Brainscape's Knowledge GenomeTM

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


See full index

AVS 471 > Immunology > Flashcards

Immunology Flashcards

1
Q

What are some infectious agents to an animals environment?

A
  • Viruses
  • Bacteria
  • Protozoa
  • Parasites
  • Fungi
  • Prions
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Health/Disease Triangle

A

Host-Agent-Environment

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

Intracellular Pathogens vs. Extracellular Pathogens

A

• All viruses, some bacteria and some protozoan parasites
replicate inside host cells
• Immune responses must recognize and destroy the infected
cell
• Many bacteria and larger parasites live in tissues, body fluids
or other extracellular spaces
• The immune system must differentiate between the two
• Intracellular pathogens exist as extracellular pathogens en
route to their target cell

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

Primary function of the immune system

A

• Eliminate infectious agents and minimize the

damage they cause.

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

external defenses in immune response

A

Effective against many organisms
• Skin, forms a thick multicellular barrier. Fatty acid secreted from
sebaceous glands keeps the skin PH between 5-5.5. This low PH is
bactericidal to certain bacteria.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

routes of access

A
  • GI epithelia
  • Urogenital
  • Nasopharynx
  • Lung
  • Direct blood contact
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

external defenses

A

• Lysozyme in tears and secretions dissolves and destroys the
cell wall of bacteria especially gram +
• Respiratory tract – cilia which lines the respiratory tract
removes foreign particles, mucous/secretions flush FB away.
• Skin – fatty acids, physical barrier commensal organisms
• Urinary Tract – flushing
• GI Tract – Commensal organisms, stomach acid, PH changes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

internal defenses

A
  • blood
  • WBC
  • Macrophages
  • Neutrophils
  • Eosinophils
  • Basophils
  • Lymphocytes
  • Monocytes
  • RBC
  • spleen
  • lymph
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Innate Immunity (non-adaptive)

A

• Non-specific, most primitive
• Phagocytosis, consisting of the phagocytic cells of the reticuloendothelial
system (Macrophages); Neutrophils, Eosinophils, and Basophils
• Does not alter with repeated exposure

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Adaptive immunity

A
  • Specific, more sophisticated
  • Includes Lymphocytes, their progeny and their extracellular products
  • Improves with each successive exposure to the same pathogen (“Memory”)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

innate immune response

A 
White blood cells(Leukocytes)
• Primarily responsible for eliciting and coordinating the
immune response
• Phagocytes
• Monocytes, macrophages, polymorphonuclear
neutrophils, eosinophils, basophils
• Bind, internalize, kill microorganisms
• Nonspecific=>Innate immune response
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Phagocytes

A 
• Innate immune response
• Derived from bone marrow stem cells
• Mononuclear phagocytes
• Engulf particles including infectious agents and destroy
them
• Strategically placed (e.g. kupffer cells-liver)
• Monocytes (blood)
• Macrophages (tissue)
• Act as Ag presenting cells
• Polymorphonuclear neutrophils (PMN)
•Majority of blood leukocytes
•Migrate to tissues in response to certain stimuli
• Engulf material, destroy it, and die.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

lymphocytes

A

•Central to adaptive immune response
• Specifically recognize individual pathogens
• Two major categories
•B-lymphocytes(B-cells)
• T-lymphocytes(T-cells)
•Wholly responsible for specific immune recognition
of pathogens=> central to adaptive immune
response.
•All derived from bone marrow stem cells
• T-cells develop in Thymus
•B-cells develop in bone marrow (in adults)
•In the fetus the immune process begins in the yolk
sac, then fetal liver, bone marrow takes over close
to parturition.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

B-lymphocytes

A

B-cells
• Combat extracellular pathogens and their
products(Antigen, Ag) by releasing Antibody (Ab)
•Originate in the bone marrow
•Migrate to and locate in the spleen and lymph
nodes throughout the body
•Genetically programmed to encode a surface
receptor specific for a particular Ag
•Undergo stimulation by Ag and increase rapidly in
numbers
•Differentiate into plasma cells which secrete Ab

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

T-lymphocytes

A

T-cells
• Control of B-cell development and Ab production
• Interact with phagocytic cells to help them kill
• Recognize cells infected with viruses
Produced in the bone marrow
• Undergo maturation process in the Thymus gland
• Migrate to lymph glands and enter circulation
• Constitute 40-60% of all circulating lymphocytes in blood.
• Secrete factors called cytokines
• Cytokines assist phagocytes and macrophages in destroying
pathogenic microorganisms
• Do not manufacture Ab
• T-cells sometimes called memory cells
• T-cell immunity=>Cell mediated immunity (CMI)
Several different types
• T-helper (TH) cells – two types
TH1-secrete Interleukin-2 (IL-2) and Interferon (INF).
These are important in the CMI response and killing of
intracellular pathogens (viruses, bacteria, parasites)
TH2 – secrete IL- 4,5,6,10. Important in antibody
mediated response (Humoral immunity) and free- living
organisms.
- T-cytotoxic (Tc) cells
- Destruction of host cells infected with viruses or other
intracellular pathogens
T-suppressor (Ts) cells – suppress immune responses
• T-cells recognize antigens in association with familiar
markers on host cells=T-cell receptor(TCR). Similar in
structure and function to B-cell antigen receptor site.
• T-cells generate their effects by releasing soluble proteins
called cytokines.

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

cytotoxic cells

A

a cell that can injure or kill other cells
•Recognize surface changes on tumor cells
and virally infected cells
•Use non-specific mechanisms
•Natural Killer activity or NK cells
•Eosinophils
•Engage and damage large extracellular
parasites
Cytotoxic Reactions
• Directed against whole cells too large for phagocytosis
• Cell recognition by TCR or Ab bound to cell surface
• Granules directed at target cells
• Perforins – create holes in target’s outer membrane

17
Q

Apotosis

A

• Cytotoxic cells can signal target cells to undergo

programmed self-destruction

18
Q

acute phase proteins

A

mediator of immunity
• Molecules normally present in serum
• Concentrations increase rapidly during infection
• Fibrinogen = acute phase protein; used in ruminants and
horses as in indicator of an acute inflammatory response

19
Q

complement protein

A

Group of serum and cell surface proteins activated by
factors such as Ag/Ab combination resulting in enzyme
cascades that have a variety of biological consequences
such as cell lysis and opsonization.
• Alternate activation pathway
• Spontaneous
• Innate, nonspecific response
• Classical activation pathway
• Ab mediated activation
• Adaptive response
• Cascade reaction = compliment cascade

20
Q

cytokines

A 
soluble mediator of immunity
Signaling molecules
• Proteins or glycoproteins
• Interferons(IFNs)
• IFNa,IFNb – virally infected cells
• IFNg – activated T-cells
• Interleukins(Ils)
• IL-1 to IL-5
• Direct other cells to divide and differentiate
• Act on cells that express the correct IL receptor
21
Q

colony stimulating factor

A

• Direct division and differentiation of bone marrow stem cells,
blood leukocyte stem cells, and further differentiation of some
cells outside the bone marrow.
• Other cytokines
• Tumor Necrosis Factor
• TNFa, TNFb
• Transforming Growth Factor
• TGFb
• Mediators of inflammation and cytotoxic reactions

22
Q

Antibody

A 
• Specifically binds to Ag
• Binding region diversity
• Mediates secondary effects
• Soluble form of B-cell Ag receptor
• Immunoglobulin
• Fab portion binds Ag
• Fc portion binds with other immune elements, e.g.
phagocytes, complement
• Act as opsonins
23
Q

neutralization

A

– Ab binds to pathogen preventing

infection

24
Q

phagocytosis

A

• Phagocytosis – Ingestion and destruction of
antigenic material
• Ab can activate complement or act as an opsonin
• Phagocyte binds to opsonized Ag
• Pseudopodia fuse with Ag enjulfing and internalizing it
(endocytosis)
• Reactive oxygen intermediates (ROIs) secreted by
phagosome
• PMNs contain lactoferrin
• Lysosomal granules=>enzymatic degradation

25
Q

antigen

A

Any molecule that is recognized by the
adaptive immune elements.

Ab does not bind to the whole of a foreign agent,
instead it binds to one of many molecules, i.e.
antigens, on the organism’s surface.
•Hence, there may be several different Abs for a
given pathogen.
•Ab binds to a specific region of the antigen, known
as the epitope.
•An Ag may have several different or repeated
epitopes.

• T-cell recognition of Ag
• Ag must be presented to a TCR(T-cell receptor)by an
Antigen Presenting Cell. (APC)
• Antigen presenting cells phagocytose Ags and process
them presenting small polypeptide fragments on the
surface of the host cell (phagocyte).
• Antigen fragments are presented on the host cell surface
by a specialized group of molecules referred to as the
Major Histocompatibility Complex (MHC) molecules

26
Q

immune responses-lymphocytes

A

Lymphocytes are the key to immune recognition in
adaptive immune responses
•Clonal selection
–Proliferation of cells that recognize a specific Ag
– Stimulated lymphocytes express new receptors allowing
them to be recognized by cytokines from other immune
cells proliferation.
–When infection has resolved some newly produced
lymphocytes remain = Memory Cells => lasting immunity.

27
Q

extracellular pathogen goal

A

Destroy pathogen and neutralize its products

28
Q

intracellular pathogen goal

A

T-cell destruction of infected cell (cytotoxicity) or
T-cell activation of phagocyte to destroy pathogen

**Many pathogens have both intracellular and
extracellular phases.
**Hence, Ab may decrease spread in blood stream and Tc
cells kill cells already having an established infection.

29
Q

auxillary immune cells

A
  • Basophils and mast cells
  • Contain granules that release mediators of inflammation
  • Platelets
  • Release inflammatory mediators
30
Q

inflammation

A

• Immune cells distributed throughout the body
• Need to focus the response to a specific site during
infection=>Inflammation
• Three major events
• Increased blood supply to infected region.
• Increased capillary permeability permitting larger than
normal molecules to breach the vessel wall (soluble
mediators e.g.complement)
• Leukocytes migrate out of venules into surrounding tissue
( Diapedesis)
• Neutrophils, Monocytes and Lymphocytes

31
Q

vaccination

A

•Utilizes two key elements of the adaptive immune
response, Specificity and Memory
•Memory cells allow the immune system to mount a
much stronger response to a second encounter with
an Ag. Faster and more effective.
•Vaccines contain altered forms of a pathogen or its
toxins which retain antigenicity but are innocuous.
• Subunit
• Killed whole organism
• Attenuated live

32
Q

immunopathology

A
  • Autoimmunity
  • Immunodeficiency
  • Hereditary
  • Acquired
  • Hypersensitivity
  • Excessive immune response to a given Ag
  • Allergy
  • Transplant rejection and transfusion reactions
33
Q

hypersensitivity reactions

A

Type I – Immediate
• Typical allergic reaction
• IgE binds Mast cells, basophils and eosinophils, via Fc
receptor>Degranulation>Release of Histamine and
Heparin
• Type II – Antibody Dependent Cytotoxicity
• Transfusion reaction, drug induced
• IgM and IgG mediated
• Complement mediated lysis or cellular cytotoxicity
• Type III – Immune Complex Deposition
• Autoantibodies form immune complexes w/
autoantigens => inflammation.
• SLE
• Local tissue damage, e.g., renal
failure(glomerulonephritis), rheumatoid arthritis.
• Type IV – Delayed Type Hypersensitivity
• Tuberculin Test
•Ag sensitized T-cells release cytokines following
secondary contact with an Ag>Attract
macrophages which release inflammatory
mediators

AVS 471 (9 decks)

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