Chapter 7 Innate Immunity Flashcards
1
Q
Name the three types of lymphocytes.
A
- T-cells (thymus cells)
- B-Cells (Bone Marrow derived)
- NK cells (Natural Killer)
2
Q
Where do T cells mature?
A
In the Thymus
3
Q
Where do B cells and NK cells mature?
A
Bone Marrow
4
Q
What are the three lines of Defenses in the body?
A
- First Line-Natural Barriers
- Second Line- Inflammation (innate immunity)
- Adaptive (acquired) Immunity
5
Q
What are Physical Barriers?
A
Keeps hazardous materials out of body
Includes hair, epithelium, secretions, skin, linings of the GI, GU, and respiratory tract
6
Q
What are mechanical barriers?
A
Act of “mechanical cleansing” of cells due to vomiting, urination, mucous production, sneezing, and coughing.
7
Q
What are Biochemical Barriers?
A
Antibacterial peptides in mucous trap organisms
Cathelicidins, defensins, and Collectins (lungs) bind to carbohydrate structures on the surface of a pathogen and recruit other cells and molecules to come destroy.
Microbiomes inhibit colonization: ex. gut and vaginal flora
8
Q
How do Microbiomes work?
A
Chemicals (Ammonia, phenols, and indoles) are released to prevent infection.
9
Q
What is an example of a microbiome in the vagina?
A
Lactobacillus creates lactic acid and hydrogen peroxide to prevent infection.
10
Q
What is an example of failed microbiome?
A
Getting C-diff from extended use antibiotics; Killed the microbiome (flora) in the gut
11
Q
What is Innate Immunity?
A
- Process of Inflammation response acts as Second line of body’s defense.
- Takes place same way every time no matter what the stimulus of pathogen is.
- Rapidly initiates
- No memory cells involved. Once the inflammation response is over
12
Q
What causes activation of the inflammatory response?
A
infection; mechanical damage; ischemia; nutrient deprivation; temperature extremes; and radiation
13
Q
What are cardinal signs of the inflammatory process?
A
Redness, Swelling, heat, inflammation
14
Q
What are the steps of the inflammatory Response?
A
- Cellular injury
- Pathogenic invasion
- Mast cells degranulate
- Vascular Response
- Activation of the plasma protien systems (Complement, Clotting, Kinin)
- Release of Cellular Products
15
Q
How long does an acute inflammatory process take?
A
8-10 days from onset to healing.
16
Q
What happens during the vascular response of the inflammatory process?
A
- Blood vessel dilates (Increases blood flow)
- Vascular permeability increases (lets macrophages in)
- WBC adhere to vessel walls
- WBC migrate thru the vessels (Diapedesis)
17
Q
Describe the Vascular Response in detail.
A
Inflammation is visible within seconds after vascular response is initiated. Arterioles near the injured area initially constrict, then vasodilation causes increased blood flow to the injured site. Increased blood flow and capillary permeability result in leakage of plasma from the vessels causing swelling in surrounding area. Increased blood flow and increasing concentration of red cells cause local warmth and redness. Biocemical mediators (histamin, bradykinins, leukotrienes, prostaglandins) stimulate the endothileal cells that line the capillaries and venules to retract allowing the tight junctions to open and let in the leukocytes and plasma into surrounding tissues. Once inside the plasma synthesis systems begin to prevent infection and further damage; limit and control the inflammatory process, elicit a more specific response; and prepare the area for healing.
18
Q
Name the three plasma protien systems.
A
- Compliment system
- Clotting System
- Kinin System
19
Q
How do the plasma protien systems work?
A
The systems are crucial for an effective immune response
They each play a unique role and when the first is activated the others are sequentially activated.
20
Q
How is the complement system activated?
A
- Classical pathway -activated by (antibodies-antigen) response
- Lectin Pathway -activated by mannose containing bacteria
- Alternative Pathway- activated by gram negative bacteria and fungal cells
21
Q
Activation of the complement system results in what?
A
Direct destruction of pathogens via:
- Opsonization- (tags microorganisms for destruction and allows phagocyte to attatch)
- Anaphylatoxin Activation-
- (induce mast cell degranulation,)
- Cell lysis
- C5-C9 form the membrane attack complex is a that create pores in the membranes of target cells allow water to pour in, leading to cell lysis and cell death.
- Leukocyte chemotaxis-
- drawing in WBC to the injured site or organism
**Starts killing right away once activated***
22
Q
What is the compliment System?
A
Part of the Plasma protien system.
Destroys pathogens directly and most potent defender mostly against bacteria.
Destroys target cell membranes
Stimulates inflammation
Attract Phagocytes
Enhances Phagocytosis
23
Q
In the Compliment Cascade, what do the complement protiens C1-C5 do and C5-C9
A
C1- initiates activities of classical pathway
C2- affects smooth muscles; promotes vasodilation & permeability
C3, C4, C5- anaphylatoxins (induce mast cell degeneration)
and release histamine.
C5- chemotactic factor to attract WBC.
C5-C9- form the membrane attack complex that bind to the lipid bilayer of cell membranes forming cylindrical channels (pores). These pores in the membranes of target cells allow water to pour in, leading to cell lysis and cell death.
24
Q
What is the complement system responsible for?
A
Destroying pathogens directly.
Activates or collaborates with every other aspect of the inflammatory response.
25
What does the Clotting System do?
Forms a fibrounous mesh via FIBRIN at an injured or inflammed site to prevent the spread of infection.
1. Stops bleeding.
2. Helps prevent the spread of inflammation and infection.
3. Keeps the invader near the site of injury, thus maximizing the access of inflammatory cells and proteins.
4. Results in the formation of two peptides (fibrinopeptides A and B) that are released during the formation of fibrin and are chemotactic for neutrophils and increase vascular permeability
5. Forms clot to Provides a framework for repair and healing
26
What is Chemotaxis?
Movement of an organism up a chemical gradient in response to a chemical stimulus.
Chemical signaling that causes leukocytes to move toward an area of inflammation. C3a and C5a are the complement components most involved in chemotaxis
Chemotactic factors attract the organism to move up the gradient to the specific destination.
\*\*\*Attract the WBCs to the injured tissue site or inflammed area.
27
What are Cytokines?
Small proteins that signal cells. Different types function within immune response and play different roles.
28
What do Cytokines do?
Regulate innate and adaptive immunity by affecting other neighboring cells and telling them what to do.
Pro inflammatory or Anti inflammatory.
Each cytokine regulates differently depending on target cell with which it binds.
Include IL, Interferons, or and tumor necrosis factorsIL-10: antiinflammatory
TGF-B: antiinflammatory
29
What is the Kinin System?
Functions to activate and assist inflammatory cells by releaseing prostaglandis to cause dilation of vessels, smooth muscle contraction, increases vascular permeability, and increase leukocyte chemotaxis.
30
How does the Kinin system work to keep the inflammatory response confined?
Plasmin regulates clot formation by degrading fibrin and fibrinogen.
Hagement factor activates clotting cascade,
31
What is the primary prostaglandin released by the Kinin system and what does it do?
Bradykinin; causes dilation of blood vessel and stimulates nerve endings which induce pain.
32
What are Phagocytes?
Remove cellular debris and respond to invasion of foreign pahtogens.
Monocytes
Macrophages
Microphage- neutrophils and eosinophils
33
How do Phagocytes work?
Remove cellular debris and respond to invasion by moving thru diapedesis and exhibiting chemotaxis.
34
What is Diapedesis?
The passage of blood cells through the intact walls of the capillaries, typically accompanying inflammation.
35
What are interluekins (IL)?
Help regulate inflammation.
IL-1: Fever; activates phagocytes and lymphocytes
IL-6: helps with healing
Il-10 anti-inflammatory
36
WHat are two important chemotactic factors?
1. Nuetrophil chemotactic factor- attracts nuetrophils to site.
2. ECF-A- attracts eosinophils to the site of inflammation.
37
When are chemotactic factors released?
During Mast Cell degranulation
38
What are chemotactic factors?
Biochemical substances that attract luekocytes to the site of inflammation.
39
What is the role of memory cells regarding immunity?
They are long lived and capable of remembering the antigen and respond more rapidly after each exposures to the remembered antigen.
40
What is hypersensitivity?
What are the four types?
Is an altered immunologic response to an antigen that results in disease or damage to the host.
Is characterized by the immune mechanism.
Type I-IgE mediated
Type II-Tissue‐specific reaction(
Type III-Immune complex mediated
Type IV-Cell mediated • Delayed
41
How do memory cells in immunity create such a rapid response?
On reexposure, memory cells have the memory from previous exposure and do not require further differentiation they instead immediately become new plasma cells or effector T cells.
42
What are interferons?
Type of Cytokine. Serve to protect healthy cells from viral infection by stimulating the cellular production of antiviral proteins
Protects agians viral infections.
Modulates inflammatory response.
Produced and released by infected host
\*\*Does not directly kill viruses but prevents them from infecting addtional healthy cells (Interferes)
43
What do INF-alpha and INF-beta do?
Induce production of antiviral protiens (Disrupt RNA synthesis)
Ex. Interferon is a tx for Hepatitis C; can also cure certain genotypes now.
44
What does INF-y do?
Increases the microbiocidal activity for macrophages.
45
How do INF-alpha and beta work?
They are released from infected host, attach to a receptor on a neighboring cell; if the neighbor is uninfected, they produce antiviral protiens to prevent other cells from becoming infected.
46
What is TNF-alpha?
A cytokine secreted by macrophages.
Produces local and systemic effects
Induces fever, increases proinflammatory proteins
Can causes muscle wasting and intravascular thrombus.
Probably responsbible for fatalities in shock related to gram negative bacteria bc TNF increases fever and gram negative thrive off of elevated temps.
47
What is opsonization?
Occurs during the compliment system to encourage the process of Phagocytosis.
The complement C3b and C5b (along with antibodies) make it easier for phagocytes to ingest bacteria.
Phagocytes have receptors on their surfaces for complement and antibodies and can thus "grab" onto the bacteria and pull them into the cell to be destroyed.
Allows the Macrophage to select and be able to phagocytize a pathogen.
48
What are the steps of Phagocytosis?
1. Macrophage recognizes foriegn material thru opsonization
2. The macrophage adheres to the foreign material to become a Phagosome.
3. The Phagosome fuses with the lysosome to form a Phagolysosome
4. The lysosome ingests the foriegn material, kills and digests and removes the cellular debris thru exocytosis.
49
What is the purpose of Margination in the inflammation process?
Alters the inside of the surface of the capillary allowing nuetrophils to stick/adhere to the capillary wall. Which then creates permeability by retraction of pores in vessel to allow the nuetrohpil to leak escape to the tissues.
50
How do Monocytes grow into Macrophages and how does this affect the inflammatory process?
Monocytes are produced in the bone marrow, they are released into the circulation and continue growing until they become Macrophages.
3-7 days after the nuetrophils (first defenders) arrive, the Macrophages arrive at the inflammatory site.
The process of phagocytosis begins upon Macrophage arrival.
51
What role do Eosinophils play in the inflammation response?
Nuetrophils and Eosinophils are primary phagocytes. Eosinophils are a weak phagocyte but do respond in large numbers during parasitic infection.
52
What is the First Line of defense?
Physical, Mechanical, and Biochemical Barriers.
1. Physical: skin
2. Mechanical: linings of the GI, GU, Resp tract (coughing, sneezing, urination, vomiting
3. Biochemical: microbiomes
53
What is the Second Line of Defense?
The Inflammatory Response
54
What is the Third Line of Defense?
Acquired Immunity
The ability for the body to have memory and continue protecting the body with subsequent exposures.
Long term immunity
55
What is the classical pathway of the compliment system?
Antigin-antibody system
Activated by protiens of the adaptive immunity system (antibodies) bout to their specific targets (Antigen)
56
What is the Lectin Pathway in the Compliment System?
Activate by Mannose containing bacterial carbohydrates
57
What is the Alternative Pathway of the Compliment System?
Gram-activated by negative bacterial and fungal cell wall
58
Which pathway is most common form of Compliment System?
Classical Pathway (antigen-antibody)
59
Which Plasma Protien System releases Chemotactic Factors?
Compliment System
60
What happens with mast cell degranulation?
Inflammatory cytokines and chemotactic factors are released.
Attracts WBC (neutrophil & eosinophil) to inflammatory site
Cause vascular effects: increased permeability and vasodilation.
61
What are the three groups of active complement components and what do they do?
C3a and C5a – chemotaxis and degranulate mast cells (anaphylatoxins);
C3b and C5b – opsonize encapsulated bacteria;
C5-C9 – membrane attack complex.
62
What does the membrane attack complex do?
C5-C9 bind to the membranes of target cells and create pores through which water pours into the cells, leading to cell lysis and death.
63
What does activation of the Kinin system do?
Activation of the kinin system causes:
1. Vasodilation (hyperemia)
2. Increased vascular permeability (fluid exudation)
3. Chemotaxis of inflammatory leukocytes
4. Smooth muscle contraction (bronchoconstriction)
5. Pain
64
Which plasma protiens system causes cell lysis and death via membrane pores?
Compliment; C5-C9 bind with membranes to form pores. The clotting and kinin systems do not do this.
65
Which Plasma Protien System causes Vasodilation (hyperemia) and increased vascular permeability (fluid exudation)?
Complement system, clotting system, and kinin system
C3a and C5a activate mast cell degranulation and, therefore, vasodilation and endothelial cell contraction with increased vascular permeability. The clotting system and bradykinin also cause these vascular effects.
66
Which Plasma Protien System activates chemotaxis of inflammatory leukocytes?
. Complement system, clotting system, and kinin system
C3a and C5a are chemotactic, as are the fibrinopeptides of the clotting system. The kinin system participates in chemotaxis as well.
67
Which plasma protien system activates opsonization?
Compliment System
68
The major inflammatory cytokines are:
Interleukins
Interferons
Tumor necrosis factor-alpha
69
Which Interluekin causes fever?
IL-1
70
What role does Cortisol and Hydrocortisone play during stress response?
Increases cortisol release by adrenal glands
Stimulates gluconeogenesis (increase blood sugar)
Powerful anti inflammatory/immunosuppressive
71
What does ACTH do during stress response?
Stimulates the adrenal glads to release cortisol
72
What happens in the body during a stress response?
1. The SNS is activates; hypothalmus releases CRH.... stimulates the pituitary glad
2. Releases ADH and oxytocin
3. Anterior pituitary relecease ACTH to release Cortisol.
73
When Adrenal Gland releases catecholemines which are released and how much?
Large amounts of Epi
Small amounts of Norepi
74
What role does Epi play in the stress response?
Increase CO, blood flow, dilates vessels and airways, increases delivery of oxygen to the body.
75
What role does Norepi play in stress response?
Increases arousal; vigilance; anxiety; mental alertness
Constricts viscera of the skin, shifts blood flow to the vessels dilated by EPI,
76
What activates cortisol?
ACTH
77
What negative effect can glucagon have on the body during stress response?
Worsens autoimmune disease
78
What role does Growth Hormone have on the body during Stress Response?
Released from anterior pituitary gland
Produced by lymphocytes and mononuclear phagocytic cells
Counters the effect of insulin
Affects protein, carbohydrate and lipid metabolism
Chronic stress leads to suppression of GF.
79
The stress response is initiated by what two systems in the body?
The CNS and Endocrine System
80
What happens during the neuroendocrine response to stress?
1. The SNS stimulates the adrenal medulla
2. Catecholamines released (epi & Norepi)
3. Hypothalmus secretes CRH
4. Stimulates the pituitary to secrete ACTH
5. Stimulates the adrenals to secrete Cortisol
81
How do antibodies nuetralize toxins?
Protective antibodies can bind with toxins to prevent their interaction with cells and neutralize effects.
Detection of the presence of these protective antibodies can aid in the diagnosis of disease.
82
What is the difference between antitoxins and toxoids?
Antitoxins- Protective exotoxins that are immunogenic and elicit production of protective antibodies.
Toxoids- Vaccines against baceterail toxins
83
What will you see on a "left shifted" CBC?
Increase in number of circulating leukocytes
(Primarlily increase in nuetrophils)
For left shift you will see:
Higher ratio of immature to mature neutrophils (bands)
84
What are Segs?
Mature White blood cells seen on a CBC
85
What are Bands?
Immature nuetrophils seen on a CBC
86
If you see that nuetrophils are increased on a CBC, what kind of infection is most likely?
Bacterial infection
87
If you see Increased Lymphocytes, what infection is most likely?
Viral
88
How do autoimmune diseases damage organs?
Immune system reacts to self-antigens.
Persons own tissues are damaged by autoantibodies and auto reactive T cells.
89
What are antigens?
Molecules that can react with antibodies or receptors on B cells and T cells
90
What are immunogenic Antigens?
an antigen that can trigger an immune response
91
What determines immunogenic capability for an antigen?
1. Degree of foreignness to the host (MOST IMPORTANT)
2. Size
* (Large=very immunogenic)
* (Small= hapten-needs carrier protien to become immunogenic)
3. Chemical Complexity-
* greater diversity the more immunogenic
4. Amount (high/low)
* either extreme can cause tolerance
92
What are the functions of prostaglandins and how are they inhibited?
Synthesized by Mast Cells
Create vascular effects and nuetrophil chemotaxis:
Dilation, increased permeability; exudation; Pain
Inhibited via ASPIRIN and NSAIDS
93
What are short acting chemotactic factors vs long term?
Histamine is a shorter acting chemotactic factor
Prostaglandins and Luekotrines are longer acting and involved in the later stages of inflammatory response.
Stimulate slower and more prolonged responses.
94
What are end products of adaptive immunity?
B and T cells
Antibodies
95
What is specificity in terms of adaptive immunity?
Each T or B cell only recognizes one antigen, but together they can recognize a host of foreign antibodies.
96
What is the role of adaptive Immunity?
Provides long term protection with memory to recognize rexposures and create protection to them
97
WHat role does humoral immunity play?
Primary cells in Humoral immunity are B cells (Bone Marrow)
Causes direct inactivation of a microorganism
Protects agains bacteria and viruses
98
What role does Cell Mediated immunity Play?
Differentiates T cells (thymus)
Kills target cells directly or stimulates activity of other leukocytes.
Protects against viruses and Cancer
99
How do Humoral and Cell Mediated Immunity work together within Adaptive Immunity?
They work together to provide immunity and memory
Create the ability for the body to respond more rapidly and efficiently on subsequent exposures to same antigen.
100
What are antibodies?
Produced by plasma B cells
Five classes of antibodies:
* IgG
* IgA
* IgM
* IgE
* IgD
101
What is IgG?
1. Most abundant type of antibody
2. Transported across the placenta (Passive Immunity)
3. Most protective immunity against infections
4.
102
What is IgM?
Largest of immunoglobulin
First antibody produced to initial exposure
Detected after 5-7 Days
Synthesized early in neonatal life
If IgM is detected; active infection present
103
What is IgE?
Least concentrated
Common in allergic responses and parasitic infections
Initiates inflammatory reaction to attract Eosinophils
104
What is IgA?
Two subclasses: Blood and body fluids
IgAs may be protected against enzyme degredation
Protects most of protective activity in body secretions
105
What are Major Histocompatibility Complexes (MHC)?
Glycoproteins on the surface of all human cells (Except RBCs)
Help with antigen expression.
In order for an effective immune response, antigens have to be expressed in a specific way.
MHC help T cells respond to antigens by binding to the T-cell at a receptor site.
MH1- present antigens to Cytotoxic T cells
(Cancer, viruses)
MH2- present antigens to T helper Cells.
(B-cell)
106
What is the role for Helper T cells?
Most numerous T cell
They help in the function of the immune system
These are the cells that become unable to work in HIV
107
What is the role of cytotoxic T (Killer) cells?
These are direct attack cell kills micro-organisms and even sometimes the bodies own cells.
Play a vital role in killing cancer cells heart transplant cells and other types of cells foreign to the body.
108
How do MHC play a role in transplanted organs?
Cells in transplant tissue have a different set of MHC surface antigens than those of the recipient.
This can form an undesired immune response against the transplant tissue (foreign MHC).
NOTE: the more similar two individuals HLA tissue type, the more successful the transplant will be.
109
What are the MHC-1?
Genes: A,B,C
Endogenous antigens
Important with viral and cancer cells
110
What are MHC-2?
Exogenous antigens
Reacts with CD4 and Helper T cells
Important with Bacterial Infections
Located where body is exposed to Environment (Lung, gut, GU tract)
111
Where are MHC-2 located?
In epithileal cells where body is exposed to the environment
Lung
Gut
GU tract
112
Where are MHC-1 located?
Inside all nucleated cells and platelets. Except Red blood cells
113
What are the roles of teh T-Helper Lymphocytes?
Help the antigen-driven maturation of B and T cells (differentiation) to create memory cells.
114
What to T-Helper 1 cells do? (TH-1)
Provide help in cell mediated immunity
Activate differentiation of macrophages and T cells
115
What do T-Helper 2 (TH-2) cells do?
Provide help in developing humoral immunity.
Activate differentiation of B cells
116
How are B cells activated?
When a B cell encounters an antigen for the first time, B cells are stimulated to differentiate and proliferate.
A differentiated B cell becomes a plasma cell
(Plasma cells are factories for antibody production)
117
Where are antibodies produced?
Plasma cells are factories for antibody production.
118
What is the difference between primary immunity and secondary immunity?
Primary- 1st exposure where immune system is primed and memory is developed. IgM first responder is detected after 5-7 days. IgG responds in similar quanitity
Secondary- subsequent exposure where response is larger and more rapid due to memory from first exposure.
IgM and IgM both produced but IgG is in larger number.
119
How long after an exposure does it take for IgM to be detected?
5-7 Days
120
What is the Type I hypersenstivity?
IgE mediated against environmental antigens (allergens)
Histamin is released
* Increases chemotactic factors
* H1- bronchoconstriction, edema, vasodilation
* H2-increase in gastric secretions
Ex. Pollen allergies most common
121
What is Type II hypersensitivity?
Tissue specific reactions.
Specific cell or tissue is the target of an immune response.
Five mechanisms:
* cell is destroyed by antibodies
* Cell destruction occur through phagocytosis
* neutrophils release granules
* Antibody dependent cell-mediated cytotoxicity is present
* Causes target cell malfunction
Ex. Myasthenis Gravis; Abo Incompatibility
122
When does an immediate hypersensitivity react?
Minutes to Hours
123
When does a delayed hypersensitivity react?
Hours to days later
124
What is anaphylaxis?
Hypersensitivity reaction resulting from sensitization to an antigen by prior contact.
Can be systemic or cutaneous
125
What is the Pnuemonic for remembering Hypersensitivity Responses?
ACID
A-Type I: Anaphlyaxis (IgE mediated)
C- Type II: Cytoxic; Cell Specific reactions (IgG and IgM)
I- Type III: Immune Complex
* (antibody binds to soluble antigen)
D-Type IV: Delayed
126
What is an allergy?
Produces deleterious effects of hypersensitivity to environmental antigens
127
What is autoimmunity?
Disturbance in immunologic tolerace of self antigens
Can cause auto immune diseases
128
What is Alloimmunity?
An immune reaction to tissues of another individual
Also called isoimmunity
Ex. Transplant rejection
129
What is a Type III hypersensitivity?
Immune complex mediated
Formed in circulation and deposited later into vessel walls or tissues
NOT ORGAN Specific
Damage comes from complement activation and nuetrophil lysosomal enzymes
Ex. Serum Sickness: affected tissue; Raynaud Phenomenon
Arthus Reaction
130
What is a Type IV sensitivity?
Cell Mediated/Delayed
Mediated by T lymphocytes
Caused by direct killing from cytotoxic T cells
Examples: Acute graft rejection; skin test for TB; contact allergic reaction; some autoimmune diseases.
131
How do you test for immunity?
1. CBC with diff
2. Quantitative determination of Immunoglobulins
3. Assay for total Complement
4. Skin Tests
132
What are replacement therapies for Immune Deficiencies?
1. IV/IM Gamma Globulin- lasts only 3-4 weeks
2. Trasplant or transfusion
* must match up HLA's for success
3. Treatement with immune modulators
* Helps with T cell function
4. Gene Therapy
133
Death from infection accounts for how much worldwide?
1/3
134
What are the phases of clinical disease?
1. Incubation- initial exposure
2. Prodromal- first symptoms; mild discomfort and fatigue
3. Invasion-
4. Convalescence- Recovery or becomes fatal or latent
135
How does HIV affect CD4 (Helper T) Cells?
HIV infects Helper T cells which have CD4
* Depletes the bodys T helper cells
* Decreases thymic production of T cells
CD4 less than 200 = AIDS
136
CD4 are specific to what type of Cell?
T cells
137
What happens in HIV to the CD4 receptor
HIV attaches to the CD4 receptor and releases RNA into the cytoplasm.
Depletes bodys Thelper cells
Decreases production
Increases susceptibility to infection
138
What is the role of nuetrophils in immunity?
Predominant phagocyte early in inflammation site.
First responder
Arrive 6-12 hours after initial injury.
Inject bacteria by phagocytosis
Eat cellular debris
Short lived
139
What is the role of Monocytes (WBC) in immunity?
Produced in the Bone Marrow
Enter Circulation and grow into Macrophages while migrating to inflammatory site
Increase Glucose metabolism; more lysosomes; secrete IL
Enter site later 3-7 days after nuetrophil and gradually replace neutrophils.
140
What is the role of Macrophages in immunity?
Larger mature cell that eats and destroys cellular debris and infectious agents
Important cellular initiator of inflammatory response
141
What do vaccines do?
Preent the initiation of disease
142
What is an attenuated vaccine?
Weakend live virus
MMR; Rotavirus; oral polio
143
What is an inactivated vaccine?
Killed virus
Flu; Hep A; Polio
144
What is a recombinant vaccine?
Hep B; HPV
145
What is a toxoid?
Vaccine against bacterial toxins
Dtap
146
What is a conjugated vaccine?
Conjugated with a carrier protein to increase immunogenicity
Hib
147
What is an Extracted Capsular Polysaccharide Vaccine?
Dead bacteria
Meningococcal; Pnuemococcal
148
What are CD4 cells?
Helper T cells
149
What are CD8 Cells?
Cytotoxic T Cells (Killer)
150
Which T cells recognize MHC 1 and 2 protiens?
MHC 1 recognize Cytotoxic T Cells
MHC 2 recognize Helper T cells
151
Which types of WBC cells are involved in Innate Immunity?
Nuetrophils
Macrophages
Natural Killer Cells (cytotoxic cells that aren't T cells)
152
What types of WBC are involved in Acquired Immunity?
B Cells
T Cells
153
How many symptoms confirm SLE?
Four
154
What are symptoms of SLE?
Eleven findings are common.
– Presence of at least four findings indicates SLE.
• Facial (malar) rash, discoid rash, photosensitivity, oral or nasopharyngeal ulcers, nonerosive arthritis, serositis, renal disorders, neurologic disorders, hematologic disorders, immunologic disorders, and presence of antinuclear antibodies (ANAs)
155
What are characteristics of Type I?
## Footnote
Type 1 DM- T-cell infiltration of the pancrease and destruction of the insulin producing beta cells, usually (not always) presents before 40.
Autoantibodies are formed against pancreatic cells
Indicative of an autoimmune disease d/t presence of several human leukocyte antigen class II alleles.
Strong evidence that some infections can contribute to the activation of the autoimmune response in Type 1 DM.
Need Insulin for life
Association of specific human leukocyte antigen (HLA) class II alleles is 40%
Those who do not have aspartic acid at position 57 of the DQ chain are 100 more times more likely to get Type 1 DM.
\*\*\*\*\*Risk Factors-
Affects males and females relatively equal
siblings face substantial risk of about 6% compared to 0.3-0.5% of general population.
Risk increases with diabetic parent especially if from father
Male diabetic parent risk is 4-6%
Female diabetic parent risk is only 1-3%
156
What are characteristics of Type II DM
Type 2 DM- accounts for 90% of all diabetes cases
Patho: Some endogenous insulin production. Can usually be treated with diet modification and/or oral drugs. TCF7L2 gene significantly associated with diabetes because it encodes a transcription factor involved in insulin secretion.
Risk Factors: positive family history and obesity.
157
