• Shuffle
    Toggle On
    Toggle Off
  • Alphabetize
    Toggle On
    Toggle Off
  • Front First
    Toggle On
    Toggle Off
  • Both Sides
    Toggle On
    Toggle Off
  • Read
    Toggle On
    Toggle Off
Reading...
Front

Card Range To Study

through

image

Play button

image

Play button

image

Progress

1/134

Click to flip

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;

134 Cards in this Set

  • Front
  • Back
  • 3rd side (hint)
what does encapsulation do?
prevents opsonization by antibodies (recognition and binding)
prevents microorg from bing phagocytized
what kind of bacteria can have endotoxins? (
gram negative bacteria
i.e. enterobacteria
describe exotoxins
polypeptides produced and released by organisms
antigenic, toxic, unstable in heat
bind to receptors in target organs, interfere with metabolic processes
describe endotoxins
immunogenic part of lipopolysaccharide bacterial cell wall that triggers a massive immune response when bacterium lyses - immune response leads to cell shock and multiple organ failure
what are the characteristics of retroviruses
contain encoding information for reverse transcriptase enzyme to create mRNA and DNA from own genome
DNA replicates when host cell replicates
lactoferrin
mucosal protein which reduces Fe+3 availability and limits bacterial growth
describe some chemical barriers of our epithelium
acidic environment of skin, urine, and vagina inhibit bacterial growth
saliva, mucus, tears, and sweat contain a bacterial killing enzyme
sebaceous gland secretions are antifungal
describe innate immunity
does not require a previous exposure to the offender to react. It is our first line of defense and works very quickly. Its response is usually local (ex: if you get a splinter in your finger. Innate immunity begins the process of reacting to the foreign invader).
what is the defining cell associated with innate immunity?
Natural Killer cell
what is another name for natural killer cells?
describe the first step that happens in the innate immune response after penetration/invastion by a foreign antigen
first, the Ag is detected by an antigen presenting cell (APC) which is a macrophage
after the Ag is detected by the APC, what happens in innate immune response?
the Ag is phagocytized by the antigen presenting cell (APC)
after the Ag is phagocytized by the APC, what happens in the innate immune response?
within the APC, the Ag is loaded onto MHCII, a protein molecule that tells the body that this is not self
after the Ag is loaded onto MHCII, what happens in the innate immune response?
the MHCII-antigen complex is displayed at the cell surface, and the APCs travel to the Lymph node, where T helper cells (CD4+) can detect them. Also in the lymph node, antigen is presented to CTL/Natural Killer T- cells/CD8+
If the T-cells recognize the Antigen as foreign, then what happens?
the helper Tcells "HELP' turn on the B Cells, and the helper T cells activate the killer T cells
after helper and Killer T-cells are activated, what happens in innate immue response?
active helper and killer T-cells replicate, including formation of memory cells, which can responds quicker to subsequent infection by that kind of pathogen
what do the killer t cells do?
they seek and destroy the antigen and execute "lethal hits" causing apoptosis
what is the alternative pathway?
if the antigen is bacterial endotoxin with lipopolysaccharide cell wall (gram - cells) then the complement is activated via the C3a alternative pathway - complement cascade leads to membrane attack complex (MAC) which kills the Ag cells.
In adaptive immunity, antigens in the blood trigger what?
b-cell activation, but only if the b-cell recognizes the specific antigen. Active helper T-cell is required for B-cell activation
If helper T-cells recognize a specific antigen presented by a macrophage (APC), then the Helper T-cell activates the
B cell
What does the activated B-cell do?
replicates and produces antibody molecules that can bind to specific antigens
what happens when the antibody molecules bind to specific antigens?
Stimulates the complement via the C1 "Classical" pathway.
what are steps to the C1 "Classical" pathway?
Precipitation
Neutralization - inflammation
Opsonization
MAC
Memory B cells come from where?
from the activated B-cells
what else does the antibody-antigen complex signal?
phagocytosis
describe what happens in adaptive immunity in the case of virus infection
nucleated cells are infected by the virus, which are then loaded to MHCI. Natural killer cells (Killer T cells) read the complex as foreign, give the virus infected cell a "lethal hit"
what are the two categories of leukocytes?
granulocytes and agranulocytes
what types of cells derive from granulocytes?
neutrophils: macrophage
eosinophils: macrophage
basophils: mast cells
what types of cells derive from agranulocytes?
lymphocytes: B and T cells
Monocytes: immature, become macrophages in tissues
what are the lymphocytes?
B and T cells

agranulocytes
GRANma POLY uses a NEBulizer
Granulocytes/polymorphonuclear
Neutrophils
Eosinophils
Basophils
where do T cells mature?
Thymus
where do B cells mature?
bone marrow
and then the lymph node
Primary organs in the immune system?
Bone marrow
Thymus
Secondary organs in the immune system?
lymph nodes
spleen
tonsils
Peyer patches in intestine
what are the primary effectors of the immune system?
Leukocytes = White Blood Cells
monocytes from the circulating blood migrate to organs and tissues to become ______
macrophages
wgat do neutrophils primarily respond to?
acute bacterial infections
what do eosinophils primarily respond to?
allergic reactions and infection by intestinal parasites (kill parasitic helminth through release of specialized molecules)
what is required for a macrophage to engulf an offender
the macrophage must recognize it as non-self?
what is the difference between mast cells and basophils?
basophils become Mast cells, However, basophils are called basophils when they are circulating in the vascular system. Mast cells are found in tonnective tissues
mature basophils can migrate to connective tissue and do not reenter the curculation (called mast cells once in the tissue)
what is the function of mast cells and basophils?
Begin the inflammatory response.
when an appropriate stimulus occurs, such as antigen binding to the IgE antibodies, mast cells and basophils release granules (degranulate) containing proinflammatory chemicals. (histamine, platelet activating factor, vasoactive amines)
what is the role of cytokines secreted by macrophages
macrophages secrete a variety of cytokines that induce inflammation (i.e. interleukins) and chemotaxis. Some macrophage cytokines stimulate the growth and defferentiation of other white blood cell types
what are the three major types of lymphocytes?
NK cells, T cells and B cells
NK cells function in _______ immunity wheras B and T lymphocytes are the cells responsible for __________immunity.
innate
specific adaptive
CD4+ cells (T helper cells) do what?
interact with antigens presented on the surface of specialized antigen presenting cells such as dendritic cells, macrophages, and B cells. Secrete cytokines that activate other T cells and macrophages, and stim b-cell proliferation adn antibody production
what do CD8+ cells (cytotoxic T Cell (CTL) do
require "help" from T helper cells to activate fully. kill through perforins and CD95 (intracellular enzyme cascades)
what is lactoferrin
Lactoferrin is one of the components of the immune system of the body; it has antimicrobial activity (bacteriocide, fungicide) and is part of the innate defense, mainly at mucoses.[1] In particular, lactoferrin provides antibacterial activity to human infants.[2
what is reverse transcriptase
a reverse transcriptase, also known as RNA-dependent DNA polymerase, is a DNA polymerase enzyme that transcribes single-stranded RNA into double-stranded DNA. It also helps in the formation of a double helix DNA once the RNA has been reverse transcribed into a single strand cDNA. Normal transcription involves the synthesis of RNA from DNA; hence, reverse transcription is the reverse of this.
where to T-cells mature?
thymus
where do b cells and natural killer cells mature
in the marrow
what happens in the lymph node?
contain large numbers of b cells, t cells , and macrophases
lymph fluid flows through for immune cells to filter, detect and react to foreign material
what do white blood cells in general do?
mediate inflammation and immunity
locate and eliminate pathogens and foreign molecules.
what are the signaling molecules?
cytokines, chemokines, and kinins
degranulation of basophils and mast cells begins
inflammatory response associated with allergic reactions and wound healing
what do dendritic cells do
similar to macrophages
summoned by cytokines/chemokines
engulf antigen
bring it back to lymph node to show antigen to B and T cells
dendritic cells are activated by the
innate response
what do macrophages do?
ingest invading microorganisms,
capable of cell division
Proliferate at site of inflammation
what are monocytes
mononuclear
immature macrophages that circulate in the bloodstream
become macrophages when they enter the tissues
macrophages secrete _________ that induce _______ and chemotaxis
cytokines
inflammation
the surface of macrophages are covered with a variety of ________
receptor proteins
Fc receptors on macrophages bind to:
the constant fragment of antibodies
macrophages present ________ to what, where?
antigens
b and c cells
lymph node
describe what Natural Killer (NK) cells do.
effectively kill tumor and virally infected cells without previous exposure
NK cells use Fc receptors to recognize
antibody-coated cells
Fc receptors are the what?
constant "handle" on an antibody that allows binding
what are the two major classes of T lymphocytes and how are they differentiated?
T helper cells: have CD4 proteins
Cytotoxic T-cells: have CD8 proteins
what do B lymphocytes do?
produce antibodies; have antibody-like receptors on cell surface
carry many copies of identical b-cell receptors
respond to only one antigen epitope
The antigen epitope must fit the b-cell receptor for activation
what is "epitope"
the specific shape of the antigen.
what are the two different complements?
Classic Pathway
Alternative Pathway
the Classic pathway is initiated by
an adaptive response
Ag/AB complex
the alternative pathway is initiated by
an innate response
what is the end result of the complement?
n matter the trigger, the end result is always a membrane attack complex. The attack causes Na+ and water to flood the offender, causing it to burst
Kinins cause what?
powerful vasodilation response
what are the three purposes of inflammatory response?
Neutralize and destroy invading and harmful
agents
 Limit spread of harmful agents to other tissue
 Prepare damaged tissue for repair
what are the five cardinal signs of inflammation
Redness
 Swelling
 Heat
 Pain
 Loss of function
what are the two types of inflammation?
Acute
 Short in duration, lasting less than 2 weeks
 Involves a discrete set of events
85
 Chronic
 More diffuse
 Extends over longer period
 May result In scar tissue formation or deformity
 Fact: inflammation has now been linked to many
pathologic processes, including CVD, diabetes, and insulin
resistance. It remains to be demonstrated if inflammation
is causitive to these and other pathologies
what is the role of vasodilation in inflammation?
allows for the emigration of neutrophils and macrophages into tissue
vasodilation in tissues leads to what?
pain, heat, redness
what are the three players in healing
fibroblasts
endothelial cells
myofibroblasts
what are the four kinds of exudate
serous exudate - serosanguineous
fibrinous exudate - sticky, thick
purulent exudate - pus
hemorrhagic exudate - RBC's mixed in with serous fluid: can be a sign of severe inflammation
what are the funxtions for inflammatory exudates
Transport leukocytes and antibodies
 Dilute toxins and irritating substances
 Transport nutrients for tissue repair
what are the signs of systemic inflammation?
Systemic
 Fever, neutrophilia, lethargy, muscle catabolism
 Acute phase proteins
 Erythrocyte sedimentation rate (ESR
what is the general role of specific adaptive innumity?
Recognizing foreign invaders
 Destroying foreign invaders
 Retaining memory of the encounter
96
g y
 Allows for more effective defense (adaptive) to
be achieved after subsequent exposure
what is MHC and what is another name for it?
major histocompatibility comples
aka
human leukocyte antigen (HLA) complex
what are MHCs?
a cluster of genes on chromosome 6. the proteins made by these genes are displayed on the surface of body cells and mark them as "self"
class I and II MHC genes code for proteins that
display or "present" antigens on the surface of cells
MHC classes 1 and 2 do what
codes for proteins that present antigens on cell surface
describe the MHC class I presentation
Found on every cell in the body
 Nucleated cells continuously produce MHC I
proteins on endoplasmic reticulum; combine
with peptide fragments in cytoplasm
 MHC I peptide complexes cycled to cell surface;
99
inspected by T‐cells (cytotoxic T cells)
what happens if there are abnormal proteins presented on MHC class i
produce immune response
describe MHC II presentation
MHC II Proteins
 Found ONLY on B cells, macrophages, Ag presenting
cells (like DC)
 Present antigens obtained from extracellular sources
 Extracellular antigens must first be ingested by
antigen‐presenting cell
101
g p g
 Antigen presenting cell degrades into fragments in
endocytic vesicle
 T‐helper cells ‘read’ the Ag and activate B cells to
begin cranking out antibodies
 MHC II proteins synthesized on endoplasmic
reticulum
 Pick up antigen from phagosome on way to plasma
membrane
t cell receptors are used to:
recognize foreign antigen displayed on
surface of antigen‐presenting cells
 T cells are specific
O l i d d i l i i

 Only recognize and respond to a single antigenic
epitope
what do t helper cells do (CD4)?
Recognize antigen in association with MHC II
molecules
 CD4 protein necessary to enable T helper cells
to bind to MHC II protein; T‐cell receptors
i ifi ti t d
104
recognize specific antigen presented
 T‐cell receptors bind to corresponding antigen
and generate signaling cascade in
T helper cell cytoplasm
 T‐cell receptors linked to cascade through CD3
what do cytotoxic t cells (CD*) do?
Recognize antigen displayed in association with
MHC I protein
 CD8 protein needed for MHC I binding
 TCR specifically recognizes presented antigen
 Bi di
Cytotoxic T Cells (CD8+)
106
Binding
 Triggers responses in cytotoxic T cells similar to
that of T helper cells
 Not enough to activate them (need costimulation
by IL‐2 cytokines)
 Costimulators usually present on surfaces of
presenting and responding cells
what do activated cytoxic t cells do? How?
Proliferate into memory cells and effector cells
 Perforins
 Proteins manufactured in cytotoxic T cell
Cytotoxic T Cells (CD8+) (Cont.)
108
 Store in cytoplasm granules with granzymes
 Granules
 Bind to target cell, migrate to contact site, and
release to target cell membrane
how do perforins work
Perforins
 Assemble into pores, allow granzymes into target
cell, degrade DNA, trigger apoptosis
 CD95 or FAS ligand—CD95 protein on cytotoxic
Cytotoxic T Cells (CD8+) (Cont.)
109
T cell
 Binding to CD95 protein to CD95 ligand causes
cell death
describe memory b cells
Memory B Cells
 Contain antigen receptors
 Memory of exposure to an antigen is stored in
memory B cell clones
describe plasma b cells as short-lived antibody producing factories
Plasma B Cells: Short‐Lived Antibody
Producing Factories
 All plasma cells in clone secrete antibodies with
identical monoclonal antibody; secretions
112
circulate in blood/body fluids
 Bind specifically to antigen that triggered its
production
 Usually die off once antigen is cleared; some live
to recognize antigen if re‐exposed
eacdh b cell receptor is coded for two types of genes:
Each B‐cell receptor coded for two types of
genes
 Variable region
 Makes up antigen‐binding site
113
 Constant region
 Same for all antibodies of a given class
 Structure similar to IgM
what are the five classes of antibodies
G, M, A, D, E
describe IgG
Most common type
120
 Smallest
 Easily escapes bloodstream to enter interstitial
fluid
describe IgM
10% of circulating immunoglobulins
 Mostly found in intravascular pool; cannot
penetrate capillary wall
121
 First to be produced on exposure to antigens or
after immunization
 Major antibody found on B‐cell surfaces
 Works best to activate complement
describe IgA
Produced by plasma cells located in tissue under
skin/mucous membranes
 Primarily found in saliva, tears, tracheobronchial
secretions colostrum milk 122
secretions, colostrum, breast milk, and GI/GU
secretions
 Secretory IgA
 Complex made by binding to secretory component
produced by epithelial cells
 Allows transport of IgA into secretions
 IgD
describe IgD
Found in tiny amounts in serum
 Located primarily on B cell membranes
(with IgM)
 Thought to be cellular antigen receptor that acts
Antibody Structure (Cont.)
123
to stimulate B cell to:
 Multiply
 Differentiate
 Secrete other specific immunoglobulins
describe IgE
IgE
 Bound by Fc tail to receptors on basophil and
mast cell surfaces
 Trace amounts identified in serum
 Helps in immunity against helminthic parasites;
Antibody Structure (Cont.)
124
responsible for initiating inflammatory and
allergic reactions
 Functions as signaling molecule
 Causes mast cell degranulation when antigen
detected at mast cell surface
what are the fxns of antibodies
Precipitation, agglutination, neutralization,
opsonization, complement activation
 Each arm of immunoglobulin Y structure can
bind an antigenic epitope
All tib di d ti t bi d t th
126
 Allows antibodies and antigens to bind together
into large insoluble complexes that precipitate
out of body fluids
Can function as antitoxins
 Neutralize bacterial toxin
 Antibodies bound to foreign antigens on cell
membranes
128
 Can also activate complement cascade
 Can trigger
 Chemotaxins
 Inflammatory mediator release
 Membrane attack complex formation
describe passive immunity
Transfer of plasma containing preformed antibodies
against specific antigen from a protected or
immunized individual to an unprotected or
nonimmunized individual
129
 B‐cell immunodeficiencies
 Following exposure of individual with high susceptibility to
a disease without adequate time for active immunization
 Antibody rejection may alleviate or suppress effects of
antigenic toxin
describe active immunity
Active Immunity
 A protected state owing to the body’s immune
response as a result of active infection or
immunization
defensins
Defensins are a family of small cationic, antibiotic peptides that contain six cysteines in disulfide linkage. The peptides are abundant in phagocytes and small intestinal mucosa of humans and other mammals and in the hemolymph of insects. They contribute to host defense against microbes and may participate in tissue inflammation and endocrine regulation during infection. Iinnate
selectins
During an inflammatory response, stimuli such as histamine and thrombin cause endothelial cells to mobilize P-selectin from stores inside the cell to the cell surface. In addition, cytokines such as TNF-alpha stimulate the expression of E-selectin and additional P-selectin a few hours later.

As the leukocyte rolls along the blood vessel wall, the distal lectin-like domain of the selectin binds to certain carbohydrate groups presented on proteins (such as PSGL-1) on the leukocyte, which slows the cell and allows it to leave the blood vessel and enter the site of infection. The low-affinity nature of selectins is what allows the characteristic "rolling" action attributed to leukocytes during the leukocyte adhesion cascade[2].
shift to the left
an increase in the number of immature leukocytes in the peripheral blood, particularly neutrophil band cells
kupffer cells
specialized macrophages located in the liver lining the walls of the sinusoids that form part of the reticuloendothelial system (RES) (aka: mononuclear phagocyte system).
Langerhans cells
In skin infections, the local Langerhans cells take up and process microbial antigens to become fully-functional antigen-presenting cells.

Generally, dendritic cells in tissue are active in the capture, uptake and processing of antigens. Once dendritic cells arrive in secondary lymphoid tissue, however, they lose these properties while gaining the capacity to interact with naive T-cells.

Langerhans cells derive from the cellular differentiation of monocytes with the marker "Gr-1" (also known as "Ly-6G/Ly-6C"). This differentiation requires stimulation by colony stimulating factor (CSF)-1.[6] They are similar in morphology and function to macrophages.
dendritic cells
Their main function is to process antigen material and present it on the surface to other cells of the immune system. That is, they function as antigen-presenting cells. They act as messengers between the innate and adaptive immunity.

Dendritic cells are present in tissues in contact with the external environment, such as the skin (where there is a specialized dendritic cell type called Langerhans cells) and the inner lining of the nose, lungs, stomach and intestines. They can also be found in an immature state in the blood. Once activated, they migrate to the lymph nodes where they interact with T cells and B cells to initiate and shape the adaptive immune response.
neutrophilia
increase in number of circulating neutrophils
arachidonic acid
Arachidonic acid does still play a central role in inflammation related to injury and many diseased states
WHAT ARE THE 5 PARTS OF AN SF-364 (G/S/D/R/C)?
- GENERAL INFORMATION
- SHIPMENT, BILLING, RECEIPT DATA
- DISCREPANCY DATA
- REMARKS
- CLOSING
1
What form is used for shipping discrepancies from dod source of supplies?
SF361
kinins
kinins are inflammatory mediators that cause dilation of blood vessels and increased vascular permeability. Kinins are small peptides They act on phospholipase and increase arachidonic acid release and thus prostaglandin (PGE2) production
diapedesis
The movement or passage of blood cells, especially white blood cells, through intact capillary walls into surrounding body tissue. Also called migration
diapedesis
the movement of leukocytes out of the circulatory system, towards the site of tissue damage or infection. This process forms part of the innate immune response, involving the recruitment of non-specific leukocytes. Monocytes also use this process in the absence of infection or tissue damage during their development into macrophages.
what are the three steps to acute inflammation
Acute inflammation has three major components:
* Alteration in vessels leading to increased blood flow to the area.
*Structural changes in microvessels that allow plasma protein and WBCs to leave the circulation. Capillaries are composed; endothelial cells and fluid leaves the capillary at the junction between the endothelial cells. Inflammatory stimulus causes these junctions to open up widder than normally which allows excess fluid to get out of vessel. After fluid leaves vessel the blood get thicker because of large protein particles and cells which stay inside vessel. This is referred to as stasis because the blood flow slows down. Now the white blood cells start to line up along the peripheral edges of the vessel. This is called margination or pavementing.
*Emigration of WBCs from vessels so they can accumulate at the site of injury.
what are the four theories of autoimmunity?
Antigenic mimicry theory
 Self/foreign antigens made of same materials, so small alterations
in self tissue lead to attack
2. Release of sequestered antigens
 Self antigens not in direct contact with lymphocytes during fetal
Autoimmunity Theories
development
 Antigens “hid” in places lymphatics couldn’t reach. When illness
hits, Ag’s released
3. T‐cell theories
 Thymus gland defects
 Decreased suppressor T‐cell function
 Altered T helper cell function
4. B‐cell theories
 B cells lose their responsiveness to suppressor
T‐cell signals: ↑↑in B cell function and autoAb production
DiGeorge Syndrome
thymic hypoplasia
total loss of thymus
t cell development decrease
what is the most important mediator of Type I hypersensitivity reactions
histamines
what is the hallmark of hiv and aids
defective cell mediated immunity: decrease in CD4 /t helper lymphocytes
HIV targets the conductor of our immune system
what does glycoprotein 120 (GP120) do in the etiology of HIV
Gp120 is important:
Allows the virus to
Attach to CD4+ (Th)
Cells with help of
Chemokine receptors
CXCR4 and CCR5
what is the HIV structure
Viral envelope
 Consists of membrane derived from host cell
 Viral glycoprotein studs protrude from cell
Etiology
membrane
 Contains proteins gp120and pg 41
how does the HIV get into the lymph node to kill T cells?
HIV adheres to the dendritic cell, the DC engulfs it, carries it to the lymph node, so the virus uses the DC as a “Trojan Horse” to sneak
into lymph node
once HIV is in the lymph node, what happens
Virus binds by gp120 envelope to the CD4
molecule on Th cell
‐gp120 has high affinity for Th cells
3. Binding to the Th cell via gp120 allows binding to
co‐receptors CCR5 and CXCR4
‐binding of the co‐receptors causes the Th cell
membrane to melt away, virus + cell fuse
what happens after the t cell membrane melts away?
Virus injects core into cell, activates
reverse transcriptase and copying begins
‐RNADNAprotein
‐virus’s DNA is now incorporated into the host Th
HIV Binding and Infection, cont.
cell’s DNA
‐all new copies of cells now infected
5. Virus buds from infected cell, tearing
holes in the membranes
6. As new copies made, gp120 protein is
replicated and allows fusion to more Th cells
what happens when the t helper cells fuse with the virus?
When Th cells fuse, a huge SYNCYTIUM forms
7. ‐syncytium is a multinucleated mass of cytoplasm
created by fusion of many cells
8. ‐this is how virus infects multiple Th cells at once
8. Syncytium prevents receptor availability for
HIV Binding and Infection, cont
Ab binding
‐Antibodies are useless
what is a poor prognostic sign for HIV
an accelerating fall in the CD4/CD8 ratio is poor
prognostic sign
why does b cell responsiveness decrease with HI'v?
as t cell numbers decline, B cell responsiveness decreases because of
dependence on T‐cell helper cytokines