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93 Cards in this Set

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What is the difference between the non-specific resistance and specific immunity?

specific = has to do with the intracellular foreign agents and defense against a particular foreign particle

non-specific = first line of defense for foreign particles

What are some of the non-specific resistance mechanisms used by different organ systems?

non-specific = lacks specificity and memory

- normal microbiota

- physical barriers

- chemical mediators

- intracellular immunity

- phagocytosis

- natural killer cells

- inflammation

What are the characteristics of skin?

has keratin and nails acting as a first line of defense

What are the characteristics of mucous membranes?

has antimicrobial secretions

has cilia

What are the antimicrobial secretions of mucous membranes?

lactoperoxidase - creates a reactive oxygen species which is toxic to microbes

lactoferrin - sequesters iron which limits multiplication

lysosome - breaks down (hydrolyzes bonds), likely in gram positive bacteria

What is the difference between bacteriocins and cationic peptides?

both have properties able to induce immune functions such as cytokines, chemotaxis, etc.

bacteriocins are found on gram+/- bacteria and are lethal to similar species

cationic peptides are produced by the host and made by positive cells which alter membrane permeability

What is the complement system?

- ability to defend against bacterial infections by increasing phagocytosis (opsonization)

- enhances antibodies and memory

- punctures cell membranes causing cell lysis

- promotes inflammatory response

What is a cytokine?

a soluble protein or glycoprotein released by cell population and act as signalling molecules

What are some of the effects of cytokines?

proliferation and differentiation

activation of chemotaxis

regulation of differentiation

activation of specific molecules

induction of apoptosis

What is chemotaxis?

movements of leukocytes to a damaged area

What is inflammation?

removal of foreign invaders

- release of neutrophils

- lactoferrin proteins

- complement proteins

- mast cells releasing histamines

What is the interferon response?

prevents nearby cells from replicating and assembling

What are acute phase proteins?

recognizing foreign material to release cytokines, liver stimulation, acute phase protein production

- activates the complement system

- enhance opsonization but more so phagocytosis

- trap microbes and debris

What is phagocytosis? How does it happen?

phagocytic cells will recognize, ingest and kill extracellular microbes

- will fuse with a lysosome

- helps destroy foreign invader by acid, lysosomal degradative enzymes and antimicrobial peptides

What is autophagy?

destroy intracellular pathogens or pathogens escaping from phagosomes

forms an autophagosome and is destroyed by chemicals as in phagocytosis

What is ubiquitin?

a protein coat which tags the foreign particles for destruction

What is the role of natural killer cells?

-release perforins to create holes in cell membrane

- granzymes will induce apoptosis

What is opsonin-dependent phagocytosis?

can be greatly increased by opsonization

- complement, acute-phase and antibodies will bind to the surface of foreign cells

What is PAMPs?


What are the four types of lymph organs?

bone marrow: site of hematopoiesis

spleen: filtration of blood

lymph node: lymph filtration

thymus: T-cell maturation

What is an epitopes?

small 3-D portions of an antigen recognized by a single immune receptor

What is an antigen?

molecules that confer immunogenicity which are recognized as foreign and unique

What is the mechanism of clonal selection?

formation of large diverse lymphocyte pool that can bind to large range of antigenic epitotes

- stimulated cells with proliferate and differentiate to produce clone cells which later form effector and memory cells

What is the MAC?

membrane attack complex which is activated upon complement proteins

- make pores on foreign particles

- leads to cell lysis

What the the names of the different complement proteins?




What is the difference between the effector response and memory response?

memory response is important for a second exposure to respond in a faster fashion and is long-lived

effector: eliminates or renders foreign entity bacteria

memory: upon second encounter with same foreign entity in a faster and more intense response

What is a antigenic determinant?

epitote which is something that is recognized by the immune system

What is the function of antigen presenting cells in the specific immune system?

helps present the antigens to cells such as cytotoxic or helper cells

present antigens endogenously or exogenously

Why should cells not expressing MHC-I be targeted for destruction?

these cells are unregulated, could be cancerous or infected with viruses but all cells will express MHC-I saying these are self-cells and should be left alone unless bound with an AOC

What is the significance of the light and heavy chain?

regions of the antibodies which will can result or partake in rearrangement to generate diversity by using DNA splicing and hypermutuations

What are superantigens?

bacterial and viral proteins which stimulate a stronger immune than normal by tricking variants of the T-cells into activation

stimulates the release of massive quantities of cytokines from T-cells and results in a hyper reaction

What contributes to generating genetic diversity?

- rearrangement of antibody-gene segments

- generation of different codons during splicing or gene segments

- insertion of nucleotides during splicing

- hypermutations

- combination of light and heavy chains

What is the secondary antibody response?

B and T cells will mount a heightened memory-based response with a shorter lag time, rapid log phase and binds with a higher affinity

What does the secondary antibody response need?

reserves of memory cells

IgM --> IgG heavy chain switch

somatic hypermutations of the V regions

What are the types of acquired immunity?

natural or artificial and later active or passive

What is microbiota?

the normal mixture of microbes in the host body

What is used to determine the different microbiota in hosts today?

use of metagenomics:

- isolate DNA from samples of specific body regions

- amplify DNA fragments using PCR and random primers

- sequencing DNA fragments

How has our knowledge of microbiota been expanded?

use of genetic sequencing (cheap, easier, and quicker)

Why is it best to use metagenomics?

not all microbiota are culturable

Where is the largest population of microbiota in the body and why?

large intestine because of elimination due to peristalsis, replaced rapidly due to reproduction and regular food intake, microbes present are anaerobes or facultative anaerobes

What are the metabolic benefits of intestinal microbiota?

- produce neurotransmitters

- produce nutrients that can be used

- convert nutrients into short chain fatty acids to feed microbes

- convert billirubin

What are superorganisms/holobionts?

- emerge when gene-encoded metabolic processes of the symbiont become integrated with those of the host

- blend of host and microbial traits where host and microbial cells co-metabolize various substrates

What is the normal immune function of microbiota?

- prevent colonization by pathogens

- environmental control

- microbial warfare

What is the the hygiene hypothesis?

living in too clean of an environment =

- immune system does not mature properly

- may not react properly

- immune related health problems

- may overact

What is the difference between probiotics and prebiotics?

pro: certain living organisms meant to be applied or ingested with providing health benefits

pre - certain foods will be ingested to provide optimal conditions for growing beneficial microbiota

Why is the significance of C. difficile?

- an infection occurring in the hospital

- host in immunocompromised

- host may lack normal microbiota

- production of endospores (difficult to kill)

What is the difference between an experimental or correlational study?

experimental: manipulate and independent variable to see if there is an effect on the dependent variable

correlational: observe two groups that differ in one variable and see if there is any correlation with another variable

What is the difference between in vivo and in vitro?

vivo: living organism

vitro: in a lab on a petri dish

What is a cytokine storm?

release of massive quantities of cytokines from T-cells

(can be done by superantigens)

How can an infectious disease not be communicable?

a communicable disease is something that can be passed directly or indirectly through a contract, vehicle or vector

not communicable would be unable to be spread in this manner ie. food poisoning

How can a carrier spread disease without being ill?

having a delayed prodromal period, some people can still be carriers during the convalescent stage of illness

What are the two forms of direct contact transmission?

horizontal: person to person through contact or sexual disease

vertical: mother to baby

What is a fomite?

inanimate objects which are involved in spreading pathogens

What is the difference between external and internal vector transmission?

external: carried outside on body of vector

internal: carried within the vector

What are the two kinds of internal vector transmissions?

haborage: does not undergo changes within vector

biologic: pathogen undergoes changes within vector

What are the two types of ways to exit a host?

active: actual movement of pathogen to exit site

passive: fecal movement, vomitting, etc

What is the chain of infection for the plague?

rat reservoir --> human + rat feces = human infection --> bloor/airborne deposits --> next human victim

What are the important factors in determining risk from infectious disease?






What is the relationship among factors determining chance and severity of disease once exposure has occured?

change & severity (a) #pathogens x virulence over host resistance

What is the ID50?

infectious dose 50 which states that 50% of the experimental hosts will become infected

What are the virulence factors?

attachment, colonization and growth


resistance to host defenses

production of toxins

How do pathogens adhere?

fimbriae, capsules, slime layers, spikes

How do pathogens colonize?

find favourable conditions in the host which allow for suitable environment

How does a pathogen invade its host?

- have ability to spread to adjacent or other tissues

- can penetrate through substances

- attack extracellular matrix, basement membranes, membranes and intestinal walls

- can degrade the attachments between cells

What is septicemia?

having both pathogens and toxins in the blood

What is the difference between extracellular and intracellular pathogens?

extra: multiply outside of cells

intra: multiply within ccells

What is the difference between a faculative or obligate intracellular pathogen?

faculative: can live within or outside a host

obligate: must live within a host to survive

How does a pathogen resist host defenses?

- hide latent within host cells

- fusing host cells to adjacent cells to prevent expose to microbial proteins

- mutations to change antigenic sites or alter expression of antigens

- interfere with interferon response

What is a biofilm?

a layer on top of bacterial pathogens which makes for cells to become less sensitive to antibiotics and antibodies

What is zoonosis?

the transmission of animal pathogens to humans

What is a holobiont?

host and their microbiota

How would cellular mechanisms be impacted by an anti-inflammatory response?

- prevent prostaglandins

- block cytokines, histamines

- no recruitment of neutrophils

- no lactoferrins = keep iron relevant and prevent proper immune response

How do APCs carry out bacterial recognition, digestion and presentation?

macrophages, dendritic cells and B-cells will attach to antigens later binding to proper MHCs to later promote an immune response

What two different proteins carry out opsonization?

completment system

acute phase proteins

What are the two types of leukocytes that use perforins?

natural killer cells

cytotoxic T-cells

What are the cardinal signs of inflammation?

redness, swelling, pain, warmth and altered functions

How does the innate respond to pathogens invading cells and pathogens invading tissue spaces?

cells invasion: use phagocytosis, lysis, etc

tissue invasion: use of first line of defense (inflammation)

Why do some vaccines require boosters?

provoke a memory response and later a stronger immune response and to protect for future infection

Why would proteins be suitable for use as antibodies?

- many amino acid combinations

- primary and secondary structures

- can be put together in different ways

- varying size

How does the immune system combat extracellular vs intracellular infections?

extra: done through inflammatory response

intra: cell-mediated and cytotoxic responses

How does the healthy immune system make so many different antibodies specific for many different antigens?

- rearrangement of antibody gene segments

- different codons during splicing

- somatic hypermutations

What are six examples of how the innate and adaptive immune system work together?

- complement system

- inflammation

- macrophages

- phagocytosis

- lysis

- many more...

What are the various T-cells?

T-helper: cytokines which later will direct other immune responses

T-cytotoxic: kill infected/transformed cells

T-regulatory: suppress immune responding to self

Why would a defect in MHC-I protein would affect the immune response?

all cells should be expressing MHC-I, if not we're un sure which cells are ours and which are not

What are the five ways antibodies help destroy pathogens?

opsonization - adds opsin/substrate to help phagocytosis

agglutination - come together and clump

neutralization - inactivation and block binding capacity

complement fixation - lysis

precipitation - formation of a new insoluble product

Why would it be beneficial that lymphocytes will require two types of signals for activation?

creates a regulatory response? ensure a proper immune response will occur

What is the difference between NK cells and cytotoxic T-cells?

NK: lack specificity and memory

cytotoxic: will be there to kill host cells expressing MHC-I

What is clonal selection?

a generation of diversity of the lymphocyte pool which can bind to many epitotes to stimulate recognized cells later becoming effector or memory cells

Is a pathogen always a pathogen under any circumstance?

pathogens are what cause disease (pathogenicity) therefore a pathogen is always a pathogen but can be active or inactive based on the viable host or mode of transmission

What the factors determining tissue tropism of a pathogen?

tissue tropism: depending on how the pathogen wants to enter the tissue:

- kinds of tissue of an organism affects

- route of transmission

- adhesion factors

- growth requirements

- invasiveness

- adhesion factors

A higher ID50 would mean a higher or lower virulence?

A higher ID50 would be a lower virulence because it would take MORE to actually infect an organism

What are some ways that a pathogen is able to evade the host immune system?

- hiding (becoming latent)

- mutating antigenic sites

- lack/prevent the interferon response

- resistance to host defenses

What would be characteristics of a good reservoir?

- cannot be killed

- can be moved around easily

- easily transmitted