W3 Immune System Flashcards
Adaptive/ Acquired immunity
Exposed to antigens
Inducible- can be activated
Specific-only certain antigens mobilized
Has memory- activates remembered response
Antibody
any molecule that to the MHC-major histocompatibility complex, a cell surface receptor on WBC that helps identify self vs nonself
Autoantigens
the ability to recognize self from nonself is disrupted. Autoimmune disease
Hapten
Must bind with larger protein to cause production of antibodies
Poison ivy must bind to molecule in skin to cause allergic reaction
Antibodies are
Y shaped glycoproteins produced by B cells (backbone of adaptive immune response)Able to ID the epitopes of specific antigens and bind to them. Once bound , they tag that antigen for attack by other immune cells.
Once bound to an antigen, the B cell is activated and can secrete more antibody specific to that antigen. The two forms are:
Soluble: manufactured and secreted by B cells where they can circulate in the blood and body cavities
Surface Bound: Found on the surface of B cells
Typical B cell will typically have 50-100,000 antibodies on its surface
IgA
In the mucosal lining and is present in tears, saliva, and respiratory endothelium.
Weak activator of complement, but has role in first line of defense.
Some bacteria have learned to overcome IgA
Neisseria gonorrhoeae has special protease enzyme that degrades and inactivates IgA
IgG
Classic complement pathway. Bind and neutralize certain antigens/ toxins. The presence of IgG means that you have been exposed to the antigen before and it can be rebound to that antigen if there’s any additional exposure
IgM
natural antibody. Can bind to any antigen even if there hasn’t been any previous exposure. First antibody to appear during infection
IgE
Allergens and parasites
IgD
Signals B cell activation
Lymphocytes
developed in Bone marrow. few develop there but most go to the thymus and become T cells. When exposed to an antigen they undergo more differentiation
The 3 types of lymphocytes
NK cells
T cells:[ Helper T (CD4), CD8]
B-Cells
Natural Killer Cells
Cytotoxic. Respond to cells that have developed into tumors and are signaling distress, DO NOT REQUIRE AN ANTIBODYTO BE ACTIVATED
(can attack tumors)
T-Cells: Helper T
(CD4) Adaptive Immunity
-ID and flag pathogens/ distressed cells for immune response
HIV fuses to CD4/ Helper T (GP120) & fuses so that cell and avoids detection by other cells
T-Cells: CD8
Cytotoxic. Bind to MHC of infected cells and induce apoptosis when signaled by helper T
-Once attached, release perforins & proteases that degrade cell membrane
B-Cells
Born in bone marrow & develop once they bind to antigen-> produce both surface and soluble antibody towards that specific antigen.
Afterwards become memory cells
The ability of the pathogen to cause a disease is dependent upon
Communicability-ability to sprea Immunogenicity- vaccine? Infectivity how quickly? MOA: Mechanism of action Portal of Entry: How does antigen get into host Toxigenicity: does it produce toxins Virulence: severity
Bacteria have a cell wall made of
Peptidoglycan (polysaccharide sugars linked by peptides)
What does a Gram+ and Gram- cecll wall mean
Gram+ means call wall of teichoic. Gram - (tin cell wall surrounded by lipid membrane)
Methanopyrus kandleri
nonpathogenic bacteria. Hyperhermophile. Lives in seas vents
Tetragenococccus Halophilus
Halophile, can lie in high Na+ concentrations. Ferments iportnat parts of soy and meso
Disease causing bacteria
Streptococcus pneumoniae
Gram+ cocci bacteria, pneumonia, sinusitis, otitis media, cellulitis, meningitis
Chest X-Ray of strep pneumonia, the lungs will fill with some fluid as an immune response
Symptoms: fever, chills, cough, SOB, chest pain
Otis media
infection of the inner eat. Can cause perminant hearing loss if left untreated
Bacterial meningitis
Inflammation of the meninges (lining of the brain)
Symptoms: fever, neck pain, stiffness, rash or confusion
Neurologic Sequelae
include cognitive, sensory, and motor deficits that may encompass emotional instability and seizure activity in the most severe cases.
Neisseia gonorrhoeae
Disease Process
Gram- DiplococciMotile, have arms called pili that help them attach to cell surfaces. Have Opa proteins that help them bind to immune cells so that they can avoid detection
Urethritis
Pharyngitis
Conjunctivitis
Clostridium tetani
Tetanus, by release of tetanospasmin, a potent neurotoxin that inhibits chemical called GABA. Inhibit GABE in muscle neuron, you overstimulate that neuron and can result in an overactive spasmodic state. 2nd deadliest toxin in the world
Characteristics of a virus
Started as parasites that degraded
Require a host cell fr replication, metabolism, and survival
Helical or structural shape
Can be DNA or RNA surrounded by a capsule
Metabolize proteins differently
Herpes simplex virus lies dormant in neurons
Mechanism of Virus Action
Attachment: via a cell surface receptor protein.
Penetration: endocytosis by cell’s own mechanism.
Uncoating: removal of the capsid
Replication: viruses use cell’s own machinery
Release: when enough versions are made, the cell is lysed
Effect on the Host: depends on the type of virus.
Influenza Epidemic: H1N1
Yeasts
Candida albicans
Unicellular eukaryotes
Ferment Carbs to CO2 + alcohols. Commensal
Commensal
they do not harm the host while they benefit
Describe Malaria
Mosquito is the vector (carries sporozoites) until it bites a human. Eggs go to the liver & reproduce & hide in cells.
Describe Malaria Symptoms
headache, fever, rashes, anemia, respiratory distress syndrome, shock, acute renal failure, and death
Benefit of Sickle Cell Anemia
Has resistance to parasites. Sickle cell can’t carry enough oxygen so some parasites die off. Also a deficiency of the Duffy Antigen in SC (Duffey antigen has resistance).
Hypersensitivity
Allergy, altered immune response to a normal nonpathogen
IgE Mediated Type 1
Most allergies. Binds to Mast cells and the degranulate, releasing histamine and heparin . Histamine binds to H1 or H2 receptors to produce allergy symptoms
IgE mediated Type I symptoms
Nausea, vomiting, diarrhea, urticaria (hives), rhinitis (nose, phlegm, cough), asthma and bronchoconstriction
Type III: Complex-Mediated Response: . Antigen-antibody reaction.
Serum sickness for a snake bite. Antibody binds to antigen and deposits it in the tissue.
Bactrim can have similar effect, mistaken for invader
Fancy serum sickness
When an antiserum is given, the human immune system can mistake the proteins present for harmful antigens. The body produces antibodies, which combine with these proteins to form immune complexes. These complexes precipitate, enter the walls of blood vessels, and activate the complement cascade, initiating an inflammatory response and consuming much of the available complement component
Raynaud’s Disease
Type III: Complex-Mediated Response: causes some areas of your body — such as your fingers and toes — to feel numb and cold in response to cold temperatures or stress. Smaller arteries that supply blood to your skin narrow, limiting blood circulation to affected areas (vasospasm).
Responding to change in temperature. Produce cryoglobulins that the antibody binds to and produces a change in the local environment (vasospasm) giving u the white tissue look
Type IV: Cell Mediated
cytotoxic T cells destroy cellular targets. Graft rejections
Autoimmunity
immune system attacks own cells. Maladaptive response that should not occur. The Proteins display proteins on their surface to display them as “self” but the body no longer recognizes it
Influenza
Symptoms
Treatment
RNA virus:fever chills malaise, cough
Rest, fluids, antipyretics
Explanation of the Flu
- Neuraminidase inhibitors which would keep the virus from spreading
- Symptoms are secondary to the release of cytokines- produced by the cells that are infected
E. Coli z157H7
Enterohemorrhagic strain
Fecal-Oral route Food poisoning, Hemorrhagic diarrhea Renal failure can occur. ANTIBIOTICS WORSEN THE DISEASE Treatment is supportive
Clostridium difficile:
naerobic spear forming rod that has spores that can survive through very harsh conditions. One of the leading causes of antibiotic associated diarrhea and colitis. Symptoms are abdominal pain and profuse diarrhea and volume lose that can lead to renal failure.
Borrelia burgdorferi
Lyme Disease. Rashes to heart block, & chronic lyme disease
Rhinovirus
Responsible for common cold, more sick days than anything else
Innate Immunity: Physical Barriers
the skin (the largest barrier), GI tract-has pH of 1-2, openings to air contains cilia (nose) have cilia, the lining of our eyes (the conjunctiva) produce tears and debris (have serialized antibodies). The innate immune system can tell when an invader is foreign and likely to cause harm. Activates the complement proteins and recrote inflammatory mediators like cytokines and leukotrienes to help combat invasion. Can also help to activate the adaptive immune system.
Innate Immunity’s inflammatory mediators
Cytokines & Leukotrienes
Endothelial derived mechanisms
Provide physical barriers creating tight seal. May be involved in antigen recognition. Helps direct inflammatory response
Antimicrobial Peptides
Innate Immunity
pH to endothelial cells are hostile and capture foreign invaders
Biochemical Barriers
Innate Immunity
Our bodies also use bacteria as defense
Our normal flora that serves an immune function. Some archaea are in the stomach & help metabolize
Mutualistic (both benefit)
Bacteroides fragilis
Fragile bacteria that are easily overwhelmed by meaner bacteria. Without causes Colitis or inflammation to colon
Lactobacillus
Normal part of the vaginal flora. Causes Dental plaque in mouth, depends on where it is
Antimicrobial peptides are:
Peptides are + while most bacteria are -
- Cathelicidins
- Defensins
Cathelicidins
- Antimicrobial peptide
- Derived from cells called Macrophages inside lysosomes. bind to cellular membrane, boring a hole through & invading
Defensins
-Expressed in a wide variety of cells & tissues including skin cells, neutrophils, the cornea, the salivary glands & the respiratory tract. Bore into cell membrane. Allows for important cellular molecules to escape from the cell. Defensins go in & disrupt important biological activities
Lack of ability to produce antimicrobial peptides include:
Link btn disease processes from Chrones to Cystic Fibrosis. Maybe we can use these instead of antibiotics
Platypus venom
one of the only mammals that has venom & lays eggs
Collectins
Defense Lectins: lectins being proteins that can bind to carbs
Lectins are
- perform recognition on the cellular & molecular level & play numerous roles in biological recognition phenomena involving cells, carbs, & proteins.
- Mediate attachment & binding of bacteria & viruses to their intended targets
Once Lectin (proteins) are attached to carbs
These proteins are soluble pattern recognition receptors
-Bind to well preserved areas called the PATHOGEN ASSOCIATED MOLECULAR PATTERN
Form an aggregate that triggers release of Interleukins & Cytokines. They can disrupt the cell membrane & enhance phagocytosis. Inactivate some gram-bateria
Inflammation includes
macrophages, dendritic cells, astrocytes, bradykinins, vasodilation
Bradykinins
peptides that are an inflammatory chemical and that is released and results in pain and can cause swelling by increasing vascular permeability
Vasodilation
The manifestation of Erythema. Allows for important immune cells and chemicals to get to the site of injury or infection. Vasodilation < the velocity of the blood to a particular vessel. Allows for important immune cells, like leukocytes, to attach to the vessel wall and then migrate into the injury. At normal velocity these cells cant’ stick
Chronic inflammation occurs when this process wont go away
asthma, IBD, rheumatoid arthritis, cellulitis and celiac disease
Complement proteins
10% of circulating plasma cells. 1) classic pathway- activates antibodies
2) Alternative pathway: reponds to surface products of antigens like their endotoxin
3) Lectin pathway: binds to mannose residues on a variety of pathogens
3 Purposes of Complement
1) Opsonization: The process of attaching (opsonins) to antigen surface, this negates the typically - charge on the antigen surface allowing immune cells to interact
2) Chemotaxis: When activated, complement cells are cleaved into smaller cells to attract immune cells to the area
3) Cell Lysis: complement proteins start to bind to the antigen and to each other in MAC: MEMBRNAE ATTACK COMPLEX-causes lysis of cell
What happens with overactivation of a complement:
C3A, stimulates an inflammatory mediator like inflammatory interleukin 17, has been implicated in the chronic inflammatory association with asthma
Angioedema
he swelling of subcutaneous tissue. Can be from a # of causes of them is the deficiency of C1 esterase. An enzyme that disintegrates the complement protein C1
Multiple Sclerosis
a demyelinating disease of neurons and may result from the dysregulation of CR3, specific complement protein
Rheumatoid arthritis
oll like receptors are complement related receptors involved in the release of a # of inflammatory modulators. Overactivation of these toll like receptors by complement is indicated in rheumatoid arthritis.
Coagulation & clotting
Damage to a blood vessel- tissue factor is exposed to blood cells, stimulates a variety of enzymes and cofactors. Overall effect will be a clot
Platelet Activation
Vessel is damaged, the underlying collagen is exposed. collagen can bind to a glycoprotein on the surface of platelets called glycoprotein 1A2A
Von Willibrand Factor
Soluble protein that can bind &strengthen this bond between collagen and platelet. This bond allows the platelet to change its shape and release& activate a number of molecules including ADP, serotonin, & thromboxane A2. These chemicals draw more platelets to the other creating a platelet plug, which attracts fibrin to the plasma plug
Fibrinolysis
the destruction of the clot once it’s completed its task. This involves many enzymes
Dysfunctions of the Clotting Cascade
Hemophilia Von Willebrand disease Antiphospholipid Syndrome (Procoagulant syndrome) Aspirin- antiplatelet Plavix-antiplatelet Warfarin-antiplatelet
Antiphospholipid Syndrome
pro-coagulant, inactivation of these cause clotting disorders (DVTs)
Warfarin is used in patients with a history of
Antiplatelet.
Afib, stroke, pulmonary embolism
Vitamin K important for the maturation of many clotting factors
What happens when you inhibit vitamin K
you inhibit the coagulation cascade, and that’s exactly what coumadin does
Platelets
Form Platelet plug
release a # of vascular & inflammatory mediators that can cause vasoconstriction which helps to form the clot & < blood flow through the area which < shear forces.
-attract other procoagulant molecules to site of injury
-release GF
Phagocytes recognize antigens by
- binding to opsonized antigens or by using toll or scavenger receptors
- release cytokines & interleukins that help attract more phagocytes to the area
- uses ROS, myeloperoxidase, & peroxide
Phagocytic Cells include
Neutrophils, monocytes, & eosinophils
Polymorphonuclear neutrophils (PMNs)
These are WBC that have multilobed nuclei. Most prominent phagocyte. First WBC on the scene of action
Macrophages
Come from monocytes. Promote healing, angiogenesis- the creation of new blood vessels. Macrophages also release the protein GF which induces cellular reproduction & growth
Eosinophil
Another type of WBC that exhibits phagocytosis. See an > when there’s a parasite.
Antiparacytic phagocytic WBC
Also have a role in vascular mediation where the engulf & degrade vasoconstrictive molecules
