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50 Cards in this Set

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dendritic cells

recruite t-cells

mast cells

release histamine which makes blood vessels more pourous (vasodilate) so the white blood cells, neutrophils, and phagocytes can come out. Initiates inflammatory response

type I hypersensitivity reaction

normal type of allergy. immune globulin IgE attaches to a recognized antigen. Mast cells release histamine when antigen-antibody complex binds with it. vasodilation and capillary leakage occurs. causes urdicaria and hives and swelling in larynx (if really bad), and anaphylactic shock (because of the dramatic drop in BP because of vasodilation)

type II hypersensitivity reaction

tissue specific reaction. ciliac disease

gluten binds with walls of bowel and immunoglobulins bind to the gluten on cell wall. . complement reactions occur which leads to inflammation which calls neutrophils which phagocize portions of cells which lead to cell death.

type III hypersensitivity reaction

antibody antigen complex reaction

caused by IgM instead of IgE. IgM has five components so it is really efficient at causing agglutination. quickly becomes ball of antigen antibody complexes which create huge molecules. lead to problems in kidneys- glomerulonephritis. this is because it is really large and sticky and will get stuck in the glomerulus.

type IV hypersensitivity

delayed hypersensitivity reaction. poison ivy.

poison ivy molecules bind with proteins in skin activate t cells which cause inflammatory reaction in tissues (dermititis)

also can be from medicine or from medicine/ sunlight photoreaction. something about UV light causes proteins to bind with NSAID molecules which leads to a similar dermititis as poison ivy

systemic lupus erythematosus

related to inheritance and acquired environmental factors (viruses)- leads to hightened activity of B cells and plasma cells

loss of self tolerance and increased activity of helper t cells. decreased activity of suppressor t cells. abnormal cell break down (apoptosis) (all of the parts are not broken down completely so a lot of phospholipids and nucleic acids enter blood stream)

anti-nuclear antibodies and antiphospholipid antibodies are created. can't differentiate between self and non self. inflammation in many systems through out the body. this makes it autoimmune.

rash, arthritis, lung lesions, raynauds disease, and nephritis

endothelial cell derived immunity

provide a tight seal so other things can't get through. involved in antigen recognition so endothelial cells can detect when cells are not self. interact with platelets and leukocytes to allow these cells to migrate to an area of intrusion. produce antimicrobial peptides. has a pH that won't allow certain bacteria and produces secretions to catch foreign antigens.

bacteria defense (biochemical barriers)

normal flora in body forms immune function in skin, oral, conjunctiva, gi tract. aids digestion and metabolizes complex sugars.

lacto bacillus creates acidic pH in vagina which is hostile to some antigens

cathelicidins and defensin

drill holes in membrane and affect protein synthesis of microbes.


attracted to bacteria and virus through charge (they are positively charged and membranes are negatively charged) electrostatic interaction

strong broad spectrum antibiotics

bind to and inhibit protein and enzyme synthesis and DNA and RNA synthesis


innate immune system. defense lectins that are proteins that bind to carbohydrates. pattern recognition receptors of patterns of carbohydrates of antigens. form aggregate which activates immune response and trigger interleukins and cytokines. disrupt cell membrane, deactivate toxins (endotoxins), enhance phagocytosis. another form of antibiotic which is innate

defence lectins- bind to carbohydrates- recognize patterns of carbohydrates and bind to pathogen associated molecular patterns- allow immune cells to recognize as dangerous

form aggregate to activate immune response


inflammatory molecule released during inflammation

peptides that result in pain and swelling

pathways for complement plasma proteins

complement immune response

1. classic pathway-activated by antibodies

2. alternative pathway- responds to surface products of antigens (endotoxins)

3. lectin pathway- responds to mannose residues (sugar residues) on antigen


process of attaching opsonins on antigen surface. negates negative charge on membrane surface so immune cells (phagocytes) can interact with them (which are normally negatively charged as well)

allows them to react


attract cells to a certain area. complement proteins are cleaved to act as a signal for the area

cell lysis/ MAC

complement proteins bind to antigen to form membrane attack complex (MAC). causes osmotic lysis of the cell by forming channels in membrane

overactivation of C3A leads to

asthma- stimulates interleuken 13


swelling of subcutaneous tissue (lips)

can be from deficiency of C1 Esterase which disintegrates complement protein C1

rheumatoid arthritis

toll-like receptors leads to inflammatory response in joints

overactivation of toll like receptors

coagulation and clotting purpose

stop bleeding, trap foreign molecules, repair and healing

activation of coagulation

tissue factor activates enzymes and cofactors of coagulation cascade leading to insoluble cross linked fiber net (clot)

or by platelet activation from collagen which blinds to glycoprotein on platelets. soluble protein binds and strengthens this bond so the platelet can change it's shape and release molecules which draw more platelets to the area to create plug. also accumulates fibrin to form stronger clot

vonwillenbran factor binds and strengthens bond of platelet and fibrin also creates platelet plug. forms fibrin net


destruction of clot. dissolves bond between fibrin, platelet, and other clot molecules

involves enzymes- fibrinolytics (TPA)


disorder with lack of cofators needed to clot blood.

von willebrand disease

lack of von willebrand factor so can't clot

antiphospholipid syndrome

procoagulant syndrome-

antibodies lead to inactivation of anticoagulants so embolisms can occur

how does aspirin help prevent formation of clots

platelet inhibitor. inhibits thromboxin A2


anticoagulant medication.


phagocytes leave circulation and enter tissue


has ability to provoke immune response by binding to antibody or MHC

epitopes- key like complex that fits in with antibody to provoke response- complex protein structures

exogenous- inhaled/ ingested bacteria or virus

endogenous- part of bacteria or virus that is put onto surface membrane for recognition

autoantigen- ability to recognize self and nonself is disrupted

tumors- abnormal rapidly growing cells that are recognized as hostile invaders

hapten is something too small to provoke response but can attach to a larger protein to provoke response (poison ivy)- urshiol must bind with molecules in skin to provoke response

allergens- not always pathogenic but can produce immune reaction


produced by b cells

y shaped


tag antigen for attack

can be soluble and circulate through blood stream

or surface bound on b- cells

identify epitopes of antigens and tag for attack

b cell receptor allows them to react to antigens

types: immunoglobulins (antibodies)



IgA- tears, saliva, respiratory endothelium,

first line defense- weak activator of compliment- some bacteria overcome it

IgG- most abundant, activates classic complement pathway, neutralizes antigens and toxins- sticks around for life and can be rebound to antigen if another exposure- presence of IgG indicates exposure to an antigen

IgM- natural antibody- can respond even if no previous exposure- first to appear in early infection

IgE- allergens and parasites

IgB- b-cell activation


lymphocytes- type of white blood cell- differentiate to b cells or t cells

3 types of lymphocytes - natural killer cells, t-cells, b-cells

type of white blood cell

natural killer cells- rapidly respond, don't require antibody but identify MHC in stressed cells- release porforins to degrade membrane

natural killer cells

large lymphocytes, rapidly respond to cells infected or in distress.

do not require antibody to be activated, but bind to MHC on surface. release porforins and proteases to degrade membrane leading to apoptosis.

identify tumor cells

t- cells

differentiate in thymus gland

CD4- t helper cells- activate immune response, no phagocytic activity, HIV uses to gain entry

CD8 t cells- cytotoxic, bind to MHC and induce apoptosis when signaled by CD4, has memory to create rapid response upon reexposure


develop in bone marrow and produce surface and soluble antibody. then become memory cells for subsequent exposure


when immune system fails to respond to antigen


agent capable of causing disease. depends on factors


ability to spread between individuals


ability to induce or avoid immune response, used for vaccines- present inactivated antigen to provoke an immune response


how quickly it multiplies in a host


mechanism of action- what it does to a host

portal of entry

how it gets into a host.


ability to produce toxins to enhance its effects


severity of the disease. measured by case fatality.


no cell nucleus- bacteria, unicellular

gram +

thick cell wall with thecoic acid

gram -

thin cell wall surrounded by lipid membrane


hibernation. able to live in inactive state for long time


unicellular eukaryotes. ferment carbs to CO2 and alcohols.

earliest domesticated microbe

commensal- benefit from host without affecting it (generally)

opportunistic pathogen


symbiotic- benefit at expense of host

require vector to survive


produce toxins or cause direct tissue damage

sometimes immune can't get rid of it