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principals of animal healthcare and diseases > topic 1: basic concepts of immunology > Flashcards

topic 1: basic concepts of immunology Flashcards

1
Q

what is the three levels of defense in vertrate immune system

A
  1. physical barriers (skin, mucous membranes - in nose, lungs)
  2. innate immune system (macrophage, neutrophils, NK cells
  3. addaptive/ aquired immune system (B cells, T cells)
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2
Q

immune system comprises

A

-cellular components
-non-cellular components: chemical mediators (cytokines) and complement proteins

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3
Q

How do drugs kill pathogens

A
  • recognise (pathogen, foreign molecule)
    -attack
    -eliminate )destroy the invading pathogens)
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4
Q

monocyte

A

immune system: inate

function: differenciates into macrophages and dendritic cells
cytokine production

activated by: cytokine

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5
Q

Macrophages

A

immune system: inate

function:
1) Engulf and digest cellular debris, foreign substances,
microbes, cancer cells, and dead or dying cells
(2) Cytokine production

activated by: cytokine, helper T cells (CD4+ T cells)

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6
Q

Dendritic cells

A

immune system: Innate

functions:
(1) Ability to capture, process, and present antigens to T helper cells
(2) Cytokine production

activated by: cytokines

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7
Q

Neutrophils
(most abundant type of
granulocytes)

A

immune system: Innate
functions:
(1) Engulfing and digesting pathogens, particularly
bacteria
(2) Cytokine production

activated by: Cytokine

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8
Q

Basophils
(least common type of
granulocytes)

A

immune system: Innate

functions: (1) Contain granules filled with histamine and involvement
in allergic responses
(2) Cytokine production

activated by: Cytokine

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9
Q

Eosinophils
(type of granulocytes)

A

immune system: innate

function:
(1) Highly effective at fighting parasitic infections,
especially those caused by worms (helminths)
(2) Cytokine production

activated by: Cytokine

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10
Q

Mast Cells

A

immune system: Innate

functions: 1) Contain granules filled with histamine and involvement in
allergic responses
(2) play a role in tissue repair and wound healing
(3) Cytokine production

activated by: cytokine

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11
Q

Natural Killer Cells

A

immune system: Innate

functions: (1) highly effective at recognizing and destroying cells infected
with viruses and tumour WITHOUT the need for antigen
presentation
(2) release toxic molecules (such as perforin and granzymes)
(3) Cytokine production

activated by: Cytokine

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12
Q

Natural killer T cells

A

immune system: immune adaptive

functions:1) highly effective at recognizing and destroying cells infected
with viruses and tumour WITHOUT the need for antigen
presentation (innate)
(2) can recognize lipid and glycolipid antigens (adaptive)
(3) release toxic molecules (such as perforin and granzymes)
(4) Cytokine production

activated by: cytokines

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13
Q

Gamma delta (γδ) T
cell

A

immune system: Innate Adaptive

functions:
(1) ability to recognize a wide variety of antigens such as
proteins, lipids, and small molecules (adaptive)
(2) highly effective at recognizing and destroying cells infected
with viruses and tumour
(3) release toxic molecules (such as perforin and granzymes)
(4) Cytokine production

activated by: Cytokine

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14
Q

B cells

A

immune system: adaptive

functions: (1) Differentiate into plasma cells to produce large
amount of Ab
(2) Some B cells become memory B cells providing long-term immunity

activated by: Helper T cells
(specifically
CD4+ T cells)

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15
Q

Helper T Cells
(CD4+ T Cells

A

immune system: adaptive

functions 1) Activate B cells, cytotoxic T cells, macrophages
(2) Cytokine production

activated by: dendritic cells, B cells

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16
Q

Cytotoxic T Cells
(CD8+ T Cells

A

immune system: adaptive

functions: 1) directly killing infected or abnormal cells
(2) release toxic molecules (such as perforin and granzymes

activated by: Helper T cells ( CD4+T cells )

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17
Q

Regulatory/Supress
or T Cells

A

immune system: Adaptive

functions: (1) preventing autoimmune diseases, where the immune
system mistakenly attacks the body’s own tissues

activated by: Helper T Cells
(CD4+ T Cells)

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18
Q

non immune cells: endothelial cells

A

immune system: innate

functions: (1) Regulate immune responses by expressing adhesion
molecules that allow immune cells to attach to the blood vessel wall and migrate into tissues during inflammation or infection
(2) Cytokine production

activated by: cytokine

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19
Q

non immune cell: fibroblast cells

A

immuune system: innate

functions: nteract with immune cells during inflammation and
wound healing
(2) Cytokine and growth factor production

activated by: cytokines

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20
Q

non immune cells: cytokines

A

immune system: innate adaptive

function: act as messengers that allow immune cells to communicate with each other, helping regulate mimmune responses, inflammation, and the body’s defence mechanisms

produced by: Wide variety of immune and non-immune cells

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21
Q

non- immune cells: Prostaglandins

A

immune sytem: innate adaptive

fnctions:(1) group of lipid compounds that have hormone-like
effects in the body
(2) critical role in various physiological processes,
including inflammation, blood flow regulation, pain,
and fever

produced by: Macrophages
Monocytes
Dendritic Cells
Endothelial Cells
Fibroblasts

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22
Q

non immune cells: complement proteins

A

immune system: inate

functions: (1) a group of more than 30 plasma proteins
(2) coat the surface of pathogens marking them fordestruction by macrophages and neutrophils
(3) forms a complex known as the membrane attack complex (MAC), which creates pores in the cell membranes of pathogens, leading to cell lysis

produced by: Plasma Proteins

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23
Q

list the components of the innate and aquired immune system

A

innate:
macrophage
dendritic cells
neutrophils
eosinophils
basophils
NK cells

innate and adaptive: T cells and NK T cells

adaptive:
B cells
T cells: CD4+ T cells and CD 8+ T cells

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24
Q

similarity and diff between innate and aquired immunity: definition

A

innate: Non-specific; natural immunity; non-antigen specific

Aquired immunity: Specific, Antigen-specific immune response

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25
Q

similarity and diff between innate and aquired immunity: order of defense

A

innate: First line of defense of immune system

acquired: Action against pathogens that are able to evade or
overcome innate immune response

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26
Q

imilarity and diff between innate and aquired immunity: presence

A

innate: Since birth; always present in the body

acquired: Acquired during lifetime; developed only exposure to
antigens

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27
Q

imilarity and diff between innate and aquired immunity: cell involved

A

innate: Physical epithelial barriers, Phagocytic leukocyte, Dendritic cells, Natural killer (NK) cell, Mast cells etc.

aquired: Killer CD8+ T-cells, Helper CD4+ T-cells, B-cells, Antigen
presenting cells etc

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28
Q

imilarity and diff between innate and aquired immunity: molecules invloved

A

innate: Cytokines, Complements, Acute phase proteins.

acquired: Antibodies, Cytokine

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29
Q

imilarity and diff between innate and aquired immunity: receptor involved

A

innate: uses receptors that recognize conserved pathogen-associated molecular patterns (PAMPs) such as LPS,
flagellin, nucleic acids.

acquired: Uses recombined B- and T-cell receptors that recognize
specific antigens on pathogens

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30
Q

imilarity and diff between innate and aquired immunity: response time and immunology memory

A

innate: Occurs rapidly from minutes to hours; Does not confer memory

aquried: Occurs over days to weeks; Confer immunological
memory

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31
Q

imilarity and diff between innate and aquired immunity: type of immune response

A

innate: nflammation, Complement mediated killing,
Phagocytosis

aquired: humoral immunity by antibodies produced by B lymphocytes, cell-mediated immunity by T lymphocytes.

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32
Q

what are the different lymphoid organs

A

spleen
tonsils
thymus gland
bone marrow
cervical lymph node
thoracic duct

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33
Q

the lymphatic system is made up of

A

1.lymphatic vessels carrying lymph
2.Lymphoid organs
* Primary lymphoid organs – bone (where the lymphocytes produced+ mature)
marrow and thymus
* Secondary lymphoid organs (where lymphocytes get activated, initiate response ) all the other organs other than thymus gland and bone marrow –
spleen and lymph nodes
mucosa-associtae lymphatic tissues (MALT)
3. lymph nodes

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34
Q

what are the different mucosal associated lymphatic tissues (MALT)

A

1.Adenoid and tonsils in humans (Waldeyer’s ring)
in humans (located behind mouth)
2.Nasal-associated lymphoid tissue (NALT) in rodents (located behind nose) protect against inhaled pathogens
3. Gut-associated lymphoid tissue (GALT), eg. Peyer’s
patches ( all over the intestines) protect against pathogens entering through ingestion.

35
Q

function of the lymphatic system

A

The lymphatic system enables the immune system to
respond appropriately
* B and T lymphocytes reach the lymph nodes, when
there is foreign particles present in lymph fluid
* Adaptive immune responses is activated

(pathogen ends up in lymphatic fluid that will flow through the lymphatic vessels to nearby lymph nodes. in the lymph node, antigen presenting cells (dendrites, macrphage) will capture and display antigen using MCH
t helper cells with specific receptors will bind, produce cytokins, stimuate b cells, differenciate, plasma cells produce antibodies)

36
Q

describe a germinal centre and what happens in it

A

b cells surrounded by antigen presenting cells, surrpunded by T cells in the follicle of a lymph node

.Filtration of Lymph:
1. Lymph nodes filter lymph, trapping pathogens, antigens, and foreign particles.
2.Activation of Immune Cells:
Lymph nodes provide a site where immune cells, particularly lymphocytes, can encounter and recognize antigens. This triggers the activation and proliferation of lymphocytes, leading to an adaptive immuneresponse.
3.Antigen Presentation: Dendritic cells and macrophages within lymph nodes present antigens to T cells, initiating and regulating
the adaptive immune response

37
Q

what is PAMPs

A

Pathogen-Associated Molecular Patterns (PAMPs):
PAMPs are specific molecular structures that are broadly shared among various classes of pathogens,
including bacteria, viruses, fungi, and parasites. These structures are conserved and unique to
microbes, distinguishing them from host molecules

38
Q

Examples of PAMPs include:

A
  1. Lipopolysaccharides (LPS) in the outer membrane of Gram-negative bacteria.
  2. Peptidoglycan and lipoteichoic acid in Gram-positive bacteria.
  3. Viral double-stranded RNA and unmethylated CpG DNA motifs in viruses.
39
Q

what is Pattern Recognition Receptors (PRRs)

A

PRRs are receptors on immune cells (like macrophages, dendritic cells, and neutrophils) that are
capable of detecting PAMPs. PRRs are germline-encoded (in their DNA alr from the parent) and do not require previous exposure to a
pathogen

40
Q

There are several classes of PRRs, including:

A

Toll-like Receptors (TLRs): Recognize a wide range of PAMPs, such as bacterial LPS, flagellin, and
viral nucleic acids.
2. NOD-like Receptors (NLRs): Detect intracellular PAMPs and trigger inflammatory responses.
3. C-type Lectin Receptors (CLRs): Bind to carbohydrate PAMPs on fungi, bacteria, and viruses

41
Q

what happens when PRRs bind to PAMPs

A

ead to an immune response, such as
the production of cytokines, chemokines, and the activation of phagocytes. This response helps to
contain and eliminate the invading pathogen.

42
Q

what are the three pathways complement proteins assist in bcterial killing (marking them for phagocytosis)

A

The classical complement pathway (require binding of antibodies) protein sticks to Ab that sticks to bac)

  1. The alternative complement pathway (does not require antibodies) (protein sticks directly to bac)
  2. The lectin pathway (binds to mannose residue of bacteria) (sticks to the sugar on the bac)
43
Q

effects of complement protein binding

A

These Complement proteins binds to the surface of the bacterium in the form
of a membrane attack complex (MAC) or can generate opsonins that label a
bacterium for destruction
MAC can insert into the cell membrane of Gram-negative bacteria, but not
gram-positive (walls are thin enough to create the pores)
MAC produces pores that allow the entry of membrane damaging molecules,
such as lysozyme (break down the cell wall)

44
Q

describe the process of pahgocytosis

A

immune proteins like acute phase proteins (like complement)
& Antibodies bind to the surface of bacteria by a process called opsonisation. (term for th porcess of this binding)
* Opsonised bacteria are coated with molecules that phagocytic cells recognise
and respond.
* Activated phagocytes engulf and destroy opsonised bacteria by a process
called phagocytosis.
* Opsonisation allows killing of gram-positive bacteria that are resistant to killing
by MAC

45
Q

Describe how phagocytes cuase humoral immune
responses eradicate bacterial infections

A

Phagocytes present the bacterial fragments on their surface via class II major
histocompatibility (MHC class II) molecules.
* Circulating helper T (Th) cells recognise these bacterial fragments and begin
to produce proteins called cytokines.
* Two major groups of helper T cells are known as Th1 and Th2 cells
Th1 cells predominantly produce interferon-gamma (IFN-g), which
promotes cell-mediated immune mechanisms
* Th2 cells produce mostly interleukin-4 (IL-4), which promotes humoral
immunity by activating B cells.
* B cells make antibodies that prevent bacterial growth & survival.

46
Q

what are the different cells/molecules involved in cell-mediated response to eradiate viral infection

A
  1. cytotoxic T cells
  2. interferons
  3. antibodies
47
Q

explain how cytotoxic t cells eradiate viral infections (cell mediated immune resoponse)

A

viral infected cells use molecules called class 1 hypercompatability complex proteins (MHC-class 1) to display pieces of viral proteins from inside the cells upon the cell surface. cytotoxic T cells have specialised proteins on their surface called T cell receptors (TCRs) that can specifically recognise the particular antigen peptide bound to MCH-Class1 molecule. if the TCR detects a peptide from a virus, it warns its T cells of an infection-> t cell release cytotoxic factors (granzymes, perforin) to kill infected cell-> preventing the survival of the invaders.

48
Q

how does interferons help to eradicate viral infection (cell mediated immune response)

A

Virally infected cells produce and release small proteins called interferons
effects:
1.Prevents replication viruses (bonds to the recepotrs of neighboring cells, so virus cannot enter cell)
2.Also, it act as signaling molecule & makes neighboring cells increase MHC class I molecule for the action cytotoxic T cells (tells neighboring cells that there is a virus on the loose, neighboring cells put their guard uo by increaseing MCH class 1 molecule, if they get infected, can quickly display viral peptide, cytotoxic t cell can quickly identify it)

49
Q

explain how antibodies eradiate viral infection (cell mediated immune response)

A

Antibodies are specifically recognise invading pathogens and bind to them.
Eradication of virus in the following mechanisms:

  • Neutrlization: 1.antibodies bind to viral surface proteins are are ciritcal for attaching to host cell receptor. by covering these proteins, antibodies prevent to virus from entering and infected host cells.
    2. antibodies also neutralise toxins produced by pathogens. they bind to active site of the toxic molecules, rendering them unable to interact with and damage host cells.
  • Agglutination: antibodies bind to atigens of multiply virus, causing pathogen to clump together -> restrict movement, easier for phagocytosis.
  • Phagocytosis: antibodies bind to pathogens ->marking them through the process of opsonization. phagocytes identify these opsonized pathogens->engulf and digest them->eradicating pathogens from host organisms
  • Activation of complement system:in the classical complement pathway, antibodies aid in the binding of complement proteins to surface of pathogen-> formation of membrane to attack complex (MAC) -> MAC can insert into the cell membrane ->producing pores and entrance of membrane damaging molecules, lysozyme
50
Q

what are the isotopes of antibodies/ig

A

igM
igG
igA
igE
igD

51
Q

what is ig M

A

the first antibody produced in every antibody response and target largest
antibody molecule (largest antibody molecule)

52
Q

where igG found and purpose

A

high in serum, important in systemic diseases in general
(found largely in the blood, circulating all around the body preparing for systemic (whole) body/multiple organ disease, non exclusive diseases)

53
Q

ig A where its found

A

important on mucosal surfaces (saliva, tears) as a dimer (2 ab tgt)

54
Q

where ig E is found and function

A

important in allergy and parasitic infection, found on mast cells under
epithelial surfaces

55
Q

ig D where its found and function

A

plays a regulatory function on the B cell surface, not secreted (just remains on the surface of B cell once it gets produced)

56
Q

effect of T helper cell in cell mediated immunity (effect on b cells)

A

Produce cytokines that regulate native and acquired immune mechanisms
1. (cytokine produced by t helper cell) Important for directing which antibody class is produced,
i.e. a B cell produces IgM and then based on cytokines from TH cells will
switch and make IgG or IgA or IgE
2. CD8+ ‐ TC cell, cytotoxic T lymphocyte (CTL), CD8+ ‐ attack and kill cell
that make foreign proteins, example viral infected cell or tumor cell

57
Q

how do B cells recognise antigens on pathogens

A

B cells recognise intact antigens (not processed/ broken down)
they recognise a wide variety of of chemicals (antigens): protein, carbohydrates via membrane- bound antibody molecules. these antibodies recognise a small portion of a molecule (epitopes) (part of antigen on the pathogen)

58
Q

how do T cells (t helper, t cytotoxic) reconise antigens on pathogens

A

T cells (helper and cytotoxic) recognise only peptides (processed proteins).
the antigen must be presented on mahor histocompatability complex (MCH) molecule (Th: MCH-2, Tc: MCH:1)

59
Q

How do antibodies behave differently in a memory response compared to the first exposure?

A

-faster than a primary response
-antigen specific clones of B lymphocytes have expanded and matured (memory B cells)
they have:
. Higher in titer than a primary response (increased concentration of AB production)
b. The antibody can bind more tightly

c. Antibody class switching has already occurred (from IgM to a different class
depending on the nature of the infectious agent)

T helper and CTL clones have expanded, matured, and circulating

60
Q

What is tolerance in the acquired immune system and how does this form.

A

its the aquired immune system ‘tolerateing’ self molecules
the process of forming “toerating” molecules
antigen presented during lymphocte maturation are recognised as self-> no attack (antigens are from the body/ presented on other cells)
antigen presented after lymphocyte maturisation-> recognised as foreign-> attack

61
Q

what happens when tolerence breaks down

A

autoimmune disease (attacking ‘self’ cells)

62
Q

what are the two types of immunity part of aquired immunity and their definition

A
  1. Active Immunity (host produces antibodies by themselves); persists a
    long time in the host, up to many years in humans. (exposed to pathgens-> make the antibody-> create memory cells-> last longer in the body)
  2. Passive Immunity (host receives antibodies that originally produced in
    another animal); typically, short lived and usually persists only a few
    weeks or months (ab is recognised as foreign-> will eventually get destroyed in the spleen)
62
Q

what is primary and secondary immune resoponse

A

Primary responses (immune response of the host to antigen occurs on
the first occasion it is encountered)

  • Secondary responses (immune response of both B- and T cells is
    observed following subsequent encounter with the same antigen
63
Q

how long does primary response take and what happens during it

A

primary response:
time: 14 days for the generation of memory cells with high specificity(reason for waiting for second dose of vaccination)
-results in antigen specific CD4 T cells helping B cells (tell them which ab to rpoduce)

64
Q

difference between primary and secondary immune response (effect)

A

primary response: Slow and small in terms of Ab
concentration
* Short-lived
* IgM- major antibody subtype
elicited; low affinity
* IgG- low levels; low affinity

secondary immune response: Fast and high Ab concentration
* Sustained long period of time
* IgM- low levels; affinity remains
essentially unchanged
* IgG- high levels; increasing affinity

65
Q

explain clonal selection theory

A

according to this theroy, each B cell or T cell has a unique receptor specific to a particular antigen. when a lymphocyte encounters its specific antigen-> it is selected for activation

activation of clonal expansion of B cells: when B cells with a specific b cell receptor binds to corresponding antigen-> undergoes activation. if it receives signals from helper t cells (cytokines and surface interaction) -> proliferates and differenciates into two types of cells: Plasma cells: produce large quanitities of Ab specific to antigen
memory B clls: long lived cells reain in the body and provide rapid and robust Ab production of the same antifen is encountered again in the future.

66
Q

importance of long term immunity

A
  1. rapid response to infection: due to previous encounter to pathogen-> prevent pathogen from establishing an infection, reducing severity of disease
  2. vaccination: vaccinations work by inducing long term immunity without causing the disease-> prepares the immune system to respond quickly if the actual pathogen is encountered
  3. protection against epidemics: long term immunity in individuals contribute to herd immunity, reduing the spread of infectious diseases within a population.
67
Q

Impact of defect in thr Innate or acquired immune system

A

unusual susceptibility to infectious or parasitic diseases.

68
Q

What is primary immunodeficiency

A

Inherited defects causing deficiencies in the immune system (eg gene mutation)

69
Q

What is acquired/ secondary immunodeficiency

A

Immune system deficiency is a direct result of some other causes (eg viral infection, chironic disease eg diabetes)

70
Q

What is Canine Leukocyte Adhesion Deficiency (CLAD)
How does it happen
Impact

A

innate primary immunodeficiency disease : breed-specific mutations in genes (irish setter type 1, german shepherd type 3)

Who it affects: Irish setter (type1), German shepherd (typeIII)
About the disease. Disease is caused by a breed specific gene mutation. It is inherited in an copies (non sex) recessive fashion means both males and female is equally affected and two complies of the defective gene is needed to cause CLAD

How it happens: mutation in a gene that encodes for protein called CD 18: responsible for adhesions of neutrophils to blood vessel wall
in CLAD, lack of CD28neutrophils cannot effectively adhere to blood vessel walls, cannot migrate to site of infection
Impact: have abnormal blood clot thing and immune system function

impact of CLAD: abnormal blood clotting (neutrophils control plateleys) and immune system functions

71
Q

what is systemic lupus erythematosus (SLE)
what does it cause (DOG)

A

What is it: Systemic lupus erythematosus (SLE) in dogs is an autoimmune disease that affects multiple systems in the body, including the skin, joints, kidneys, and blood.
• SLE causes the immune system to attack the body’s own tissues, leading to inflammation and tissue damage.
• Can be either inherited or acquired disease
• Causes of lupus in dogs include genetic factors, immunologic disorders, and environmental factors.

Who it affects ( these breeds are more susceptible)
German Shepaherds • Brittanys
• Alaskan Malamutes • Siberian Husky
• Chow Chows
• Shetland sheepdogss

How it happens: Immune cells like B cells and T cells become overreactive and produces too much antibodies that recognise and attack the host cells leading to inflammation and damage in affected organs.

72
Q

what is feline immunodeficiency virus (FIV)

A

what is it: acquired immunodeficiency (from feline immunodeficency virus)

how ot affects body: FIV invades cell via primary receptors (will go attack these first) on feline CD4+ T cells, B cells and activated macropgages. and secondary recepors, normally and chemokine receptor

impact of FIV: increase susceptability to infection

73
Q

what is feline leukemia virus (FLV)

A

it is an aquired immunodeficency (viral infection)
FeLV can result in leukemia (blood cancer) as it affects the bone marrow cells genome

Who it affects: kittens as they have immature immune response

how it is aquired: invade lymph tissues-> directly into CD4+ T cell-> destroy and replicate the virus-> imparied function-> immune suporession
-since CD4+ is affected-> less B cells activated-> decrease in antibody production-> harder to fight FLV
-immunosupressive properties alter monocyte morphology and destribution-> reduce ability to respond to infection

74
Q

what is feline hypotrichosis in birman cats

A

what is it: rare innate primary immunodeficiency disease (genetic mutation) characterised by hair loss and thymi’s aphasia (absent or underdeveloped thymus)

Who it affects: Birman cats , kitten with this disease are born hairless and have increased susceptibility to infection , most die soon after birth.

how does it happen: hypotrichosis is caused by a point mutation in the FOXN1 gene-> aplasia (incomplete/abnormal developemnt) of the thymus, abnromal developement of lymphoid tissues in multiple organs (spleen, peyers patch, lymph nodes) thymus appasia -> t cell cannot mature properly–> reduce number of functional T cells -> increases susceptab

Cells affected: Helper T cells (CD4+ T cells): Thymus is responsible for the maturation of T cells, which helps the immune system fight infection and regulate immune responses ➔Thymus aplasia, thymus is underdeveloped or absent.
➔This makes it harder for the skin to defend against infections that could damage
hair follicles and result in hair loss
Cytotoxic T cells (CD8+ T cells): Identify and eliminate infected or abnormal cells within the skin
➔Dysfunction of CD8+ T cells increases susceptibility to bacterial, viral, and
fungal infections
➔Impair immune defense around hair follicles to responds to threats effectively ility to bacterial, viral and fungal infection , hair loss

75
Q

. Explain how long-term immunity is generated

A

Antigen‐specific T cells are selected during a primary immune response and expand to produce clones of T cells with high specificity for the activating antigen.

• In a B cell primary response to a thymus‐dependent (need activation of T cell) antigen, the immune system selects B cells with a high affinity (better binding) and specificity for the antigen and these become memory cells.
• In a secondary response to the same antigen, memory B cells are rapidly activated. This process is quicker and more effective than the primary response.

76
Q

What is colonial deletion (part of final selection theory)

A

Self reactive b cells (with Ab that recognise self antigens) will be deleted from the pool. Only b cells that do not react with self antigens are allowed to leave the bone marrow (to prevent autoimmune disease)

77
Q

Bone marrow function

A

Primary site for the production of all blood cells including lymphocyte
It is also where B cells mature before they enter thr bloodstream

78
Q

Thymus function

A

Where T cells mature. Immature T cells (thymocytes) migrate from the bone marrow to the thymus where they undergo selection process to ensure that they can recognise foreign antigens while ignoring self antigens

79
Q

Lymph node function and what are they

A

Filter lymph, trapping pathogen and foreign particles. They are sites where immune cells such as lymphocytes encounter antigens and initiate an adaptive immune response (germinal centre)

What they are. Small bean shaped structures along the lymphatic vessel.

80
Q

Spleen function

A

Filters blood, removing old or damaged red blood cells and pathogen.
Also serves as a site where the immune cells can interact with antigens and mouth an immune response

81
Q

Fucntion of tonsil

A

They are lymphoid tissue located at the back of the throat. They trap pathogens entering through the mouth or nose and contain immune cells that initiate an immune response.

82
Q

activation of humoral immune responses to eradicate bac

A

.Antigen Recognition:
1. The humoral immune response begins when B cells, a type of lymphocyte, encounter a specific antigen on the surface of
a bacterial pathogen. B cells have membrane-bound antibodies (B cell receptors) that recognize and bind to specific
antigens.
2.B Cell Activation:
1. Upon binding to the antigen, the B cell processes it and presents fragments (peptides) of the antigen on its surface using
MHC class II molecules. Helper T cells (CD4+ T cells) recognize this antigen-MHC complex through their T cell receptors
(TCRs).
3.T Cell Help:
1. The interaction between the B cell and the helper T cell leads to the activation of the T cell, which in turn releases
cytokines. These cytokines are crucial for fully activating the B cell.
4.B Cell Differentiation and Clonal Expansion:
1. The activated B cell undergoes clonal expansion, producing a large number of identical B cells. These cells differentiate
into plasma cells and memory B cells.
2. Plasma Cells: Plasma cells are the effector cells that produce and secrete large amounts of antibodies specific to the
antigen.
3. Memory B Cells: Memory B cells persist in the body and can quickly respond to future exposures to the same antigen

principals of animal healthcare and diseases (5 decks)

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