micro 2 Flashcards
Elie Metchnikoff
1st to observe phagocytes
father of immunology
Innate (nonspecific) immunity
Anatomical barriers
mechanical
- Skin
2. Mucous membranes—-saliva/mucus/urine
Innate (nonspecific) immunity
Anatomical barriers
chemical
- skin
2. mucous membranes (Lysozyme and phospholipase A of tears and saliva)
Innate (nonspecific) immunity
Anatomical barriers
biological factors
- skin and mucous membranes (antimicrobial substances, etc)
Innate (nonspecific) immunity
Humoral components
- Complement
- coagulation system
- lactoferrin and transferrin
- lysozyme
- cytokines
neutrophils
kill by
phagocytocis
intracellular killing
(cause inflamation and tissue damage)
Innate (nonspecific) immunity
cellular components
- neutrophils
- monocytes/microphages
- NK and LAK cells
- Eosinophils
Humoral components
complement
lysis of bacteria
increase in vascular permeability
recruitment of phagocytic cells
Humoral components
coagulation system
increase vascular permeability
recruitment of phagocytes
B-lysin from platelets
B-lysin
a cationic detergent
Humoral components
lactoferrin and tranferrin
compete with bacteria for iron
Humoral components
lysozyme
breaks down bacterial cell wall
Humoral components
cytokines
various effects
monocytes and microphages
kill by
phagocytosis and intracellular killing
extracellular killing of infected or altered self targets
monocytes and microphages
special
antigen presentation for specific immune response
NK cells and LAK cells
do what
kill virus infected and altered self targets
eosinophils
do what
kill certain parasites
Acquired immuity (specific)
react with a specific pathogen, discrete determinates
Acquired immuity (specific) 2 kinds
cell-mediated immunity humoral immunity (Ab)
Acquired immuity (specific) hallmarks
self/non-self discrimination
memory
specificity
diversity
Primary lymphoid organs
bone marrow
thymus
FETAL LIVER
secondary lymph organs
Spleen
lymph nodes
tonsils
MALT
humoral root
fluid contained
blood cells
RBC
Platelets
WBC
WBCs include
1.monocytes/macrophages
2.Polymorphonuclear granulocytes
neutrophils
eosinophils
basophils
3.Lymphocytes
NK cells
T cells
B cells
NK cells are what % of WBC
15
Lymphocytes are what % of WBC
20
Neutrophils are what % of PMN
95
monocyte lysosomes contain
peroxidase
acid hydrolases
monocytes become
tissue macrophages
neutrophils primary granules contain
lysosomes with acid anhydrolases, myeloperoxidase,
muramidase
neutrophils secondary granules contain
lactoferrin
lysozyme
eosinophils are what % of WBC
2-5
eosinophils do what upon stimulation
degranulate,
release histamine, and
aryl sulphatase
basophils are what % of WBCs
<.2
basophils are similar to
mast cells in tissue involved in allergic response
large lymphocytes
NK cells
small lymphocytes
T cells
B cells
NK cells are part of
cell mediated immunity
innate immune response
do Nk cells require prior activation
no
What molecules do NK cells attack specifically?
MHC class I molecules
T and B cells are principal cells involved in what
adaptive immune system
Do T and B cells retain a memory of previous infection?
yes
B cells are primarily responsible for
humoral immunity
B cells mature in
bone marrow
B cells differentiate into
plasma cells
T cells are primarily responsible for
cell mediated immunity
T cells mature in the
thymus
T cells begin in the
Bone marrow
when T cells are activated they secrete
specific proteins
when T cells are activated they secrete specifically
cytokines
cytotoxic granules
helper (CD4)
cytotoxic (CD8)
Antigen presenting cells
microphages
dendritic cells
B cells
immunogen
ability to induce a humoral and/or cell mediated response
antigen(Ag)
ability to specifically bind to an antibody or cell mediated receptor
Haptens
incomplete antigens
need a large carrier such as Hapten-carrier conjugate
Adjuvant
agents which modify the effect of other agents
few direct effects
Epitopes
antigenic determinants
specific active regions for lymphocyte antigen receptors and antibodies
Allergin
substance that causes an allergic reaction
Factors influencing immunogenicity
- contribution of the immunogen
- contribution of the biological system
- method of administration
- chemical nature of immunogens
contribution of immunogen
- foriegness
- size >6000 MW
- Chem composition
- physical form
- degradability (Ag processing by Ag Presenting cells)
contribution of biological system
- genetics
2. Age
method of administration
- dose
- route
- adjuvant
method of administration
dose
subcutaneous>intravenous>intragastric
method of administration
adjuvant
substances that enhance an immunogen response to an Ag
Chemical nature of immunogens
proteins
polysacchirides
nucleic acids
lipids
Antibody
gamma globulins that are produced by plasma cells in response to stimulation by foriegn antigen
gamma globulins
immunoglobulins
glycoproteinmolecules
antibodies are aquired through
natural infection and recovery transplacental (only class Ig G) breast milk feeding for secretory Ig A (sIg A) vaccine immunization recieving antibodies
Structure and function of antibody
Y config
heavy chain
light chain
disulfide bond
contains FAB AND FC REGION
what is Fab
site of antigen binding
variation in Fab allows
a wide range of specific activity
recognition of many antigens
Fc is what
constant part of the Ab molecules
functions of Fc
complement activation
attraction of inflammatory cells
opsonization
what is opsonization
phagocytosis by macrophages with the assistance of antibodies and complement
do macrophages have receptors for Fc molecules
yes
what enhances macrophages opsonizational activity
Fc and complements
how do antibodies digest
by papain and pepsin
different fragments
5 classes of antibodies
- Ig G
- Ig A
- Ig M
- Ig D
- Ig E
most abundant antibody
Ig G
smallest antibody
Ig G
Ig A
two types
serum type
secretory type
4th highest concentration antibody
Ig D
binds to basophils and mast cells
Ig E
antibody in secretory mucosomembrane, tears, mouth
sIg A
3rd highest concentration antibody
Ig M
transplacental antibody
first few weeks of birth
Ig G
antibody associated with parasitic infections
Ig E
agglutinins
combine with Ag to cause agglutination
WIDAL TEST for TYPHOID FEVER
preciptins
combine with a soluble Ag to form a preciptiation complex
OUCHTERLONY PRECIPTIN TEST
lysins
Ab that will lyse particulate Ag
usually needs the prescence of a complement to complete this reaction
antitoxin
soluble Ab that neutralizes toxins
TETANUS TOXIN
DIPTHERIA TOXIN
BOTULISM TOXIN
Ag-Ab reaction
affinity
strength of the reaction between a single antigenic determinant and a single Ab combining site
Ag-Ab reaction
Avidity
overall strength of binding between an Ag with many determinats and multivalent Abs
Ag-Ab reaction
specificity
ability of an individual antibody combining site to react with oly one antigenic determinant & the ability of a population of antibody molecules to react with only one antigen
Ag-Ab reaction
cross reactivity
ability of an individual Ab combinig site to react with more than one antigenic determinant & the ability of a population of Ab molecules to react with more than one Ag
Hemocytoblasts
stem cells of bone marrow
hemocytoblasts origin
embryonic liver and embryonic yolk sac
T lymphocyte development
bone marrow—-thymus—-peripheral lymphatic tissue
T cells chief responsibility
cell mediated immunity
T cells action in humoral immunity
antigen presenting process
Cytotoxic T cells AKA
CD-8
Cytotoxic T cells appear _____ and release _____
early and granules
T- helper subscripts
CD4, T4, Th
T-helper action
interact with Ag before B cells
stimulates activity of CD8
***helps B cells synthesize Ab by secrection of interleukin
Suppressor T cells action
dampen the activity of B and T lymphocytes
inhibits immune response—autoimmunity
B lymphocytes development
origin in Bone Marrow from hematopoiesis— enter circulation and got to peripheral lymph organs
B cells (upon stimulation)
differentiate and form effector plasma cells and memory cells
B cells mainly involved in
humoral immunity
immunoglobins AKA
Ab
Six participants involved in B cell conversion to plasma cells (namely Ab-forming cell)
- Microphage
- CD4 lymphocyte
- Exogenous antigen
- MHC CLASS 2
- Cytokine
- B cells
MHC
Major Histocompatibility Complex
MHC definition
set of molecules displayed on cell surfaces responsible for lymphocyte recognition and antigen presentation
*****control the immune response through recognition of “self” and “non-self”
MHC chromosome location
Chromosome 6
MHC classes
1,2,3
MHC class 1
expressed on virtually every cell
**presents endogenous peptide antigens to Tc cells
MHC class 2
primarily on Antigen presenting cells
**present processed exogenous peptides to Th cells
MHC class 3
various secreted protiens that have immune functions
APC
Antigen presenting cells
APC found where
skin lymph nodes spleen underneath mucosal epithelium thymus
APCs include
dendritic cells follicular dendritic cells interdigitating dendritic cells B cells macrophages
Definition of Atigen processing and presentation
processing-protein antigen degraded into peptides
presentation-peptide-MHC complex transported to cell membrane and displayed
Endogenous Ag bind to
MHC class 1
Endogenous Ag are processed within
cytoplasm
Endogenous Ag examples
cellular proteins
tumor proteins
viral and bacterial proteins
Exogenous Ag bind to
MHC class 2
Exogenous Ag internalized by
phagocytosis or endocytosis
Exogenous Ag processed within
endocytic pathway
TCR means
T cell receptor molecule
TCR structurally similar to
BCR
TCR provides
specificity for an individual T cell to recognize a particular Ag
Why is the TCR “MHC restricted?”
because the TCR is required to interact with MHC
CD4 interacts with
MHC class 2
CD8 interacts with
MHC class 1
interactions between the CD4 and CD8 with their repective MHC acts to
stabilize and consummate the antigen recognition process
*****this allows helper T-cells to respond to “exogenous” antigens (leading to B-cell production of antibody)
**also alows Cytotoxic T-cells (CD8) to respond to “endogenous” antigens leading to target cell distruction
Where does antigen dependent stages of B-cell differtiation begin?
secondary lymph organs
Ab have what 3 main functions
neutralization
opsonization
complement activation
B-cells differentiate into what 2 types of cells
plasma
memory
immune memory AKA
anamnestic response
Is a lag phase present in the secondary immune response?
no
Why is IgM response limited?
They use to much protien and energy to keep on
Cell-mediated immunity is especially important for
destroying intracellular bacteria
eliminating viral infection
destroying tumor cells
what are the effector cells involved in CMI
cytotoxic T-cells (CTLs)
NK
K cells
CTLs are restricted in what way?
antigen
MHC
CTLs require
specific antigen determinant
recognition of self MHC
CTLs principally eliminate
endogenous antigens
CTLs recognize
specific antigens MHC class 1
CTLs express
CD8
NK cells AKA
large granular lymphocytes
NK cells are primarily involved in
elimination of neoplastic or tumor cells
K cells contain
immunoglobin Fc receptors
K cells are involved in
ADCC (antibody-dependant Cell-mediated Cytotoxicity)
ADCC occurs as a consequence
of antibody being bound to a target cell surface via specfic antigenic determinants expressed by the target cell
ADCC can result in
CMIR type 2 hypersensitivities
the complement system in mammal blood is composed of
26 protiens
The compliment proteins combine with
antibodies or cell surfaces
complements are numbered or refered to as
factors
Do complements have to be activated?
yes
What 2 pathways activate complements
classical
alternate
What happens after a complement is activated?
complement cascade
what are the functions of the comlement cascade?
opsonization
clearance of the immune complex
inflammation
MAC—-membrane attack complex
Inflammation during the complement cascade produces and this provides
chemotactic substances (C3a, C5a)
**increased vascular permeability; causing smooth muscle contraction and promotin mast cell degranulation
Classical pathway of complement activiation
immune complex initiation, from C1 to C9
Alternate pathway activation of complement
carbohydrates on bacterial surface
Does most phagocytic binding occur without opsonization?
no
Pagocytic cells express receptors that bind what molecules
opsonin including Fc receptors
Vaccine
usually killed or attenuated bacteria, virus, or attenuated toxin
Booster injections
additional inoculations introduced to **increase immune response, causing quicker anamnestic response
attenuated
rendered incapable of causing disease, but capable of inducing immunity
Titer
concentration
Different modes of aquiring immunity
Natural
artificial
active
passive
natural aquired immunity
naturally exposed to pathogen
artificial aquired immunity
oral intake (or injection) of attenuated organism
active aquired immunity
host makes own antibodies
passive acquired antibodies
recieve antibodies from others (or animal serum)
4 types of immunization
natural aquired active immunity
artificial active immunity
artificial passive aquired immunity
natural aquired passive immunity
natural aquired active immunity
Ab formation is stimulated by the presence
natural aquired active immunity
length of immunity
may be lifelong
artificial active immunity
Ag composed of attenuated microorganism or detoxified product administered to the host which stimulates Ab. production
artificial active immunity
example and length of immunity
flu shot
long term
artificial passive aquired immunity
confeerd by injection of serum from an immune animal, or human being, to a susceptible individual
artificial passive aquired immunity
example and length of immnity
Antitoxin of tetanus
short term
natural aquired passive immunity
Ab aquired in utero while the baby is in the womb, and later while the baby is nuresing on mother’s breast
natural aquired passive immunity
example and length of immunity
Ab in uterus and breast milk
short term
Hypersensitivity
undesirable overreactions produced by the normal immune system to certain allergens
Hypersensitivity reactions require
a pre sensitized (immune state) of the host
Desensitization AKA
allergy shots
allergy shots work by
turning down immune response to the allergen
less Ig E
more Ig G
4 types of Hypersensitivity
Type 1
Ig E mediated immediate AKA anphylactic
Type 1 hypersensitivity involves
mast cells and basophiles
Type 1 hypersensitivity
2 types
Localized anaphylaxis
systemic analphylaxis
systemic analphylaxis
worst case scenario of hypersensitivity
smooth muscle contraction—causing life threatining respitory distress
systemic analphylaxis
immediate treatment
epinephrine injection
Type 2 hypersensitivity
Antibody dependent cytotoxicity
Ig G or Ig M
Type 2 hypersensitivity
what happens
complement enhances cytotoxicity
Type 2 hypersensitivity
examples
autoimmune hemolytic anemia
tranfusion reactions
goodpasture’s syndrome
graves’ disease
Type 3 hypersensitivity
immune complex
Ig G or Ig M-mediated immune complex hypersensitivity
Type 3 hypersensitivity
AKA
arthus reaction and serum sickness
Type 3 hypersensitivity
example
rheumatic fever (strep infection)
immune complex glomerulonephritis
subacute bacterial endocarditits
systemic lupus erythematosus
Type 4 hypersensitivity
cytotoxic T cell CD8-mediated immune response AKA delayed
Type 4 hypersensitivity
Ab role
none
Type 4 hypersensitivity
example
tuberculosis
poision ivy
skin test
fungal disease
Regulation of the Immune response
Immunodeficiency & autoimmunity
Major method of regulation
a balance of T helper and T supressor activities
Regulation of the Immune response
Immunodeficiency & autoimmunity
Major method of regulation
a balance of T helper and T supressor activities
Regulation of the Immune response
Immunodeficiency & autoimmunity
Suppressor T-cell release what?
factors that suppress the B-cell response
Regulation of the Immune response
Immunodeficiency & autoimmunity
Suppressor T-cell release what?
factors that suppress the B-cell response
Regulation of the Immune response
Immunodeficiency & autoimmunity
suppressor T-cells don’t release what?
lymphokines
Regulation of the Immune response
Immunodeficiency & autoimmunity
suppressor T-cells don’t release what?
lymphokines
Regulation of the Immune response
Immunodeficiency & autoimmunity
what does a disturbance in the balance cause?
immunodeficiancy syndromes
(state of unresponsiveness is created)
lack of helper
or excess of suppressor activity
Regulation of the Immune response
Immunodeficiency & autoimmunity
what does a disturbance in the balance cause?
immunodeficiancy syndromes
(state of unresponsiveness is created)
lack of helper
or excess of suppressor activity
Regulation of the Immune response
Immunodeficiency & autoimmunity
autoimmunity caused
excess helper
or reduced suppressor activity
Regulation of the Immune response
Immunodeficiency & autoimmunity
autoimmunity caused
excess helper
or reduced suppressor activity
Tissue/organ transplantation
Autografting
tissue moved from one location to another
Tissue/organ transplantation
Autografting
tissue moved from one location to another
Tissue/organ transplantation
synergenic graft
isografting; transplant from identical twins
Tissue/organ transplantation
synergenic graft
isografting; transplant from identical twins
Tissue/organ transplantation
allografting
homografting; transplant from geneticall different members of the same species
Tissue/organ transplantation
allografting
homografting; transplant from geneticall different members of the same species
Tissue/organ transplantation
xenografting
from different species
Tissue/organ transplantation
xenografting
from different species
Tissue/organ transplantation
rejection
hyperacute
in minutes to hours, because of preformed antidoner Ab and complement
Tissue/organ transplantation
rejection
hyperacute
in minutes to hours, because of preformed antidoner Ab and complement
Tissue/organ transplantation
rejection
accelerated
in days; reactivation to sensitized T cells
Tissue/organ transplantation
rejection
accelerated
in days; reactivation to sensitized T cells
Tissue/organ transplantation
rejection
acute
days to weeks, primary activation of T-cells
Tissue/organ transplantation
rejection
acute
days to weeks, primary activation of T-cells
Tissue/organ transplantation
rejection
chronic
months to years; causes not clear, may be Ab and CMI
Tissue/organ transplantation
rejection
chronic
months to years; causes not clear, may be Ab and CMI
Tissue/organ transplantation
rejection
graft-versus-host rejection
especially found in bone marrow transplantation, grafted T-cells attack host; symptoms include rash, jaundice, diarrhea, GI hemorrhage
Tissue/organ transplantation
rejection
graft-versus-host rejection
especially found in bone marrow transplantation, grafted T-cells attack host; symptoms include rash, jaundice, diarrhea, GI hemorrhage
