetus through placenta or by baby from mother’s milk

Front 39

4) artificial passive immunity

Back 39

-obtained by medical intervention
-body does not make its own Abs; receives them from an outside source
-ex: treatment for someone bitten to prevent rabies or snake anti-venom for snake bite treatment

-injected with Ab obtained from a vaccinated animal (often horses)

Front 40

Types of specific immunity based on how the body responds

Back 40

cellular (or cell-mediated) immunity & humoral (antibody-mediated) immunity

Front 41

cellular (or cell-mediated) immunity

Back 41

-lymphocytes directly attack the pathogen
-may lyse, release toxic chemicals, cause inflammation, etc.

Front 42

humoral (antibody-mediated) immunity

Back 42

-uses antibodies
-Abs do not destroy pathogen directly, but “tag” it for attack by other cells

Front 43

Components involved in specific immunity

Back 43

antigens

T lymphocytes

B lymphocytes

Antigen-presenting cells

interleukins

Front 44

antigen

Back 44

a molecule that triggers an immune response
-includes free molecules, like toxins
-also includes cell membrane or bacterial cell wall molecules
-each organism has unique Ags in their cell membranes
-body can tell self and non-self

Front 45

T lymphocytes

Back 45

develop before birth in the thymus
-they can recognize Ags presented to them by Ag-presenting cells (described below)
-they have specific receptors on their surface for recognizing Ags

(many types of t cells each is unique)

Front 46

B lymphocytes

Back 46

-develop before birth in the bone marrow
-develop surface receptors for diff. Ags

-then leave marrow and reside throughout lymph system

Front 47

d) Antigen-presenting cells

Back 47

-cells that “present” an Ag to T cells so they can respond to it
-APCs can be macrophages, B cells, or others called reticular cells and dendritic cells
-APC engulfs a bacterium, digests it, displays the Ag on its surface
-wandering T cells “inspect” APCs for displayed Ags, then respond by launching an immune response

Front 48

Interleukins

Back 48

-are chemical signals from one leukocyte to another (hence the name)
-made by WBCs and macrophages
-there are many, with new ones being discovered

Front 49

Cell-mediated (Cellular) Immunity

Back 49

Recognize, React, Remember

Front 50

Recognition
Two parts:

Back 50

antigen presentation & T-cell activation

Front 51

antigen presentation (Recognition)

Back 51

-antigen-presenting cell processes the pathogen, displays its antigen (Ag)
-APC then goes to lymph node & displays the Ag to T cells
-Tc and T¬h cells “patrol” lymph nodes and tissues
-when they contact a displaying APC, they start an immune response

Front 52

T-cell activation (recognition)

Back 52

Tc or Th cell binds to the APC at the displayed Ag
-this triggers clonal selection

Front 53

clonal selection (recognition)

Back 53

-T cell is “activated” & divides to produce a clone of identical T cells
-some cells in the clone will attack any cell with that Ag

-some cells in the clone will become memory T cells

Front 54

React

Back 54

-three types of cells will attack: Th, Tc, and Tr

Front 55

1) Th (helper T ) cells (react)

Back 55

-respond to presented Ag
-secrete interleukins
-attract neutrophils, NK cells & macrophages
-stimulate T and B cells to multiply & mature

Front 56

2) Tc (cytotoxic T) cells (react)

Back 56

-respond to presented Ag’s
-release toxic chemicals to destroy the target cell
-some chemicals are: perforin, lymphotoxin, tumor necrosis factor
-secrete interferon: interferes with virus replication
-secrete interleukins to activate macrophage

Front 57

3) Tr (regulatory T) cells (react)

Back 57

-release interleukins to inhibit T and B cells
-keeps the immune response under control

Front 58

CD4 cells & CD8 cells

Back 58

CD4 = Th

CD8 = Tc & Tr

Front 59

Remember

Back 59

-some Tc and Th cells become memory T cells
-long-lived; can be present for year, or a lifetime
-cause rapid, intense response to a second (or later) exposure to an Ag

destroys a pathogen quickly, before symptoms appear: no disease; the individual has immunity to the pathogen

Front 60

Antibody-mediated (Humoral) Immunity

Back 60

in this type of specific immunity, B cells make antibodies which bind to Ags
-“tags” the Ags for destruction by other means

Front 61

Recognition

Back 61

individual B cells are specific for one Ag

Front 62

steps in B cell response - 1

Back 62

1) Ag binds to B cell receptors

Front 63

steps in B cell response - 2

Back 63

2) B cell takes in the pathogen, digests it, & displays its Ag on its surface (acts as an APC)

Front 64

steps in B cell response - 3

Back 64

3) T¬h cell binds to displayed Ag on B cell
-Th cell starts to release interleukins

Front 65

steps in B cell response - 4

Back 65

4) this triggers clonal selection of the B cell
-B cell divides many times to produce a clone of identical B cells that will recognize that Ag

Front 66

steps in B cell response - 5

Back 66

5) most clone cells become plasma cells
-most plasma cells migrate to bone marrow
-there, they make Abs continually until they die (about 4-5 days)

Front 67

structure of antibodies (Ab’s)

(react)

Back 67

made of four proteins: 2 heavy chains, and 2 light chains

ends of all four chains are variable regions

rest of chain is constant region

Front 68

classes of antibodies

(react)

Back 68

IgM is main class made on first exposure
IgG is main class made on second exposure
IgG is also a class that crosses placenta from mother to fetus
IgA goes from mother to newborn in breast milk
IgE is produced in response to allergic reactions

Front 69

antibody facts

Back 69

it is believed we can produce 2 million different Ab’s
-how is this done when we have fewer than 20,000 genes??
-achieved by “gene shuffling”
-different parts of genes are cut and spliced to produce new genes

Front 70

antibodies have four main methods of attacking a pathogen - 1

Back 70

1) neutralization: Ab’s bind to the active regions of a toxin or virus

Front 71

antibodies have four main methods of attacking a pathogen - 2

Back 71

2) complement fixation
-Ab binds to invading cell and exposes its complement-binding sites
-complement binds to invader, causing lysis, inflammation, attraction of macrophages
-this is main method used to attack bacteria

Front 72

antibodies have four main methods of attacking a pathogen - 3

Back 72

3) agglutination
-Ab binds to pathogen, producing clumps of them
-important in stopping spread of pathogen

Front 73

antibodies have four main methods of attacking a pathogen - 4

Back 73

4) precipitation
-clumps the Ag’s, forming complexes that precipitate out of solution
-they can then be phagocytized by other cells

Front 74

how antibodies work

Back 74

Ab’s do not directly destroy the invader; they “tag” the invader for destruction by other cells or immune system processes.

Front 75

1st exposure to an Ag causes the primary response

Remember

Back 75

-slow; takes several days
-some cells of the clone become B memory cells
-they make Ab’s very quickly & in high numbers on 2nd exposure

Front 76

2nd exposure to an Ag causes the secondary response

Back 76

-fast; memory B cells make Ab’s within hours of invasion by pathogen
-pathogen may be destroyed before any symptoms appear

Front 77

Autoimmune Diseases

Back 77

-autoantibodies attack the body’s own tissues
-failure of self vs. non-self recognition
-possible causes:

Front 78

1) cross-reactivity

Back 78

-infection causes production of an Ab that reacts with both the invader and a self Ag
-some self Ag’s are structurally similar to the Ag’s of pathogens
-example: an Ab attacks both the streptococcus bacterium and self-Ag’s of heart tissue

Front 79

2) abnormal exposure of self-Ag’s to blood

Back 79

-may occur during early development (before birth)
-some Ag’s are not normally exposed to blood
-example: sperm are separated from blood by the BTB (Blood-Testis Barrier)
-if barrier is broken, Ab’s against sperm can be produced; can cause sterility later in life

Front 80

3) change in structure of self-Ag’s

Back 80

-may be caused by a viral infection
-viral genes may be inserted into self-Ag genes, altering them
-self-cell genes then make an abnormal version of the Ag, are attacked as non-self Ag’s

Front 81

some common diseases believed to be likely autoimmune diseases

Back 81

rheumatoid arthritis: cells of joints are attacked

Type I diabetes mellitus: insulin-producing cells of the pancreas are attacked

Systemic lupus erythematosis: connective tissue cells throughout the body are attacked

multiple sclerosis: myelin sheaths of nerve cells are attacked

Crohn’s disease: cells of the intestine are attacked

Front 82

Action of TH cell

Back 82

PC ingest pathogen  displays Ag  TH binds to displayed Ag  APC release IL-1  IL-1 stimulates the TH cell  TH cell releases IL-2  T & B cells stimulated & multiply

(This stimulation of a B cell is further shown in next pathway.)