Immunity Flashcards
(61 cards)
1
Q
Inflammation
A
- recruitment of other WBCs = chemotaxis
- stabalizes tissue for repair
- swelling localizes damage
- vasodilation & increased capillary permeability
2
Q
Innate Immune system vs Adaptive Immune system
A
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
3
Q
stress and disease
A
Physiostress (infection, disease, external factors of stress) release CORTISOL during times of stress from adrenal cortex and stress makes us IMMUNOCOMPROMISED
4
Q
Immunity
A
- 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
5
Q
Adaptive Immunity
A
- 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
6
Q
Innate- immunity
A
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
7
Q
innate immunity - 1st line of defense
A
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
8
Q
Innate- Innate Immunity - 2nd line of defense
A
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”
9
Q
Innate- Why is inflammation physiologic?
A
it is a normal, good-functioning response in the body
- stabalizes tissue
- recruits WBCs
- stops spread of infection
10
Q
Innate- Why is inflammation pathologic?
A
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
11
Q
Innate- Diapedesis
A
leukocyte extraction, cells leave blood stream for tissues
- monos (in blood))/macros (in tissues) pacman, phagoctes
- neutrophils
- eosinophils
12
Q
Innate- chemotaxis
A
moving leukocytes to injured site
13
Q
Innate- phagocytes
A
= monocytes & macrophages, neutrophils
14
Q
Innate- hematology of immuno
A
- 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”
15
Q
Innate - Neutrophils
A
- 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
16
Q
Innate mast cells
A
- 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
17
Q
Innate - mast cell - synthesis
A
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
18
Q
Innate- mast cell arachidonic acid pathway
A
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
19
Q
Innate- Monocytes and Macrophages
A
- 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
20
Q
Innate- Eosinophils
A
- primary defense against parasitic worms
- regulate vascular mediators from mast cells histamine
- NOT phagocytic
21
Q
Innate- phagocytosis
A
- 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
22
Q
Innate - Natural Killers (NK) cells
A
- 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)
23
Q
Innate - cellular products - proteins
A
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
24
Q
Innate- plasma protein systems
A
- 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
25
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
1. opsonization = taggin a cell for destruction
2. chemotactic = attracts WBCs
3. produces membrane attack complex - pokes holes in bacterial membrane
26
Innate - cytokines
cell communication for immunity
27
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
28
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:
1. memory of antigens
2. specificity
3. antibodies
29
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
30
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
31
adaptive - Tolerance
* tolerance = us not killing "self cells" because we recognize them
- if you loose tolerance then you get autoimmune issues
TWO ARMS:
1. ab mediated/humoral - B cells
- antibodies = bacteria, viruses, toxins
2. 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
32
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:
1. memory cells
2. cytotoxic T cells (poke holes in cell)
3. helper T cells (stimulate both T and B cells)
4. Suppressor T cells (ramp down response)
Antigen activates B CELLS:
1. memory cells
2. plasma cells --> antibodies
33
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
34
adaptive - APC cell
antigen-presenting cell, lymphocyte
- accessory cells (also dendritic)
- APC activates helper T cells --> tell antibodies to release
35
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
36
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)
37
MHC2
APCs - dendritic, B cells, macrophage
| Fxn- presents processed antigen fragment to -> CD4 T cells
38
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
39
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
40
Secretory (mucosal) immune system
- lymphoid tissue that protects the external surface of the body
- Ab present in tears, sweat, saliva, mucus and breast milk
41
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
42
adaptive immunity
tighly regulated
| **MORE INFO**
43
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
```
44
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)
45
Immune Dysfunction
1. hypersensitivities
2. infection
3. immune deficiencies
46
humoral immunity
antibody mediated, b cell activation to make antibodies
47
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
48
IgM
- largest antibody
- 1st responder
- shows if you have a current infection
- synthesized during fetal life
- type ii hypersensitivity
49
IgA
- secretions
| - tear, saliva, mucous, breast milk
50
IgE
- allergic responses: stimulates mast cells and inflammation
- parasite infections
- Type i hypersensitibity - anaphylactic
51
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
52
Primary Immune Response
initial exposure -- latent period (B cells start to differentiate) -- after 5-7 days IgM antibodies are detected -- an IgG response follows
53
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
54
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
55
AIDS
- helper T count falls below 200
| - anywhere above = HIV
56
inappropriate immune responses
1. exaggerated - allergies
2. misdirected - autoimmunity (against self)
3. against beneficial foreign tissues - alloimmunity (transplant rejection)
4. insufficient - immune deficiency
57
Type I Hypersensitivities
1. ANAPHYLACTIC HYPERSENSITIVITY
2. Type 1
3. IgE antibody
4. Immediate (minutes)
5. Mast Cells
6. 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
58
Type II Hypersensitivities
1. Cytotoxic Hypersensitivity = Automimmunity against healthy tissue Specific
2. Type II
3. IgG, IgM
4. hours - days
5. Phagocyte
6. graves disease (creates antibodies against thyroid), rheumatoid arthritis, lupus (attacks muscles, cells)
EXP: systemic lupus erythematosus
- antibodies against nucleic acids, erythrocytes, coagulation proteins, etc.
59
Type III Hypersensitivity
1. Complex Mediated/ Antigen-Antibody - antigens get "stuck" in healthy tissue
2. Type III
3. ANY antibody
4. days - months
5. rare to no leukocyte involvement
6. wrong blood transfusion, serum sickness,
* C3B + neutrophils
* alloimmunity - rejection of foreign transplanted tissue, blood
60
Type IV Hypersensitivity
1. delayed reaction
2. Type IV
3. Years
4. NO antibodies
5. T Cells
6. 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)
61
Bacterial Infection
START HERE
