Chapter 21 (Lecture) Flashcards
ability of the body to resist many agents (both living and nonliving) that can cause disease; resistance to disease
immunity
- first line of defense: surface barriers such as intact skin and mucosae
- second line of defense (internal): antimicrobial proteins, phagocytes, fever, NK cells, and other cells; hallmark is inflammation
- NO MEMORY
innate (nonspecific) immune system
- takes considerably longer to mount
- humoral immunity
- cellular immunity
- MEMORY; each response is unique, and second exposure is quicker
adaptive (specific) defense system
- a functional system rather than an organ system in an anatomical sense
- structures are a diverse array of molecules plus trilions of immune cells (especially lymphocytes) that inhabit lymphoid tissues and circulate in bodily fluids
immune system
harmful or disease-causing microorganisms
pathogens
benefits of keratin
resistant to most weak acids, alkalis and bacterial enzymes
protective chemicals of the innate immune system
- acid (acid mantle)
- enzymes
- mucin
- defensins
- lipids, sebum and dermicidin
protective mechanism: normally acidic pH inhibits bacterial growth; cleanses the lower urinary tract as it flushes from the body
urine
protective mechanism: continuously lubricate and cleans eyes (tears) and oral cavity (saliva): contain lysozyme, an enzyme that destroys microorganism
tears, saliva
protective mechanism: inhibits growth of most bacterai and fungi in female reproductive tract
acid mantle of the vagina
protective mechanism: contains concentrated hydrochloric acid and protein-digesting enzymes that destroy pathogens in the stomach
gastric juice
protective mechanism: propel debris-laden mucus away from nasal cavity and lower respiratory passages
cilia
protective mechanism: filter and trap microorganisms in respiratory and digestive tracts
nasal hairs
protective mechanism: traps microorgansim in respiratory and digestive tracts
mucus
protective mechanism: skin secretions (sweat and sebum) make epidermal surface acidic, which inhibits bacterial growth; also contain various bactericidal chemcials
acid mantle of skin
vesicle formed as a result of phagocytosis
phagosome
- phagocytes
- about 126B/day produced
- usually the first WBC to make it to an infection
- 1 time use
neutrophils
made up of dead neutrophils, microbes, pathogens
pus
- monocytes in blood, this in tissue
- leave blood and increase in numbers at site of infection
- cleanup crew
- dendritic cells, microglia, alveolar, hepatic
macrophages
- mobile
- release factors that attract more WBCs
basophils
- immobile
- are found near sites of possible pathogen influx
- release chemotaxic factors
- can also phagocytize bacteria
mast cells
factors that attract more WBCs
chemotaxic factors
act as moderators of inflammatory response and kill parasites by releasing enzymes all over them
eosinophils
- B cells and T cells
- Natural Killer Cells (NKC)
lymphocytes
recognize tumor and cancerous cells in general
NKC (natural killer cells)
- prevents the spread of damaging agents to nearby tissues
- disposes of cell debris and pathogens
- sets the stage for the repair process
inflammatory process
cardinal signs of inflammation
- redness
- heat
- swelling
- pain
- happens after first exposure, involves the creation of killer T cells and memory cells
- usually takes about 3-7 days, and you will feel sick during this time
primary response
occurs upon a repeated exposure to the same antigen or a similar formand the memory clels recognize it and the response is faster and of greater magnitude
secondary response
long-lived and require less activation to respond than do other APCs
memory T cells
- production is regulated by helper T cells and antigen presenting cells
- once activated, proliferate and produce Killer Ts and memory T cells
cytotoxic T cells
effects of cytotoxic T cells
- cause cells to lyse (contact killing) by releasing perforins
- cause the release of cytokines that attract cells such as macrophages and WBCs (inflammatory response)
caused by the release of histamines, prostaglandins, etc. from the injured tissues
vasodilation
allows protein rich fluid to seep into the injured region from the blood vessels
vascular permeability
which factors cause edema in the injured area
vasodilation and vascular permeability
steps of phagocyte mobilization
- leukocytosis
- margination
- diapedesis
- chemotaxis
follows chemical signals to injured site
chemotaxis
true or false:
inflammatory response can be localized or systemic in nature
true
functions of antimicrobial proteins
- preventing entrance to cell
- vasodilation
- increased permeability
- attracting WBCs
- increasing phagocytosis
- protects body against viral attack
- mobilize NK cells
- can be released by lymphocytes to cause widespread immune mobilization
interferon
virus infected cells produce interferon which
stimulates neighboring cells to produce antiviral proteins
A group of bloodborne proteins, which, when activated, enhance the inflammatory and immune responses and may lead to cell lysis.
complement system
classical complement pathway is stimulated by
antibodies
alternate complement pathway is stimulated by
factors C3 which break down into different compounds
complement works in which response
both the innate and adaptive resopnses
a systemic response that involves the release of pyrogens
fever
events of phagocytosis
- phagocyte adheres to pathogens or debris (using receptors)
- phagocyte forms pseudopods that eventually engulf the particles, forming a phagosome
- lysosome fuses with the phagocytic vesicle, forming a phagolysosome
- toxic compounds and lysosomal enzymes destroy pathogens
- sometimes exocytosis of the vesicle removes indigestible and residual material
- wander throughout the tissue spaces in search of cellular debris or “foreign invaders”
free macrophages
such as stellate macrophages in the liver, are permenant residents of particular organs
fixed macrophages
when neutrophils enter blood from the bone marrow
leukocytosis
neutrophils cling to the capillary wall
margination
neutrophils flatten and squeeze out of capillaries
diapedesis
steps of interferon release/production
- virus enters cell
- interferon genes switch on
- cell produces interferon molecules
- interferon binding stimulates cell to turn on genes for antiviral proteins
- antigen-antibody complex
- C1, C4, C2 complex
classical pathway of complement system
coats pathogen surfaces, which enhances phagocytosis
opsonization
steps to contact killing
- cytotoxic t cell binds tightly to the target cell when it identifies foreign antigen on MHC I proteins
- Tc releases perforin and granzyme molecules from the granules by exocytosis
- perforin molecules insert into the target cell membrane, polymerize, and form transmembrane pores similar to thsoe produced by complement activation
- granzymes enter the target cell via the pores. once inside, the proteases degreade cellular contents, stimulating apoptosis
- Tc detaches and searches for another prey
steps TH cells use to help in humoral immunity
- TH cells binds with the self-nonself complexes of a B cell that has encountered its antigen and is displaying it on MHC II on its surface
- TH cell releases interleukins as a co-stimulatory signals to complete B cell activation
steps of TH cells in cell-mediated immunity
- previously activated TH cell binds dendritic cell
- TH cell stimulates dendritic cell to express co-stimulatory molecules needed to activate CD8 cell
- dendritic cell can now activate CD8 cel with the help of IL2 secreted by TH cell
steps to the activation of T cells
- dendritic cells engulfs an exogenous antigen, processes it,, and displays its fragments on class II MHC protein
- immunocompetent CD4 cell recognizes antigen-MHC complex. both T-Cell Receptor and CD4 protein bind to antigen-MHC complex
- CD4 cells are activated, proliferate, and become memory and effector cells
- fixes complement, often first produced
- powerful agglutinogen
IgM
secreted into tears and colostrum, protects body surfaces
IgA
binding site on B-cells
IgD
activates complement, found in plasma
IgG
binds to mast cells and basophils, stimulates inflammation
IgE
types of active immunity
- naturally acquired
- artificially acquired
types of passive immunity
- naturally acquired
- artificially acquired
types of humoral immunity
- active
- passive
immunity that comes from infection; contact w/ pathogen
naturally acquired active immunity
acquired from vaccines; dead or attenuated pathogens
artificially acquired active immunity
comes from antibiodies passed from mother to fetus via placenta; or to infant in her milk
naturally acquired passive immunity
acquired from injection of immune serum (gamma globulin)
artificially acquired passive immunity
why can B-cells act as APCs
their receptors are antibodies
- dendritic cells, macrophages, activated B lymphocytes
- engulf antigens and produce fragments on their surface attached to MHC complexes
antigen presenting cells
- spontaneous activation
- stabilizing factors B, D, and P
- no inhibitors on pathogen surface
alternative complement pathway
- secreted by macrophages and neutrophils exposed to foreign substances
- stimulates the hypothalamus to make prostaglandin E
pyrogens (IL1)
what is the role of prostaglandin E
raises the set point for the body’s internal temperature
how do NSAIDs reduce fever
by inhibiting PGE synthesis
benefits of fever/pyrexia
- promotes interferon activity
- elevate metabolic rate to promote healing
- inhibit reproduction of pathogens
anything above what internal temperature will cause delirium and higher temperature cause irreversible damage
105
- found in macrophages, B cells, and monocytes
- processed antigens will cause costimulation to occur
MHC II
found in nucleated cells, causes red flag to be raised if they display a foreign antigen
MHC I
- displayed by all body cells, usually by MHC I complexes
self antigens
- region on the surface of an antigen that is immunogenic
- simple antigens may have only one or two of these
- more complex ones may have hundreds that bind and activate different types of antibody
antigenic determinants/epitopes
usually polymers that are not deemed reactive by the body
implants
- both immunogenic and reactive
- viruses, bacteria, fungi, etc
complete antigens
haptens, pet dander, poison ivy, cosmetics, perfumes
haptens
reactive, but not immunogenic so they only cause a reaction if they bind to other proteins in our body
haptens
- any molecule that triggers an immune response
- usually have a fairly high molecular weight
- complex molecules that are unique to individuals (proteins, polysaccharides, glycoproteins, glycolipids)
- body usually only attacks “non-self”
antigens
Ag, antigen generating
- antigen-specific
- systemic
- memory
- two major components: humoral and cell-mediated immunity
adaptive response
which lymphocytes are responsible for humoral immunity
b cells
which lymphocytes are responsible for cell-mediated immunity
T cells
produced from lymphoblast precursors in red bone marrow
lymphocytes
reach maturity in the bone marrow before being released
B cells
immature T-cells migrate where before maturation
thymus
- created in red bone marrow, but soon leave
- mature in thymus gland–undergo positive and negative selection
- after selection they colonize lymphatic tissue and organs everywhere in the body
T-cells
if they do not react to foreign antigens or if they DO react to self antigens they are culled from the population
negative selection
if they react to foreign antigen, but not to self antigen
positive selection
- mature in bone marrow
- undergo a similar type of seletion as T cells
- once they are mature they colonize many of the same tissues as T cells
B cells
overall goal of any cell that acts as an APC
interact the antigen and then stimulate the two arms of the specific immune response
true or false:
T cells can detect antigens on their own
false
the process wherein the MHC II complex of an APC binds with a helper T cell and this stimulaates the release of cytokines between the two cells which causes the helper T cells to either:
* proliferate and produce more helper T cells
* stimulate B or T cells
costimulation
- most effective agianst intracellular microorganisms such as viruses, fungi, bacteria, and parasites
- activation regulated by antigen-presenting cells and helper T-cells
T-cells
types of T cells
- cytotoxic
- helper
- memory
killer, CD8, or T8 t-cells
cytotoxic T cells
CD4 T-cells, activate CD8 cells and also stimulate antibody mechanisms
helper T cells
come from cytotoxic cells and remember the pathogens
memory T cells
- have receptors on their surface for an antigen
- when they are challenged by an antigen, activates specific receptors and begins stimulating them to divide
naive B cells
rapidly creates plasma cells and memory cells
clonal selection of B cells
secrete antibodies at rates up to 2000/s for 4-7 days
plasma cells
long lived and retain the imprint of the antigen so they can respond almost immediately to future attacks
memory cells
effects of antibodies
- neutralization
- agglutination
- precipitation
- complement
antibody can bind directly to the antigenic determinant and interfere with or deactivate the antigen
neutralization
antibody can combine with the antigenic determinants on two antigens rendering them ineffective adn making them more susceptible to phagocytosis
agglutination
small water soluble antigens are settled out of solution and are then engulfed
precipitation
antibodies can activate the complement cascade, and release factors which induce the inflammatory response and cell lysis
complement
variable regions of the antibody
heavy and light chains
regions of the antibody that bind and activate the complement
constant regions
what are B cells most effective against
extracellular bacteria, parasites, and viruses
B cells respond to invasion by producing antibodies that are specialized globulins known as
immunoglobulins (Ig)
antibodies are injected from another source
passive immunity
w
individuals will produce their own antibodies
active immunity
individual is exposed and develops antibodies and memory cells
active natural immunity
- vaccination; antigen is introduced in altered form
- memory cells formed
active artificial immunity
- passed from mother to newborn through placenta/milk (IgA)
- effects wear off in a few months as the child’s own immune develops
passive natural immunity
- antibodies taken from another source are given via a vaccination
- quick fix as body will produce no antibodies naturally
passive artificial immunity
steps to fever onset
- hypothalamic thermmostat is reset to higher set point
- onset: body temp rises
- stadium: body temp oscillates around new set point
- infection ends, set point returns to normal
- defervescence: body temp returns to normal
steps to lymphocyte maturation
- lymphocytes destined to become T cells migrate (in blood) to the thymus and develop immunocompetence there. b cells develop immunocompetence in red bone marrow
- immunocompetent but still naive lymphocytes leave the thymus and bone marrow. “seed” the lymph nodes, spleen, and other lymphoid tissues where they encounter their antigen
- antigen-activated immunocompetent lymphocytes (effector cells and memory cells) circulate continuously in the bloodstream and lymph and throughout the lymphoid organs of the body
steps to endogenous protein processing and display
- endogenous antigen is degraded by protease
- endogenous antigen peptides enter ER via a transport protein
- endogenous antigen peptide is loaded onto class I MHC protein
- loaded MHC protein migrates in vesicle to the plasma membrane, whete it displays the antigenic peptid
steps to exogenous protein processing and display
1a. class II MHC synthesized in ER
1b. extracellular antigen is phagocytized
2a. class II MHC is exported from ER in vesicle
2b. phagolysosome degrades antigen
3. vesicle fuses with phagolysosome, invariant chain is removed, and antigen is loaded
4. vesicle with loaded MHC migrates to the plasma membrane
MHC II display can cause
costimulation
fluid containing clotting factors and antibodies
exudate
- a lipid-based chemical messenger synthesized by most tissue cells; acts locally as a paracrine
- produced from arachidonic acid
prostaglandins
vasodilation of local arterioles cause
local hyperemia
increased blood flow due to vasodilation of blood vessels entering the injured area
hyperemia
which minerals needed for bacterial reproduction do both the liver and spleen sequester during a fever
iron and zinc
when collagen fibers are laid down to a wall of a sac of pus, what structure is formed
abscess
mechanism of complement proteins
foorming pores in the membranes of target cells
function of neutrophils
phagocytes, will migrate to the site of an infection within a few hours
fever inducing molecules are secreted by leukocytes and macrophages
pyrogens
which defense cells are common antigen presenting cells (APCs)
macrophages
caused by excess tissue fluid in the injured area; helps to dilute harmful substances and brings in excess oxygen
edema
nonspecific defense cels specialize in attack cancer cells and virus-infected cells
natural killer cells
enzyme in saliva and lacrimal fluids that destroys bacteria
lysozyme
a process of coating a pathogen to enhance phagocytosis
opsonization
fluid that seeps from the capillary contains clotting factors and antibodies during inflammation
exudate
when a localized area exhibits increased capillary filtration, hyperemia, and swelling, it is indication that
inflammation is occurring
an increase in the number of white blood cells that are in circulation
leukocytosis
process in which neutrophils squeeze through walls of capillaries into the tissues
diapedesis
a person may harbor pathogens walled off in … for years without displaying any symptoms
granulomas
first line of defense against pathogens
skin and mucous membranes
which of the following is the most specific internal defense against disease
a. inflammation
b. NK cells
c. T cells
d. phagocytes
T cells
T cells are a part of the adaptive (specific) defenses against disease. They are involved in cell-mediated immunity as they defend the body against specific pathogens.
brings more leukocytes to the site of infection
inflammation
true or false:
virus-infected cells secrete interferons to “warn” other cells of the presence of virus and these other cells and inhibit viral replication
true
role of interferons in defense against disease
protects cells that have not yet been infected by viruses
- requires that circulating antibodies are bound to antigens
- an example of overlap between innate and adaptive immune function
- will result in enhanced inflammation, opsonization as well as formation of MAC proteins
classical activation of complement system
- sets the stage for repair processes
- prevents the spread of injurious agents to nearby tissue
- disposes of cellular debris and pathologies
functions of the inflammatory process
redness and heat of an inflamed area are due to local hyperemia caused by
vasodilation
unless they are attached to protein carriers, haptens have … but not …
reactivity but not immunogenicity
how do vaccines work
by priming the adaptive immunity with a relatively harmless primary exposure
artificially acquired active immunity
results when naive lymphocytes are activated
primary response
result of activating memory cells
secondary response
A class I MHC protein presents an antigen. What type of cell is likely presenting and to what type of cell would it be presented?
Any nucleated cell would present antigens to a CD8 cell.
Which lymphocytes act as the bridge between the cellular and humoral responses?
helper T cells
What types of antigen do mature T cells normally not recognize?
self antigens
