Immunity Flashcards
Inflammation
- recruitment of other WBCs = chemotaxis
- stabalizes tissue for repair
- swelling localizes damage
- vasodilation & increased capillary permeability
Innate Immune system vs Adaptive Immune system
INNATE: you are born with these
- Physical Barriers - skin, mucous membranes
- Chemical Barriers - saliva, tears, stomach acid, sweat, earwax = lysosomes
- Inflammation - nonspecific laukocytes
* external system within the body = GI tract, Respiratory tract
ADAPTIVE: aquired
- changes within us due to exposure
- build and change across our lifetime
- hygenine hypothesis - we are too clean and not getting the exposure we need for healthy immune systems
stress and disease
Physiostress (infection, disease, external factors of stress) release CORTISOL during times of stress from adrenal cortex and stress makes us IMMUNOCOMPROMISED
Immunity
- BARRIERS: Integumentary System (skin and mucous membrane)
- first line of dense against infection and injury
- constant/continuous defense
- nonspecific
- Inflammatory response - hematology mediated
- very hard to turn off once stimulated
- second line of defense in response to injury or infection
- Immediate response
- nonspecific
- mast cells, granulocytes (neutrophils, do’s, bass’s) Mono’s/Macro’s, platelets, endothelial cells = non-specific white blood cells
- mast cells and bass cells are Pro-inflammatory = release histamine and heparin as an immediate inflame response
Adaptive Immunity
- Lymphocytic System
- 3rd line of dense
- specific, acquired, memory. humoral
- in response to antigen exposure
- VERY Specific
- delay between exposure to antigen and maximum response
- T & B lymphocytes, macrophages, and plasma cells
- anitbodies
- cell-mediated immunity = t cells
- anitbody-mediated immunity = b cells
Innate- immunity
multilevel system of interactive defense
- 1st line of defense = innate resistance, barriers
- physical and biochemical (skin and mucous membranes)
- 2nd line of defense = inflammation (innate)
- rapid, non-specific
- 3rd line of defense = adaptive (acquired) immunity = memory
- specific, memory
innate immunity - 1st line of defense
BARRIERS
- physical and mechanical
- skin
- linings of GI, GU and Resp. Tracts
- sloughing of cells removes bacteria from layers, coughing, sneezing, vomiting, mucous and cilia
- Biochemical Barriers
- synthesized and secreted - “washing” saliva, tears, ear wax, sweat, mucus
- antimicrobial peptides (skin, urethra)
- normal bacterial flora
Innate- Innate Immunity - 2nd line of defense
Inflammatory Response - response to injury or vascularized tissue
- Classic symptoms of local effect
S swelling - increased blood flow
H heat - vasodialtion
A a loss of function - damages, inflammation, trigger to not use
R redness - bloodflow
P pain - tissue releases chemicals to tell body “don’t use me”
Innate- Why is inflammation physiologic?
it is a normal, good-functioning response in the body
- stabalizes tissue
- recruits WBCs
- stops spread of infection
Innate- Why is inflammation pathologic?
hard to turn off inflammation chronic inflammation 1. fluid dynamics change - edema, BP 2. Stress on system - effects heart rate, BP, heart muscle 3. immunosuppressed - low WBC count
Innate- Diapedesis
leukocyte extraction, cells leave blood stream for tissues
- monos (in blood))/macros (in tissues) pacman, phagoctes
- neutrophils
- eosinophils
Innate- chemotaxis
moving leukocytes to injured site
Innate- phagocytes
= monocytes & macrophages, neutrophils
Innate- hematology of immuno
- WBCs = leukocytes
1. Granulocytes: cytoplasmic pockets - B basophils
- E eosinophils
- N neutrophils
2. Agranulocytes
Lymphocytes, monocytes (immature in bloodstream) - T & B cells = specific fighters
- NK cells “take out bad guys”
Innate - Neutrophils
- first responder
- most abundant of WBCs
- primary phagocyte
- ingest, destroy anything foreign or damages
- chemotaxis = called to injured site
- diapedesis = go in blood to injured site
- phagocyte - 1st in early inflammation (6-12 hours)
- mediators - attract and activate complement proteins and mast cells (cytokines)
- pus = “war zone” = dead tissues, cells, dead reg. tissue
Innate mast cells
- release histamine and heparin
- start the inflammation process
1. vasodilation
2. increased capillary permeability: gives us signs of SHARP
Degranulation: cytomplasmic granules activate and release
- histamine release = vascular effects
- increased blood into microcirculation
- histamine also increase vascular permeability
- histamine increases adherence of leukocytes to the endothelium
* these all equal inflammation - Chemotaxis of more neuters
- chemotaxis of more dos
Chemotactic factors:
- neutrophil chemotactic factor = kill bacteria in early stages
- eosinophil chematic factor = regulate inflammatory response
Innate - mast cell - synthesis
causes 3 major effects: 1. paltelet activation factors: clotting Activation of arachnoid acid to: 2. vascular effects via leukotienes 3. vascular effects and pain via prostaglandins
Innate- mast cell arachidonic acid pathway
mast cell synthesis produces 4 products
- leukotrines: leukocytes = increase inflammation
- similar effects to histamine in late stages. inreaseses inflammation and brings more WBCs - prostaglandins: endothelium = inhibits platelet agreg and induces vasodialtion
- similar effects to leukotrines and PAIN
- increase inflame and cap perm and pain - platelet-activation factor (thromboxanes) = platelets
- increase platelet agree and vasoconstriction
- increase clotting and inflame - Prostacyclin = regulates other 3 effects = decreases clotting, inflame, and pain = apririn, ibuprofen
Innate- Monocytes and Macrophages
- appear 24 hours ager injury - replace neutrophils
- attracted by macrophage chemotactic factor from neutrophils
- phagocytic cell
- APC activates adaptive immune system “antigen-presenting cell”
- ingests pathogen, takes parts of the protein it ingests and shows off to other cells to show them what to kill
Innate- Eosinophils
- primary defense against parasitic worms
- regulate vascular mediators from mast cells histamine
- NOT phagocytic
Innate- phagocytosis
- process by which a cell ingests and disposes of foreign material
- cells migrate out of the blood - though basement membrane
- pavementing = line up along basement membrane
- diapedesis = leukocyte extraction into blood stream
Innate - Natural Killers (NK) cells
- special kind of T cell
- nonspecific lymphocyte
- primary fxn is to kill - viruses, abnormal host cells (cancer or tumor cells and non-specific abnormal cells that don’t look right)
Innate - cellular products - proteins
Cytokines: cell communication signals
- interleukins - pyrogens (cause fever)
- interferons - viral infections (let neighbor cells know about it)
- tumor necrosis factor
Chemokines: chematic cytokines
* induce leukocyte chemotaxis - causes chemotaxis at injured sites
Innate- plasma protein systems
- proteins made in the LIVER and circulate the blood
- inactive enzymes (proenzymes)
- sequential activation = cascade communication confirmation. are you sure? are you really sure? really really?
3 plasma proteins essential to effective inflame/immune response:
- complement system: immune responses series of protein cascades
- coagulation system: clotting
- Kinin system: increase pain and inflammation
Innate- complement system
- activates innate and adaptive responses
- triggers and modulates a variety of immune activities and acts as a linker between the two branches of the immune response
- maintains cell homeostasis by eliminating celuarl debris and immune complexes
- opsonization = taggin a cell for destruction
- chemotactic = attracts WBCs
- produces membrane attack complex - pokes holes in bacterial membrane
Innate - cytokines
cell communication for immunity
Innate immunity Inflammation
- local manifestations: increase vasodilation & permeability
- vascular changes with leakage
- vasodilation and increase permeability
- SHARP
*exudative fluid - serous (watery, early), fibrous (thick, blotted, more advanced. amber color, thick, sticky, more proteins), Purulent (bacterial infection, pussy and smelly), hemorrhagic (bloody)
Inflammation causes systemic effects:
- fever = infection
- endogenous (within, interleukins), exogenous (pathogen produced
- act on hypothalamus - reset and turn on pyro
- leaukocytosis , increase number WBCs
- increases plasma proteins (LIVER)
- acute phase reactants - 10-40 hours. increase clotting factors
- CHONIC INFLAMM = lasting longer than 2 weeks. often unsuccessful acute inflammatory response
- stimulus isn’t removed
- chronic injury, smoking-related
adaptive immunity
- 3rd line of defense = T & B cells
- Aquired, specific
- cell-mediated T cells
- humoral/antibody-mediated B cells
3 important things to remember about adaptive:
- memory of antigens
- specificity
- antibodies
adaptive - Immunity Terminiology
active vs. passive
natural vs. artificial
ACTIVE = acquired
- producing memory, activates T & B cells
PASSIVE = straight antibodies, no memory
NATURAL= we get exposed naturally in our environment ARTIFICAL = injection into body
- Natural Active = common illness and infection, memory
- Artificial Active = injection and produce B and T cells = vaccination
- Natural Passive = mother breastfeeding passing on antibodies through breatmilk; in womb antibodies travel through placenta
- Artifical Passive = inject antibodies; AFTER the fact - rabies shot, ebola antigens, anti-venom
adaptive - Anitgens and Antibodies
- Antigens = Foreign or non self particles/proteins(ag)
- viruses, bacteria, cancer ,fungi, parasites
- noninfectious = pollens, foods, bee venom
- dugs, vaccines, transfusions, transplants
- B cells produce antibodies
- antigens react with antibodies or receptors on B and T cells
- Antibodies = proteins produced by immune system
- immunogens/immunoglobins/ig
*EPITOPE = region of the antigen that is recognized by antibody
adaptive - Tolerance
- tolerance = us not killing “self cells” because we recognize them
- if you loose tolerance then you get autoimmune issues
TWO ARMS:
- ab mediated/humoral - B cells
- antibodies = bacteria, viruses, toxins - cell-mediated - T Cells
- react directly with ag on cell surfaces - NK
- stimulate other leukocytes (cell to cell or cytokines) T
- cytotoxic cells - verses infected cells and cancer
adaptive - T cells vs. B Cells
- T cells = made in bone marrow, mature in thymus
- thymus teaches the cells self vs. non-self. Starts in puberty then shrinks to fatty tissue by adulthood
- B cells = made and mature in bone marrow
T CELLS:
- memory cells
- cytotoxic T cells (poke holes in cell)
- helper T cells (stimulate both T and B cells)
- Suppressor T cells (ramp down response)
Antigen activates B CELLS:
- memory cells
- plasma cells –> antibodies
adaptive - Clonal diversity
produces millions of T and B cells each with different receptors
- immunocompetent cells become active if meet up with specific antigen
- hang out in lymphatic tissue waiting for antigens to come or helper T cell to activate them
= recognition and activation of lymphocytes
- first phase in fetus
- recognition of millions of antigens
adaptive - APC cell
antigen-presenting cell, lymphocyte
- accessory cells (also dendritic)
- APC activates helper T cells –> tell antibodies to release
adaptive - MHC
Major Histocompatibiity complex = flagging to determine self from non-self
- 2 classes:
- *MHC1 = endogenous pathogens = viruses & cancer
- on all nucleated cells
- ag binds with MCH1 to activate cytotoxic T cells (CD8)
- *MHC2 = extracellular pathogens = bacteria & toxins
- on phagocytic cells: macrophages, APC, B lymphocytes
- Ag bings with MHC2 to activate helper T cells (CD4)
- **MHC1 = CD8
- **MCH2 = CD4
MHC1
all nucleated cells
fxn: present processed antigen to - 1. cytotoxic CD8 and T cells = cancer prevention. 2 .NK cells = constant screening (no binding with MHC needed)
MHC2
APCs - dendritic, B cells, macrophage
Fxn- presents processed antigen fragment to -> CD4 T cells
CD cells
cluster of differentiation
- additional membrane bound proteins
- FXN: aids in the function of the immune cells
- defines the functionally distinct subset of cells
- CD4 helper T cells - binding receptor-from APCs
- CD8 cytotoxic T cells - binding receptor: from all nucleated cells
adaptive - Antibodies
IgG - most abundant, transported across placenta, four classes
IgA - secretions
IgM - largest, fetal life
IgD - low concentration
IgE - allergic responses, parasite infections
- Direct Functional Effects: neutralization, agglutination, precipitation
- Indirect Functional Aspects: opsonization, complement
Secretory (mucosal) immune system
- lymphoid tissue that protects the external surface of the body
- Ab present in tears, sweat, saliva, mucus and breast milk
cell-mediated immune response
- viruses, tumors, pathogens resistant to neutrophils and macrophages
- mature T cells: cytotoxic (Tc, attack and destroy directly by using cells); Regulatory Helper T (Th, cell mediated, humoral mediated, suppressors); memory cells
adaptive immunity
tighly regulated
MORE INFO
Primary and secondary Immune Responses
PRIMARY
- initial exposure
- latent period (B cell differentiation)
- after 5-7 days (igm antibodies detected)
- an IgG response follows
SECONDARY - more rapid - large amounts of Ab are produced - rapid response 2 hours to memory cells - IgM - similar 1 hour response IGg - greater number
active vs. passive immunity
ACTIVE
- antibodies or T cells produced after either a natural exposure to an antigen or after immunization
PASSIVE
- performed Ab or T lymphocytes are transferred from a donor to a recipient
- passive immunity of the fetus = IgG (crosses placenta)
Immune Dysfunction
- hypersensitivities
- infection
- immune deficiencies
humoral immunity
antibody mediated, b cell activation to make antibodies
IgG
- most abundant
- lasts a long time in the blood
- transports across the placenta
- Type ii hypersensitivity
- the amount of it shows the level of immunity you have to something
IgM
- largest antibody
- 1st responder
- shows if you have a current infection
- synthesized during fetal life
- type ii hypersensitivity
IgA
- secretions
- tear, saliva, mucous, breast milk
IgE
- allergic responses: stimulates mast cells and inflammation
- parasite infections
- Type i hypersensitibity - anaphylactic
direct and indirect functional effects of antibodies
direct: neutralization, agglutination, precipitation
indirect: opsonization - tagging for killing by phagocyte & Complement - assists both innate and adaptive responses
Primary Immune Response
initial exposure – latent period (B cells start to differentiate) – after 5-7 days IgM antibodies are detected – an IgG response follows
secondary immune response
- explosive, more rapid
- large amounts of antibodies are produced
- IgM appears within an hour
- IgG in much great numbers
- can clear within 2 days
active vs. passive immunity
ACTIVE: antibodies or T cells produced after either a natural exposure to an antigen or after immunization
PASSIVE: preformed antibodies or t lymphocytes are transferred from a donor to a recipient exp: IgG for hepatitis A exposure or tetanus toxoid
AIDS
- helper T count falls below 200
- anywhere above = HIV
inappropriate immune responses
- exaggerated - allergies
- misdirected - autoimmunity (against self)
- against beneficial foreign tissues - alloimmunity (transplant rejection)
- insufficient - immune deficiency
Type I Hypersensitivities
- ANAPHYLACTIC HYPERSENSITIVITY
- Type 1
- IgE antibody
- Immediate (minutes)
- Mast Cells
- allergic asthma, hay fever, urticaria (hives), conjunctivitis, rhinorrea (runny nose), gastroenteritis (vomiting, diarreah)
EXP: bee sting
1st profuce IgE antibodies – 2nd IgE binds to antigens – activates mast cells – creates inflammation
Type II Hypersensitivities
- Cytotoxic Hypersensitivity = Automimmunity against healthy tissue Specific
- Type II
- IgG, IgM
- hours - days
- Phagocyte
- graves disease (creates antibodies against thyroid), rheumatoid arthritis, lupus (attacks muscles, cells)
EXP: systemic lupus erythematosus
- antibodies against nucleic acids, erythrocytes, coagulation proteins, etc.
Type III Hypersensitivity
- Complex Mediated/ Antigen-Antibody - antigens get “stuck” in healthy tissue
- Type III
- ANY antibody
- days - months
- rare to no leukocyte involvement
- wrong blood transfusion, serum sickness,
* C3B + neutrophils
* alloimmunity - rejection of foreign transplanted tissue, blood
Type IV Hypersensitivity
- delayed reaction
- Type IV
- Years
- NO antibodies
- T Cells
- poison ivey, latex sensitivity, celiac disease,
- mediated via T cells and takes time to develop
3 types: DElayed type = antigen is injected into dermis (PPD test TB exposure); Contact Hypersensitivity = absorbed into epidermis (latex sensitivity); gluten-sensitive enteropathy = absorbed by the GI (celiacs)
Bacterial Infection
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