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Immuno Physiology Flashcards

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1
Q

Organs of Immune System

A 
Tonsils/Adenoids
Lymph Nodes & Vessels
Thymus*
Spleen
Peyers Patches
Appendix
Bone Marrow*

*primary lymph organs

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2
Q

Immune system stem cells develop in which organsn during prenatal development?

A

Spleen and Liver

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3
Q

Lymphocytes develop and mature in which organs?

A

B cells develop and mature in bone marrow

T cells develop in bone marrow but mature in Thymus

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4
Q

Differences between Innate and Adaptive Immunity

A

Innate: no memory, its just there, not learned.

  • Surface Barriers: skin & mucous membranes
  • Internal Defenses: phagocytes, fever, NK cells, antimicrobial proteins, inflammation

Adaptive: memory, specificity, systemic

  • Humoral Immunity (B cells)
  • Cellular Immunity (T cells)
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5
Q

What are the body’s main 3 lines of defense?

A

Innate:

  1. ) Skin and mucosa (physical barriers)
  2. ) antimicrobial proteins, phagocytes, inflamm (most important)
    * kill anyone

Adaptive:
3.) attacks SPECIFIC foreign substances, takes longer time to react than Innate

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6
Q

Innate Defenses: Types of physical barriers

A
  • surface: skin, mucous
  • protective chemicals: skin acidity, sebum, HCl (stomach), saliva, lacrimal fluid
  • Respiratory: mucus-coated hairs, cilia of upper respiratory
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7
Q

Innate Defenses: Internal Responses

A
  • Phagocytes
  • NK
  • Inflamm response (Mf, mast cell, WBC, inflamm chemicalss)
  • antimicrobial proteins (INF & complement)
  • fever
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8
Q

Phagocytic Cell Types

A

Mf- free and fixed, develop from Monocytes, cheif phagocytic cells

Neutrophils- roaming around looking for infectious material, become phagocytic once they encounter infectious material in tissues

Dendritic Cells

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9
Q

Phagocytosis Mechanism

A
  1. ) Phagocyte adheres to pathogen via opsonization (yummy)
  2. )Phagocyte forms pseudopods, engulfs particles forming phagosome
  3. ) Lysosome and phagosome fuse forming phagolysosome
  4. ) Lysosomal enzymes (acid hydrolase), digest particles
  5. ) Exocytosis of particles
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10
Q

Steps in Phagocytic Mobilization

A

1.) leukocytosis: neutrophil release from bone marrow in response to leukocytosis-inducing factor released from injured cells
(neutrophil enter blood from marrow)

2.) Margination: neutrophils cling to walls of capillaries in inflamed area
(neutrophil cling to capillary wall)

3.) Diapedesis of neutrophils: when phagocytic cell migrate out of capillary
(neutrophils flatten and squeeze out of capillary)

4.) Chemotaxis: inflamm chemical promote movement of neutrophil
(neutrophil follow chemical trail)

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11
Q

Phagocytosis: Methods of destruction of pathogen mechanism (when pathogen is in phagolysosome; how it dies)

A
  1. ) Acidification & digestion by lysosomal enzymes
  2. ) Respiratory Burst: release of cell killing free-radicals
  3. ) Oxidizing Chemicals
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12
Q

Natural Killer Cells

A
  • target non-self cells
  • induce apoptosis in cancer cells/ virus infected cells
  • secrete chemicals that enhance inflamm response
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13
Q

5 Cardinal Signs of Inflamm

A 
Redness
Heat
Swelling
Pain
Decreased Movement
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14
Q

Inflamm. Response

A
  1. ) Tissue Injury
  2. ) TLR of Mf, epithelial, DC, neutrophils, T cell, B cell, & others becomes activated by seeing Ag and secrete cytokines promoting inflamm.
  3. ) Other inflamm mediators: Histamine, kinins, prostaglandins, leuoktrienes, and complement increase cytokine release.
  4. )Inflamm. chemicals cause dilation of arterioles, increased permeability, edema & exudate (made up of proteins, clotting factors, and abys)
  5. ) Healing
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15
Q

Function of Exudate in Edema

A

moves foreign material into lymphatic vessels

delivers clotting proteins to form scaffold for repair

isolates the area

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16
Q

Please Review This!!!

A

SLIDE 26

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17
Q

What are Antimicrobial Proteins and how do they function?

A

Interferons and complement proteins: interfere w/ microorganism ability to reproduce

*interferon especially interfers w/ viral replication

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18
Q

Mechanism of Interferon Action

A
  1. ) Virus enter cell A
  2. ) IFN genes switch on
  3. ) Cell produces IFN molecule
  4. ) IFN binding on cell B (non-infected cell) stimulates cell production of antiviral protein
  5. ) Antiviral protein blocks viral reproduction
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19
Q

Interferons are produced by which body cells?

A
  • lymphocytes produces gamma IFN
  • WBC produce alpha IFN
  • Fibroblasts produce beta IFN
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20
Q

Complement circulates in blood in inactive form? True or False

A

-TRUE

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21
Q

Function of IFN

A
  • antiviral
  • inflamm
  • activate MF and NK
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22
Q

Complement Pathways and Mechanisms

A

1.) Classical Pathway- complement (C1) binds to aby-Ag complex….activation of proteins in orderly sequence until C3—> c3B initiates MAC & opsonization, forms pore, cell lysis. C3A- causes inflamm. response

Alternative Pathway:
inactivated complement proteins are activated when they are exposed to mediators (MBL, CRP,), series of enzymatic rxns that cleave complement proteins, C3 into C3B and C3A. C3B=MAC & opsonization, form pore, cell lysis C3A- inflamm response

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23
Q

Fever Mech. & Benefits

Study These Flashcards
A
  • Leukocytes and MF exposed to foreign substances and secrete pyrogens
  • pyrogen reset body thermostat

Benefits: causes liver and spleen to sequester iron and zinc

increases metabolic rate (speeding up repair)

24
Q

Immunogenicity

Study These Flashcards
A

Ag ability to stimulate proliferation of lymphocytes and aby

25
Reactivity
ability of Ag to react with products of activated lymphocytes and abys
26
2 important functional properties of Complete Ag
Immunogenicity Reactivity
27
What is an Antigenic Determinant?
certain parts of an entire Ag that are immunogenic, this is the site where lymphocyte receptors and abys bind
28
Hapten
(incomplete Ag) when alone does not elicit immune repsonse when paired w/ body protein it can function as an Ag (immunogenic)
29
What is MHC? | Classes of MHC?
Major Histocompatabilty Complex. ``` protein molecules (self-Ag) on the surface of ALL cells. -unique to all individuals ``` MHC I- all body cells except RBC MHCII- on APC
30
Cells of the Adaptive Immune System
B lymphocytes T lymphocytes APC (Mf, DC, B cell)
31
Immunocompetence Def
lymphocytes able to recognize and bind to specific Ag
32
Self- Tolerance
lymphocyte unresponsive to self-Ag
33
Basic Lymphocyte Maturation process
B cells "mature" in Bone marrow, T cell "mature" in Thymus, then exported to lymph nodes, spleen, & other lymph organs where they encounter Ag, then they become active and MATURE, circulate in blood & lymph.
34
T Cell Maturation
Undergo Positive and Negative selection *Those who are positively selected are capable of binding self-MHC proteins (MHC restriction) * Those who are negatively selected cannot recognize self-Ag displayed by self-MHC, if recognize self apoptosis occurs. ---ensures self-tolerance. - eliminates self-reactive T cells that could cause autoimmune disease. *only 2% make it through the process.
35
Self-Reactive B Cells undergo_____ to reverse self-reactivity
1. ) apoptosis 2. ) Receptor Editing *if self-reactive B cells escape from bone marrow, they become inactivated.
36
Genes determine which foreign substances the immune system will recognize and resist, True or False?
TRUE!
37
``` APC; function types of cells ```
- engulf Ag and present to T cell * Mf remain fixed in lymphoid organs * DC internalize pathogen and enter lymphatics to present Ag to T cell in lymphoid organs. -DC, Mf, Bcell
38
DC cells are unique because_____.
They are the only APC able to induce primary immune response in a resting naive T-lymphocyte. To do this, DC are capable of capturing, processing, and presenting Ag on the cell surface along w/ appropriate co-stimulation
39
B cell Activation/Clones
1. )B Cell become activated when Ag bind to its receptors & cross-link them 2. ) Receptor-mediated endocytosis of cross-linked antigen-receptor complex occurs 3. ) stimulated B cell grows to form clone of identical cells bearing the same antigen-specific receptors. (T cells required to help B cells achieve full activation)
40
Fates of B cell Clones
Plasma Cells- secrete Abys which may circulate in blood/lymph, bind free Ag, mark Ag for destruction. Memory Cells- provide memory, mount immediate response to future exposures for same Ag.
41
Immunological Memory: Primary and Secondary Immune Responses
Primary:- occurs w/ 1st exposure - lag period: 3-6days - Peak level of plasma aby: 10day - Aby levels decline Secondary: -occurs on re-exposure to same Ag, respond within hours - Peak Level of plama: 2-3days at much higher levels - Aby bind w/ greater affinity - Aby level can remain high or weeks/months *review pictures slides 61&62
42
Active Humoral Immunity When does this occur? Name 2 types
OCCURS when B cells encounter Ag and produce specific abys against them -the body is exposed to an antigen and works to create an immune response, creating a memory for that antigen Natural: exposure to antigen through the environment Artificial: vaccine
43
Passive Humoral Immunity When does this occur? Name 2 types
B cells are not challenged by antigens. The body is given antibodies for a specific antigen so memory cells are not produced. Natural:mother to fetus Artificial: injection of serum (after snake bite) (hep C)
44
Aby Structure
T or Y shaped - 2 identical heavy chains - 2 identical light chains - Variable region of each chain at tip from two identical ag-binding sites - Constant region (everything but variable) determines aby class (IgM,IgA,IgD,IgG,IgE)
45
Aby Types and Facts
IgM- first responder to acute infection, can activate complement, may be monomer/pentamer IgA- breast milk, saliva, sweat, protects mucous membranes IgD- found on B cells, needed for maturation of B cells IgG- most abundant, only Ig that crosses placenta, activates complement, binds Mf IgE- binds eosinophils, Basophils, Mast cells; parasitic infections, allergy, hypersensitivity rxns
46
Defense Mechanisms for Abys | *INACTIVATION
Ag-Aby complex INACTIVATES BY: -neutralization- simplest, aby blocks specific sites on Ag & prevents binding to other cell receptors....phagocytosis - agglutination- ABy bind same determinant on more than one cell-bound Ag * cross linked Ag-Aby complex agglutinate -precipitation- soluble molecules are cross-linked, complexes precipitate and are subject to phagocytosis & enhances inflammation
47
Defense Mechanisms for Abys | *FIXES AND ACTIVATES
COMPLEMENT: ***main aby defense against cellular Ag -leads to cell lysis, amplifies inflamm respsonse opsonization, and enlists more and more defense elements such as *INACTIVATION
48
Monoclonal Aby
commercially prepared PURE ABY proliferate indefinately and have ability to produce a singly type of Aby * used in research, clinical testing, and CANCER TREATMENT
49
Types of T cell Ag Receptors and what do they become?
T cell receptor Types: CD4 and CD8 CD4 becomes Thelper CD8 becomes Tcytotoxic Review slid 79*
50
Humoral Immunity targets:
Bacteria and molecules in extracellular environments
51
Cellular Immunity Targets:
Viruses, bacteria, cancerous cells, transplanted foreign tissues
52
MHC proteins synthesized in....?
Endoplasmic Reticulum
53
MHC I binds _____ Ag in ____ where the Ag-MCH complex then travels & binds to _____.
endogenous Ag Endoplasmic Reticulum plasma membrane where it displays the Ag on surface of cell.
54
MHC II binds _____ Ags. _____ prevents incorrect Ag from binding in ER. _____ and _____ vesicles form. Vesicles fuse, ____ is removed and antigen is ____. Vesicle then travels to ____.
exogenous Invariant chain phagolysosome (containing exogenous antigen and lysosome) MHC II Invariant chain Loaded (with MHC) plasma membrane where is displays the AG on the surface of the cell.
55
T cell activation (2 step process)
1. Antigen binding | 2. Co-stimulation

Immunology/Allergy (8 decks)

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