Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Immunology/Allergy > Immuno Physiology > Flashcards

Immuno Physiology Flashcards

1
Q

Organs of Immune System

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

*primary lymph organs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

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

A

Spleen and Liver

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Innate Defenses: Internal Responses

A
  • Phagocytes
  • NK
  • Inflamm response (Mf, mast cell, WBC, inflamm chemicalss)
  • antimicrobial proteins (INF & complement)
  • fever
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Natural Killer Cells

A
  • target non-self cells
  • induce apoptosis in cancer cells/ virus infected cells
  • secrete chemicals that enhance inflamm response
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

5 Cardinal Signs of Inflamm

A 
Redness
Heat
Swelling
Pain
Decreased Movement
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Please Review This!!!

A

SLIDE 26

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Interferons are produced by which body cells?

A
  • lymphocytes produces gamma IFN
  • WBC produce alpha IFN
  • Fibroblasts produce beta IFN
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Complement circulates in blood in inactive form? True or False

A

-TRUE

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Function of IFN

A
  • antiviral
  • inflamm
  • activate MF and NK
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

Fever Mech. & Benefits

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

A

Ag ability to stimulate proliferation of lymphocytes and aby

25
Q

Reactivity

A

ability of Ag to react with products of activated lymphocytes and abys

26
Q

2 important functional properties of Complete Ag

A

Immunogenicity

Reactivity

27
Q

What is an Antigenic Determinant?

A

certain parts of an entire Ag that are immunogenic, this is the site where lymphocyte receptors and abys bind

28
Q

Hapten

A

(incomplete Ag)
when alone does not elicit immune repsonse

when paired w/ body protein it can function as an Ag (immunogenic)

29
Q

What is MHC?

Classes of MHC?

A

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
Q

Cells of the Adaptive Immune System

A

B lymphocytes

T lymphocytes

APC (Mf, DC, B cell)

31
Q

Immunocompetence Def

A

lymphocytes able to recognize and bind to specific Ag

32
Q

Self- Tolerance

A

lymphocyte unresponsive to self-Ag

33
Q

Basic Lymphocyte Maturation process

A

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
Q

T Cell Maturation

A

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
Q

Self-Reactive B Cells undergo_____ to reverse self-reactivity

A
  1. ) apoptosis
  2. ) Receptor Editing

*if self-reactive B cells escape from bone marrow, they become inactivated.

36
Q

Genes determine which foreign substances the immune system will recognize and resist, True or False?

A

TRUE!

37
Q 
APC; 
function
types of cells
A
  • 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
Q

DC cells are unique because_____.

A

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
Q

B cell Activation/Clones

A
  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
Q

Fates of B cell Clones

A

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
Q

Immunological Memory:

Primary and Secondary Immune Responses

A

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
Q

Active Humoral Immunity
When does this occur?
Name 2 types

A

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
Q

Passive Humoral Immunity
When does this occur?
Name 2 types

A

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
Q

Aby Structure

A

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
Q

Aby Types and Facts

A

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
Q

Defense Mechanisms for Abys

*INACTIVATION

A

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
Q

Defense Mechanisms for Abys

*FIXES AND ACTIVATES

A

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
Q

Monoclonal Aby

A

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
Q

Types of T cell Ag Receptors and what do they become?

A

T cell receptor Types: CD4 and CD8

CD4 becomes Thelper
CD8 becomes Tcytotoxic

Review slid 79*

50
Q

Humoral Immunity targets:

A

Bacteria and molecules in extracellular environments

51
Q

Cellular Immunity Targets:

A

Viruses, bacteria, cancerous cells, transplanted foreign tissues

52
Q

MHC proteins synthesized in….?

A

Endoplasmic Reticulum

53
Q

MHC I binds _____ Ag in ____ where the Ag-MCH complex then travels & binds to _____.

A

endogenous Ag

Endoplasmic Reticulum

plasma membrane where it displays the Ag on surface of cell.

54
Q

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 ____.

A

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
Q

T cell activation (2 step process)

A
  1. Antigen binding

2. Co-stimulation

Immunology/Allergy (8 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions