Physiology_Exam 4 - Chapter 15

Front 1

Innate Immunity

Back 1

-is inherited as part of structure of each organism
-distinguished between "self" and "non-self"
-FIRST line of defense again invading pathogens

-epithelial barriers, high acidity of gastric juices, phagocytosis, fever

Front 2

Adaptive immunity

Back 2

-aquired ability to defend against pathogens with prior exposure

-lymphocytes produce specific antibodies to mediate

Front 3

Phagocytosis

Back 3

fill this in

Front 4

Neutrophils

Back 4

phagocytose

first to arrive at infection sited

Front 5

Mono-nuclear phagocytes

Back 5

macrophages and monocytes

Front 6

Organ-specific phagocytes

Back 6

Liver
Spleen
Lymph nodes
Lungs
Brain
-Fixed phagocytes line all of the above except brain

Front 7

Mobile leukocytes

Back 7

Connective tissue and blood contain these WBCs

Front 8

Chemokines

Back 8

White blood cells are attracted to infection (chemotaxis) by these

Front 9

Extravasation

Back 9

Method by which WBCs from blood exit capillaries and digest pathogens

Front 10

Physical process of phagocytosis

Back 10

-Pseudopods surround pathogen
-Form vacuole
-Vacuole fuses with lysosomes which digest pathogen

Front 11

Fever

Back 11

-Innate immunity
-Occurs when hypothalamic thermostat is reset by endogenous pyrogens and other cytokines (IL1-beta)

-pyrogens are released by WBCs in response to endotoxin from Gram(-) bacteria

Front 12

Interferons

Back 12

-Produced by cells infected with virus
-a,b,g, interferons
-provide short-acting, non-specific resistance to viral infection in nearby cells

Front 13

Antigens

Back 13

-elicit production of antibodies that bind to them specifically
-large molecules foreign to body
-normally makes antibodies against non-self antigens
-immune system can determin between self and non-self antigens

Front 14

Haptens

Back 14

-small antigenic molecules
-become antigens when bound to proteins
-form an antigenic determinant site

-useful for creating antibodies for research and diagnosis

Front 15

Immunoassays

Back 15

-Tests that use specific antibodies to identify a particular antigen

-binding of antibody to antigen causes agglutination

Front 16

Lymphocytes

Back 16

-Derived from stem cells in bone marrow
-replace by cell division
-seed thymus, spleen, and lymph nodes with self replacing colonies

Front 17

T Lymphocytes (Cells)

Back 17

-Don't secrete antibodies
-Attach infected host, cancer and foreign cells
^cell mediate immunity

-majority of blood WBCs and almost all in lymph node centers and spleen

Front 18

B Lymphocytes

Back 18

Fight bacterial infections
-secrete antibodies into blood and lymph
^humoral immunity

Front 19

Thymus

Back 19

-large in childhood, regresses after puberty
-contains T cells that supply other tissues
-T cells can deplete due to AIDS or CHEMO

-after childhood re-population in secondary lymphoid organs

Front 20

Secondary lymphoid organs

Back 20

-Nodes, spleen, tonsils, Peyer's patches
^basically where antigens could gain entry to blood or lymph

-lymphocytes constantly circulation through blood and lymph to enhance chance of antibody meeting antigen

Front 21

Local inflammation initial

Back 21

initiated by non-specific mechanisms of phagocytosis and complement activation

complement activation attracts phagocytes to area

Front 22

opsinization

Back 22

phagocytic activity of neutrophils, macrophages, and monocytes

Front 23

Local inflammation progresses

Back 23

B cells produce antibodies against bacterial antigens

antibody attachment amplifies response because of complement activation

Front 24

Local inflammation and leukocytes

Back 24

Neutrophils - Monocytes - T Cells (NMT)

-attach to surface of endothelial cells
-move by chemotaxis to inflammation site
-undergo extravasation

Front 25

Mast cell secretions

Back 25

heparin
histamine
prostaglandins
leukotrienes
cytokines
TNF-a

Front 26

Mast cell effects

Back 26

Produce redness, warmth, swelling, pus, pain (RWSPP)

recruit more leukocytes

endogenous pyrogens release if infection continues

Front 27

B lymphocytes

Back 27

-have antibodies that are receptors for antigens

-when bound to antigen they divide and secrete antibodies

Front 28

B lymphocytes divide

Back 28

some progeny become memory cells

others become plasma cells that produce a sh!t load of antibodies that are specific for original antigen that initiated division (active immunity)

Front 29

Complement proteins

Back 29

can kill antigen-bearing cells
can promote phagocytosis

B cell binding activates these proteins

Front 30

Immunoglobulins

Back 30

are antibody proteins

part of gamma globulin class of proteins

Front 31

antibody specificity

Back 31

same basic structure but not exactly the same

Front 32

IgG

Back 32

main form of antibody in circulation

production increased after immunization

secreted during secondary response

Front 33

IgA

Back 33

main antibody type in external secretions

saliva and mother's milk

Front 34

IgE

Back 34

responsible for allergic symptons

immediate hypersensitivity response

Front 35

IgM

Back 35

Antigen receptors on lymphocyte surface prior to immunization

secreted during PRIMARY response

Front 36

IgD

Back 36

function as antigen receptors on lymphocyte surface prior to immunization

Front 37

Antibody structure

Back 37

-Shape of Y
-Heavy chain (interior Y)
-Light chain (exterior add on)
-Bottom half constant among different antibodies
-Two tips of y are variable that confer antibody specificity

Front 38

Antibody diversity

Back 38

Antigen independent diversity:
-Many combinations of H and Y
-recombination in the bone marrow

Somatic hypermutation (antigen dependent):
-Occurs as B-cells proliferate in the secondary lymphoid organs in response to antigens
-Occurs by gene recombination (class switch recombination) whereby original IgM antibodies can convert to any other

Front 39

Complement system

Back 39

-Nonspecific defense system
-proteins activated by binding of antibodies to antigens
-bacterial coat polysaccharides
-antigen binding does not destroy antigen or pathogen
-antibodies label targets for attack, stimulate opsonization

Front 40

Opsonization

Back 40

The ability of antibodies to stimulate phagocytosis

Front 41

Complement proteins: recognition

Back 41

C1

Front 42

Complement proteins: activation

Back 42

C4, C2, C3 in that order

Front 43

Complement proteins: attack

Back 43

C5 through C9

-complement fixation

Front 44

Complement fixation

Back 44

complement proteins attach to the cell membrane and destroy the victim cell

C4b

Front 45

classic pathway

Back 45

-initiated by binding of antibodies of IgG and IgM
-activate C1 which causes C4 to break into subunits
-C4 binds to membrane
-C3 and C5 stimlates mast cells to release histamine
-C5 serves as chemokine

Front 46

alternative pathway

Back 46

-initiated by polysaccharides that coat bacteria cells
-slower than classic

Front 47

Membrane attack complex

Back 47

karge pore that can kill the bacterial cell through osmotic influx of water

C5-C9

Front 48

Complement fragments

Back 48

-Attract phagocytes (chemotaxis)
-C3b receptors on phagocytes serve as bridge to victim cell
-stimulate mast cells to secrete histamine
^vasodilation, capillary permeability, more phagocytes

Front 49

Cytotoxic T Cells (killer)

Back 49

-CD8 surface markers
-destroy foreign antigens with direct contact
-cell-mediated destruction

Front 50

cell-mediated destruction

Back 50

-in contact with victim cell

perforins: create pore in membrane cause lysis

granzymes: cause destruction of victim's DNA

Front 51

Helper Ts

Back 51

-CD4 marker

-indirect - enhance response of killer t and b cells

Front 52

Regulatory T cells

Back 52

CD25 marker (and CD4)

decrease responses of killer Ts and Bs

help protect against autoimmune response

-suggested that some diseases suppress regulatory cells to exert control over immunity

Front 53

Stem cell differentiation B and T

Back 53

B and T

B turn into memory cell and plasma cell producing antibodies

T turns into helper, regulatory, and killer cells

Front 54

Lymphokines

Back 54

Are cytokines secreted by lymphocytes.

Labeled interleukin when differentiated

remember a cytokine is a autocrine or paracrine regulator

Front 55

T Receptor Proteins

Back 55

-Cannot bind to free antigens
-respond to foreign antigens when theyare presented on surface of antigen-presenting cells
-main antigen presenting cells are macrophages and dendritic cells

Front 56

Dendritic cells

Back 56

-Originate in marrow
-prominent where pathogens might enter body
-engulf protein antigens, partially digest
-display polypeptide fragment on cell surface for T Cells to see

Front 57

Dendritic cell and t cell activation

Back 57

1. Dendritic cell processes antigens
1a. travels to secondary lymphoid organs
2. dendritic cell acitvates T cell
3. activated T cell travels through lymphatic system
4. activated T cell extravasates to combat infection

Front 58

Histocompatibility Antigens

Back 58

-Cell surface compatibility identifiers
-On all but RBCs
-MHC Complex
^4 genes (ABCD) with multiple alleles

Front 59

MHC Types

Back 59

1. Associated with Killer T cells, require CD8 coreceptor

2. Associated with Helper T, require CD4 coreceptor, activate helper Ts so they can promote B cell activity

both also require foreign antibody

Front 60

T Cell Response to Virus

Back 60

-Phagocytized by macrophage or dendritic cell
-fragments and antigens displayed on surface
-Class 2 MHC complex present to helper T
-Helper T binds to promote B cell activity

Front 61

Macrophage - T Cell Interaction

Back 61

-Macrophages secrete Interleukin 1 and TNF

-IL 1 stimulates cell division and proliferation of helper T

-Helpers promote macrophage activity and activate B cells by secreting M-CSF, G-Interferon, IL 2

Front 62

B Cell - T Cell Interaction

Back 62

-Bind by surface antigen and MHC Class 2
-B Cells Proliferate
-Convert to Plasma Cells that produce specific antibody
-Convert to memory cell

Front 63

T Cell Destruction

Back 63

-FAS production increases during infection

-after a few days Ts produce FAS ligand

-binding of FAS to FAS ligans triggers apoptosis

Front 64

Primary response

Back 64

Exposure to a pathogen for the first time - slow creation of antibodies

Front 65

Secondary response

Back 65

Rapid response, maintained at high level, second time seeing antigen

Front 66

Clonal Selection Theory

Back 66

-Secondary immune response mechanism
-B cells inherit ability to produce only one antibody
-exposure to antigen stimulates cell to clone identical cells

-plasma cells secrete antibodies, memory cells can be stimulated to produce second antibody response down the road

Front 67

Germinal Centers

Back 67

Develop in lymph nodes and spleen from cloned B cell

proliferate and undergo hypermutation

secretes antibodies for secondary immune response

Front 68

Active immunity

Back 68

-development of secondary response

-cause development of B cell clones that provide secondary response

Front 69

Immunilogical tolerance

Back 69

-Ability to produce antibodies against non-self antigens while tolerating self-antigens
-1st month of life

Lens of the eye hidden from blood

Front 70

Autoreactive T Cells

Back 70

Killer T cells that attack self-antigens

Front 71

Immunological Tolerance Mechanisms

Back 71

Clonal Deletion theory: thymus, T cells that recognize self-antigens are destroyed

Clonal anergy: not understood, lymphocytes directed against self-antigens present but don't attack. something about B cells

Front 72

Passive Immunity

Back 72

-Produced by transfer of antibodies from recipient to donor

-Donor actively immunized

-Person who receives these antibodies passively immunized

Front 73

Colostrum

Back 73

produced by mother in first 2-3 days of nursing, rich in antibodies given from mother to infant

Front 74

Immunological competence

Back 74

Ability to mount own immune response
-does not develop until 1 month after birth

Front 75

Monoclonal antibodies

Back 75

-B cell harvested in animals
-Hybridized with cancerous myeloma to make immmortal

-take the correct one and clone it

Front 76

Tumors

Back 76

-Normally killed by immunology
-Cancer is failing of immunological surveillance

-tumors are clones of single cells whose division is not inhibited by natural mechanisms

Front 77

Tumors again

Back 77

dedifferentiated cells

surface antigens absent at time immunological competence established

Front 78

Natural Killers

Back 78

-Stimulated by interferon from T cells
-Attack cells that lack Class 1 MHC antigens

-Related to Killer T cells
-First line of cell-mediated defense
-Innate Immune System
-Array of surface receptors

Front 79

Autoimmune disease

Back 79

Produced by failure of immune system to recognize and tolerate self-antigen

afflicts women twice as often as men

Front 80

Autoimmune causes

Back 80

-antigen that does not normally circulate in blood is circulating (hashimoto's)
-Combination of self-antigen that is other wise tolerated with a foreign (thrombocytopenia, low platelet count)
-Antibodies being produced that are directed against other antibodies (rheumatoid arthritis)
-Antibodies against foreign antigens cross-reacting with self-antigens (rheumatic fever)
-Self-antigens being presented to helper T cells together with class 2 MHC molecules (Type 1 diabetes)