Reading...
Play button
Play button
Use LEFT and RIGHT arrow keys to navigate between flashcards;
Use UP and DOWN arrow keys to flip the card;
H to show hint;
A reads text to speech;
68 Cards in this Set
- Front
- Back
|
Small pox vaccine
|
production began 1867
effective vaccine 1977 no animal resovoire asymptomatic - easily identified |
|
|
Polio vaccine
|
eratication initiated by politics
countries in need don't trust westerners with vaccine |
|
|
Active Immunization
|
results in immune response that creates memory
artificial - vaccine, bypass natural disease/infection natural - get sick, produce memory response |
|
|
Passive Immunization
|
transfer of protection
instantaneous w/ Ab temporary - Ab decay artificial - injection of Ab, possibility of response against foreign serum and anaphylaxis natural - transfer of Ab from mother to child through placenta or breast milk |
|
|
Herd Immunity
|
idea that one vaccine won't work for everyone due to variations in MHC and TCR or by hole in repotoire, but the chance of an unprotected person coming in contact with an infected person is very rare
|
|
|
Live Whole Organism Vaccines
|
attenuated by adapting ways in which it grows
pathogenicity decreased, immunogenicity stays the same Ex. BCG for m. Tb grown on concentrated bile 13 years Sabin Vaccine (OPV) in chimp kidney cells Measle Vaccine in duck embryo cells |
|
|
Adv/Disadv of Live Whole
|
adv - very good immune response (humoral and cell mediated), one booster
disadv - effects if immunosuppressed, possibility of reversion and contamination (SV40 and OPV) |
|
|
Dead Whole Organism Vaccines
|
killed/inactivated by radiation or chemicals
ex. IPV |
|
|
Adv/Disadv of Dead Whole
|
adv - don't run risks of immunosuppression effects, reversion, or contamination, are more stable than live vaccines
disadv - not as good, mainly humoral response since virus can't replicate, poor Class 1 mediated response, organism might not be completely killed, requires multiple boosters |
|
|
Sub-Unit Vaccines
|
remove many of risks associated with the whole organism vaccines
|
|
|
Inactivated Toxins
|
neutralized toxins = toxoids
toxoid retains immunogenicity while preventing toxin from binding cell |
|
|
Capsular Polysaccharides
|
vaccines against sugars of capsule
Ab generated are against sugars, so no T-cell response, T-cells don't help B-cells, no class switching, no affinity maturation = poor memory |
|
|
Recombinant Vaccines
|
copy surface proteins to be used as vaccines
recombinant vector vaccines insert genes encoding different protein from the pathogen into another cell, immune response against that cell. Hep B first successful DNA vaccines and peptide vaccines |
|
|
DNA vaccine
|
encode antigen for pathogen using recombinant vectors.
DNA gun injects DNA w/ gold into muscles produce cell-mediated and Ab response cheap, easily made, highly stable, no reversion risk, require only 1 injection |
|
|
Cytokines on Recombinants
|
vaccines can also encode cytokines on recombinant vectors to produce additional responses
-encode IL-4 to produce Th2 response |
|
|
Tetanus
|
identified late 1800s
isolated Clostridium Tetani 1889 WWI passive immunizations 1924 tetanus toxoid for active immunizations in WW2 gram +, anaerobic, must infect deep tissues by deep wounds forms spores under unfavorable conditions Tetanus Ig-passive DTP-active |
|
|
Tetanospasm Toxin
|
highly toxic toxin produced by tetanus
less than 1mg causes infection but is not enough to induce immune response death rate 30% |
|
|
Neonatal tetanus
|
in newborns by inproper cutting of the umbilical cord
results in infection and death 500,000 deaths per year |
|
|
Hypersensitivity
|
misguided response against foreign antigens
Types 1-3 Ab mediated, minutes to hours Type 4 cell mediated 48-72 hours |
|
|
Type 1 hypersensitivity
|
mediated by IgE
B-cells bind and activate T-cells which produce IL-4 turning IgM to IgE IgE + mast cells/basophils = sensitized cells 2nd exposure allergen binding results in activation and histamine release |
|
|
FcER
|
two receptors must be cross-linked
type 1 has 4 chains abgg, b for signaling, a has Ig domains binding of aFcER1 can be enough to trigger release type 2 has membrane bound and soluble components, can be secreted, plays bigger role in IgE circulation |
|
|
Primary Mediators
|
preformed, already in granules
histamine from mast cells cause swelling ECP and NCF chemotatic factors for cell recruitment |
|
|
Secondary Mediators
|
produced by cell after granule release
leukotrienes, prostaglandins, cytokines (IL-4 and IL-5 from Tcells, IL-6 and TNF from macs) and kinins |
|
|
Systemic Response
|
results in shock and death
2-4 minutes in severe cases instantaneous inflammatory response by masts ans basophils |
|
|
Localized Response
|
more restricted to specific area, much less dangerous
|
|
|
Genetic involvement of Hypersensitivity
|
50% change of inheriting allergies from parents
not transfered w/ MHC - no allergen epitopes...downstream |
|
|
Influences in Ig isotype response
|
dose - low dose in BDF1 mice IgE response, high dose IgG response
presence of adjuvant (can also boost response and direc to either Th1, Th2 or Treg cells) |
|
|
number Th1/Th2 cells
|
w/ allergies more Th2
w/out allergies more Th1 |
|
|
Allergy screening
|
branching
type 1 in minutes type 2 and 3 in hours type 4 in days can possibly be dangerous and produce systemic response...epinephrine required RAST radio allergosorbent test, quantitates IgE specific for allergen, no diagnostic |
|
|
Wheal and Flare
|
swelling/redness indicating allergy response
wheal from edema flare from vasodilation |
|
|
Allergy treatments
|
avoid
allergy shots-hyposensitization, delivering small doses allergen over time to switch IgE response to IgG Antihistamines-block histamine receptor Cromolyn Sodium-block 2nd mediator production Theophylline turns off signaling cascade Epinephrine blocks mediator effects Cortisone reduces histamine production in granules |
|
|
Type 2 Hypersensitivity Response
|
5-8 hours
classical transfusion reactions mediated by IgM - blood type anti Ab by gut flora non-classical transfusion rxns mediated by IgG - RH, Kdd, Kell, Duffy cells need to see Ag first to make Ab response breakdown of these results in anemia or backup of blood particles |
|
|
Hemolytic Disease of Newborn
Drug induced Hemolyitic Anemia |
mother Rh- baby Rh+
IgG response against baby's blood cells treatment rhogan drug induced - allergy to penicillin |
|
|
Type 3 Hypersensitivity
|
mediated by immune complexes
2-8 hours complexes not cleared, high Ag/Ab leads to more complement activation, more breakdown products,neutrophil recruitment to breakdown complexes |
|
|
localized type 3
|
arthus rxn
complement intermediates mediate mast cells degranulation, recruits neutrophils and stimulates lytic enzyme release |
|
|
systemic type 3
|
foreign serum plus Ab
serum sickness/anaphylaxis |
|
|
Type 4 Hypersensitivity
|
cell mediated by Tdth
48-72 hours sensitized Tdth cells release cytokines that activate macrophages and Tcells that mediate direct cellular damage ex. poison ivy/oak |
|
|
B-cell immunodeficiency
|
more prone to extracellular pathogens (bacteria)
|
|
|
T-cell deficiency
|
more prone to intracellular pathogens (viruses)
|
|
|
Primary Immunodeficiencies
|
genetic/inherited
|
|
|
Secondary Immunodeficiencies
|
aquired by infectious agent (HIV) or treatment from hospital (chemo, immunosuppressants)
|
|
|
HIV Retrovirus
|
seconary deficiency
RNA virus reverse transcribed to DNA into genome,there for life proteins p32 integrase, p160 (p120 binds CD4, p41 binds chemokine receptors) |
|
|
Methods of HIV infection
|
sex, IV drug use, born from HIV parents
exchange of blood cells (cellular delivery of particles) |
|
|
Infection of HIV
|
gp120 binds to CD4 on target cells (tcells, macs, dcs) by conjugate formation.
lipid membranes fuse, mediated by CCR5, CXCR4 and gp41 |
|
|
lytic phase
|
period in which more HIV particles are made/released
|
|
|
latent phase
|
"provirus" responsible for latency in progression of HIV to AIDS
|
|
|
Seroconversion
|
weeks to months after infection p24 Ag levels drop, Ab levels rise
|
|
|
HIV progression to AIDS
|
by wiping out CD4 cells to under 200 cells/micL
activate provirus CD4 to make NFkB (HIV promotor) kill cell by complement, ADCC, or CTLs |
|
|
HIV treatment
|
AZT, ddC, Norvir (HIV drugs)
HAART - 3 drugs at once SCI HAART - HAART w/ interruptions disadv. multiple side effects, high costs, need for rest of life |
|
|
Knowledge to develop vaccine
|
agent 90%
immune response 50% what's protective 10% major problem |
|
|
situations favoring HIV existance
|
virus enters inside cell
progression time varies no good animal model repeated exposures money HIV drugs different general HIV types danger of some vaccines |
|
|
X-linked Agammaglobulinanemia
|
XLA
1/200,000 people absence of Bcells, no Ab BTK protein deficiency, preBcells dont become Bcells presents after 9 months when baby loses mothers Abs |
|
|
X-linked hyper IgM syndrome
|
high IgM levels
low IgG IgA and IgE levels T-cell defect, no CD40L so no class switching and no affinity maturation, IgM never gets better |
|
|
IgA deficiency
|
most frequently found Ig deficiency
lowers mucosal immunity |
|
|
DiGeorge Syndrome
|
no thymus-no Tcells
negative effect of Ab (Tcells can't help Bcells) Nude Mice thymic transplant |
|
|
SCID
|
most common missing IL-2Rg chain effects many other chemokine receptors, wipes out humoral responses
2nd ADA PNP deficiency, buildup of AMP and GMP, destruction of B/Tcells gene therapy bone marrow transplant bubble |
|
|
Bare Lymphocyte Syndrome
|
MHC definiencies
type 1 - no class 1 no CD8 type 2 - no class 2 no CD4 type 3 - no MHC, no CD8 or CD4 bone marrow/thymic transplants |
|
|
Leukocyte Adhesion Deficiency
|
deficiency in CD18 resulting in non functional LFA1, problems in cells getting from one place to another, no conjugate formations.
|
|
|
Chronic Granuloma Disease
|
CGD
problems with neutrophils phagocytize by can't kill granulomas form when neuts harbor pathogen death by age 7 IFNg therapy gets neuts to kill |
|
|
Autoimmune Diseases
|
immune responses against self proteins
5% US pop, more women (hormones) organ specific/systemic |
|
|
Organ specific
|
insulin dependent diabetes mellitus specific to pancreas beta cells preventing insulin production
|
|
|
systemic autoimmunity
|
systemic lupus erythematosus (SLE) immune complex disease response against DNA, RBC
major inflam response |
|
|
Tcell anergy
|
prevents signal 2 to turn off self reactive cells
|
|
|
Release of sequestered Ag
|
Ag hidden from immune system released and not recognized so attacked...myelin basic protein causes MS
Trauma eyes and testes |
|
|
Molecular Mimicry
|
induction of autoimmunity by a pathogen that looks like self
cross rxn responses measles virus P3 looks like Myelin basic protein |
|
|
Inappropriate MHC Class 2 expression
|
centered around IFNg
contributes to diabetes MHC expressed on beta cells of pancreas lymphocytes attack and kill pancreatic infection activated Th1 cells produce IFNg which binds to Bcells and kills them. |
|
|
Polyclonal B-cell activation
|
attacking wide range of clones
EBV targets and activates Bcells including self reactives. person w/ EBV has DNA Abs, IgG Ab, histone Ab Rheumatoid arthritis by IgG specific IgM causing immune complexes in joints |
|
|
Autoimmune therapy
|
immunosuppression w/ corticosteroids
may make patient more suseptible to infectious diseases targeting self reactive CD4 Tcells |
