Immunology I Flashcards
antigens
anything that causes an immune response
can be a bacteria virus, fungi, parasite, or a smaller protein they express
these are also known as pathogens
how are a pathogen’s presence announced to the immune system
antigens, act as name tags
are antigens specific or general
they can be both, they are general ones that say danger, but there are other that tell what it is and what it will do
what is an antibody
immunoglobulin or Lg is protein molecule created by our immune system to to target an antigen for destruction
how do antibodies worl
the proteins bing to the foreign antigen and disable the anti, tagging it for destruction by the other immune system defenses
cytokines
cell to cell communication proteins that control cell development differentiation and movement to a specific part of the body
how are cytokines produced
a variety of leukocytes
interleukins
(IL) are 13 cytokines that are regulators of the immune responses inflammatory reactions and hematopoiesis
which IL’s are responsible for fever
1 and 6
what causes the acute phase response
IL 6 causes acute phase responses
tumor necrosis factor
activates neutrophils
mediates septic shock and causes tumor necrosis
chemokine s
`type of cytokine released by infected and injured cells, they initiate an immune response
and signals to circulating neutrophils and macrophages
which cells are responsible for warning neighboring cells of a threat
chemokine
interferons
IFN block virus replication 3 types alpha beta and gamma
gamma interferons
are the strongest type of interferon and are produced by the T cells
they activate macrophages natural killer cells and neutrophils
what cells do gamma interferons activate
macrophages, NKC, and neutrophils
classifying interferons
2 types, type one and two
type one are alpha and beta
type two is gamma
Type I Interferons
function to induce viral resistance in cells, can be produced by almost any cell type in the body can at times under some circumstances suppress the T cell responses and memory T cells
Type I cells in influenza
limit viral replication but create pathological inflammation in the lung
type I cells and bacteria
may interfere with bactericidal mechanisms
type II Interferons
secreted only by NTC and T lymphocytes
main purpose is to signal to the the immune system to respond to infectious agents or cancerous growths
basic roles of the immune system
barrier, recognition of foreign none self and mutated cells, and destruction through processes such as phagocytosis
the two branches of the immune system
innate and adaptive, however cross over occurs between the two functions of both of these branches
Innate immune branch
considered natural and non specific
acts fast
adaptive immune system
considered specific, humoral, and cell mediated
acts slow
hematopoiesis
the formation and development of cells that make up the blood
in an embryo and fetus this occurs mainly in the liver and spleen
birth to adult hematopoiesis occurs primarily in bone marrow small amount in lymphatic tissues
innate immunity characteristics
immediate, non specific response so there is no stored memory (a lot of cells will die anyways) and one response does not increase the next response, or no greater responses occur with repeated exposure
skin
physical barrier, protects against invasion, the acidic of sweat acts as barrier, fattry acids and enzymes form pores and follicles
lysoymes
contain lysozyme thigh protects against gram + bacteria
commensal bacteria
physical barrier, out normal bacteria flora, both internal and external that will compete with potential pathogens for resources, however they can be upset by antibiotic use leading to reduced concentration greater opportunities for pathogens to use resources
inflammation
damaged tissues and cells release histamine, prostaglandin and leukotriene which causes vasodilation and leaky capillaries
there is also cell mediated heparin realize which decreases clotting
heparin
reduces clotting
result of inflammation
Increased blood flow to area, immunologic factors leak out of capillaries into interstitial space to do their jobs
first step of inflammation response
damaged tissues release histamine, increasing blood flow to the area (redness)
second step of inflammation response
histamine = leaky capillaries releasing in the release of phagocytes and clotting factors into the wound
third step of inflammation response
the phagocytes engulf bacteria dead cells and cellular debris
fourth step of inflammation response
plates move out of the capillaries to seal off the wound
adhesion molecules in the inflammation process
membrane proteins that connect cells to other cells to the ECM
their major role is the recruitment of neutrophils to the site of inflammation
how do neutrophils come to the site of inflammation
are recruited by adhesion molecules and roll along the luminal surface of blood vessels towards the site of injury and then will squeeze out of leaky capillaries (between the cells of capillary walls)
describe chronic inflammation
cause a chronic release of cytokine and leukocyte infiltration and the release of lysozyme and free radicals which cause an overall tissue damage
what are possible complications of mutations in the adhesion molecules
atherosclerosis in the macular system, skin and kidney issues muscles, alzhemiers and autism (chronic inflammationP
basophils
granulocytes are the least common and mature in the bone marrow
circulate the blood stream
cause allergic and helmet responses
release histamine (increase blood flow) and heparin (reduce clotting)
eosinophils
derived from the bone marrow (1-6% CWBC)
are weakly phagocytic
and act as an APC
eosinophils location
in organs and bloodstream particularly the GI tract and respiratory tract
what do eosinophils release
release H202 and other oxygen radicals to kill microbes such as viruses and parasites
and leukotrienes
what may kill off a helminth
eosinophil by releasing h202 and oxygen radicals
what does the release of leukotrienes stimulate
cause smooth airway smooth muscle contraction
this is a lipid signaling molecule
when are eosinophils active
allergic reactions
what cells do eosinophils stimulate
T lymphocytes
neutrophils
granulocytes
most abundant of the. granulocytes
circulate the bloodstream
when are neutrophils primary active
bacteria and fungi defense
neutrophil mechanism
arrive within minutes
strongly phagocytic
how are neutrophils called to cite of injury
chemotaxis, respond to chemokins
neutrophils release other cytokines to recruit monocytes and macrophages
what are neutrophil extracellular traps
extracellular fibers released bu neutrophils that bind bacteria
mast cells
release histamine and heparin causing again the inflammatory cascade
mast cell maturation
leave the bone marrow as immature cells and mature in tissues
mainly present in issues that lie on boundaries
why do mass cell degranulate (and release histamine)
if they are injured
encounters antigen or allergen
exposed to complement proteins
anaphylaxis
massive release of histamine by mast cells vasodilation is body wide and leads to edema and decreased blood pressure
how are RBCs and PLYS derives
from the myeloid stem cell
monocytes
agranular
give rise to dendritic cells and macrophages
first developed int the bone marrow and the half are stored in the spleen and the other half migrate to tissues and differentiate into dendritic cells and macrophages
Monos, Macros and Dendros 3 primary functions
phagocytosis, APC, cytokine production
Dendritic Cells
aganular derived from monocyte
Antigens are captured by dendritic cells
what is the strongest APC
Dendritic cells best at activating helper-T lymphocytes
after finding antigen dendritic cell then migrates to the nearest lymph node & presents the antigen to T Cells and B Cells
langerhans cells
Specialized dendritic cells in skin
initial cellular targets in the sexual transmission of HIV,[8] and may be a target, reservoir, and vector of dissemination
macrophages
aganular derived from monocyte
Large phagocytes
release TNF and Interleukins (ILs)
Also act as APCs
macrophages location
the skin, lungs, GI tract and most other tissues
3 stages od macrophages
1) resting = cleaning up cellular debris (scavengers)
b) primed = more active engulfing of bacteria, display fragments of bacteria for T cells (act as APCs)
c) hyper-activated = inflammatory cytokines cause macrophages to enlarge and start rapidly destroying pathogens and/or cancerous cells
After digesting a pathogen, a macrophage will
present the antigen to a helper T cell
this occurs because
Antigen is integrated it into the cell membrane and displayed attached to an MHC class II molecule (MHCII)
The MHCII indicates to other white blood cells that the macrophage is not a pathogen, despite having antigens on its surface
Kupffer cells
Specialized macrophages within the liver
Destroy bacteria & old RBCs
Chronic activation of Kupffer cells
leads to overproduction of inflammatory cytokines & chronic inflammation
this happens through repeated exposure to toxins and alcohol
result is liver damage
macrophages and pathogens
phagocytes, macrophages may become hosts for pathogens!
for example with TB, leishmaniasis and cikigunya
Natural Killer Cells
cytotoxic lymphocytes, but don’t need to “recognize” or remember a pathogen to kill it
killing enhanced by cytokines secreted by macrophages, can still kill in resting state
bloodstream, liver and spleen
Natural Killer Cells active on
cancer and viruses
and cells that have unusual surfaces receptors
Natural Killer Cells granules
contain destructive enzymes
Natural Killer Cells maturation
mature in bone marrow lymph nodes spleen tonsils and thymus
how do Natural Killer Cells kill
releasing performs and proteases that cell cell membrane lysis or trigger apoptosis in the target cell
can also be accomplished by surface contact
Natural Killer Cells and viral infections
contain the viral infections while the adaptive immune response is generating antigen specific cytotoxic T cells (takes time) that will work to clear the infection
Major Histocompatibility Complex (MHC) Proteins/ Human Leukocyte Antigen (HLA)
Cell surface molecules which help the immune system to determine if a protein is “self” or “not-self”
Bind antigen to cell surface and display for recognition by T cells
3 sub-groups: MHC I,II & III
MHC key points
Determines organ donation compatibility
Autoimmune disease is a malfunction in this recognition system
Participates in T & B cell activation
how are Acute phase proteins produced
produced by the liver in response to inflammation induced release of IL 1 and IL6 and TNF from the T cells and macrophages
what are the Acute phase proteins
C-reactive protein (CRP)
mannose binding lectin (MBL)
lipopolysaccharide -binding protein
Acute phase proteins role
mark pathogens or injured cells for destruction
CRP example
CRP binds to bacterial and fungal cell walls and damaged or dead human cells, then activates complement
The Complement System
enhances the ability of phagocytic cells to destroy pathogens
comprised of 30 different proteins working together to signal the other cells that a pathogen is present and they have begun destroying it
The Complement System is activated. by
antigens
The Complement System are made in the
liver
The Complement System activation pathways
3 possible
Classical (requires triggering)
Alternative (continuously activated at low level)
Lectin Pathway (requires very specific type of triggering)
the most abundant complement protein in humans
c3
functions of complement
opsonization, chemotaxis and lysis
opsonization
enhancing phagocytosis of antigens by ‘marking’ them for destruction
Chemotaxis
attracting and activating macrophages and neutrophils; inducing mast cells & basophils to degranulate
Lysis
rupturing pathogen cell-membranes by forming the Membrane Attack Complex (MAC)
Complement Fixation
antigen combines with an antibody and its complement, causing the complement factor to become inactive or fixed exposing the patient’s serum to antigen, complement, and specially sensitized red blood cells.
Complement-fixation tests can be used to detect
antibodies for infectious diseases, especially syphilis and viral illnesses
MAC
Membrane Attack Complex
C5b forms a complex with c6 c7 c8 and c9 to form MAC
causes lysis of cell by disturbing osmotic balance
more concentrated within the cell so microbe will swell and burst
antibodies
recognizes only one nation and bind to a specific site on the invader
how do antibodies function
directly blocking binding of invader to the cell
inactivate viruses and neutralize the toxin
mark the pathogen for destruction by phagocytes called opsonization
antibody structure
2 light chain 2 heavy changes
antigen binding site
fab legion and fc region
Fab region
antigen specific variable
Fc region
constance class effect
IgM
big first class to be produced
half life 10 days
increase Igm is a recent exposure to antigen
IgM location
because it is Large molecule- usually confined to intravascular space but inflammations opens capillaries and also entrance of Igm to interstitial space
igG
4 subclass only class that crosses the placenta longest half life 23 days use it for passive immunity in rabies and hepatitis
IgG location
blood lymph CSF and peritoneal fluid
evenly distributed in the intra and extra vascular space
IgG placenta
passes mothers immunity to child
bad if the mom forms IgG against fetal antigens
difficult to use IgG as an indicator of infection in the baby
IgG functions
helps natural killer cells find their targets through opsonization
immobilizes bacteria by binding to cilia
activates complement
neutralizes toxins and viruses through binding
polyclonal antibodes
Prepared from immunized animals
Each Ab can interact/bind with multiple sites on an antigen (human antigens can only interact with one )
monoclonal antibodies
Produced in the lab
Bind only to one site on an antigen
IgA locaion
external secretions
mucus tears salvia gastric fluids colostrum (first breast milk) and sweat
IgA function
protect of infants through breast milk
prevents viruses from entering the cells
prevent pathogens from attaching to and penetrating epithelial surfaces
high function in respiratory and GI tracts
IgE
present in low amounts
2 day half life
bind to mast cells and basophils when it discovers and antigen and trigger degranulation which releases mistime and leukotriene
and heparin from granulocytes
when is IgE increased
atopic (hyper allergic) individuals and in the presence of parasites
IgD location
surface of naive B cells
present in low amounts in the serum
IgD function
unknown
components of adaptive immune system cell mediated
T-cells
B-cells
components of adaptive immune system
T-cells B-cells Antibodies Complement APCs
adaptive immune system
requires days to develop
specific to an antigen
response is enhanced through repeated exposure
develops a memory that is more rapid and intense in its immune response
primary Lymphoid Organs
where the lympocycces grow up and proliferate
thymus (T cell in children)
and bone marrow
Secondary Lymphoid Organs
Where antigens are presented to mature (but naïve) B & T lymphocytes to initiate the adaptive immune response
spleen lymph nodes tonsils and adenoids and appendix
B-Cells (B-lymphocytes)
eliminate extracelular pathgens
is an APC with MHC
will produce antibodies
Has membrane-bound antibodies
Recognition of antigen by the B-cell receptor coupled with a signal from “Helper” T-cells (CD-4), prompts the B-cell to divide into “clones”
some of these are effector cells produce antibodies
others are memory B cells
T-Cells (T-lymphocytes)
destroy the intracellular patens viruses and intracellular bacteria
has subtypes
Killer” T-cells (CD-8)
T-Cell T-lymphocytes)
cytotoxic
specialize in identifying and killing cells infected with virus
Helper T cells (CD4)
Does not directly kill pathogens- raises the “alarm” via cytokines
Assists in the activation of “killer” T-cells
Signal B cells to begin secreting antibodies (Ig)
Activated cell differentiates into effector cells & memory cells
acquired immunodeficiencies
medications (steroids, chemotherapy), malnutrition, splenectomy (or functional asplenia), some cancers, AIDS
congenital or primary immunodeficiencies
autosomal recessive or X-linked, impaired or absent granulocyte, complement or lymphocyte production. May be an immunoproliferative disorder
