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LQB201- MICROBIOLOGY > wk 7-adaptive immunity > Flashcards

wk 7-adaptive immunity Flashcards

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1
Q

types of lymphocytes in adaptive immunity and their differences

A

B lymphocytes- humoral immunity
mature in bone marrow
produce antibodies
target exogenous antigens produced by extracellular pathogens (bacteria/fungi)

T lymphocytes- cell mediated immunity
mature in Thymus
target endogenous antigens in the intracellular space

two main types of lymphocytes (helper T cells, CD4+: and
Cytotoxic T cells, CD8+)

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2
Q

antibody is ineffective with what?

A

viruses (inside cell)

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3
Q

adaptive immune self is capable of distinguishing?

A

self and non self in a specific manner

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4
Q

Recognition of self-antigens versus pathogen-associated antigens occurs via?

A

cell-surface antigen recognition proteins including the Class I and Class II major histocompatibility complex (MHC) molecules.

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5
Q

ways you can develop humoral immunity

A

active (you do the work for antibodies) and passive (someone else does the work for antibodies)

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6
Q

active humoral immunity

A

host generates immune response to antigen and creates an immunological memory
can be:
-naturally acquired if individual acquires infection
-artifically acquired through vaccination

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7
Q

passive humoral immunity

A

when individuals recieve preformed antibodies via direct transfer (artificially acquired) or by vertical transmission from mother to child (naturally acquired). only provides short term protection and does not create any immunological memory.

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8
Q

activation of B-lymphocytes process 4

A
  1. Antigens bind to B cells activating the B cell.
  2. B cells present antigen peptides on the cell surface via MHC class II. They present the antigen peptides to activated T follicular helper (Tfh) cells, which then secrete cytokines that further enhance activation of the B cell.
  3. Activated B cells differentiate into blast cells and undergo mitotic division to produce a large population of cells bearing the same antigen receptors (clonal selection).
  4. The expanded clones differentiate into plasma cells (antibody producing cells) and memory B cells (persist in the body for months to years).
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9
Q

antibodies functions 4

A

opsonization- coats antigen to enhance the ingesting by phagocytic cells of innate immune system

neutralisation- antibodies bind to and block specific attachment sites on viruses and bacterial toxins.the pathogen Is then unable to attach and is eventually destroyed by phagocytic cells

complement fixation- binding of antibodies to antigens can lead to complement activation

agglutination- clumping of antibody-coated microbes makes them easier targets for phagocytic cells

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10
Q

5 major classes of antibodies and what they do

A

IgG- persists for months - years. responsible for long term immune protection

IgM- only lasts weeks-months. first type of antibody after primary antigenic stimulate. used to see if a patient has correct/recent infection.

IgA- found in mucosal surfaces. protects body from invading pathogens.

IgD- present on surface of B cells and is an antigen receptor

IgE- immunity to helminth infections and allergic reactions

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11
Q

first type of antibody produced after exposure

A

IgM

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12
Q

involved in allergic reactions

A

IgE

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13
Q

dimeric version found at mucosal sites

A

IgA

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14
Q

persist for months-years

A

IgG

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15
Q

b cell receptor is what antibody

A

IgD

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16
Q

what are antibody producing cells called

A

plasma cell (b cells differentiate into plasma cells)

17
Q

activation of t lymphocytes 5 steps

A

antigen presentation
1. antigen presenting cell phagocytoses microbe
2. microbial antigens are degraded into small peptides and associate with intracellular MHC class II molecules to form a complex
3. antigen peptide-MHC class II complex transported to cell surface
4. T cell receptors on CD4+ T. lymphocytes recognize MHC peptide complex
5. activation of CD4+ T LYMPHOCYTE

18
Q

why are antigen presentations important? 2

A
  1. T lymphocytes cannot recognise full antigens (only short antigen peptides)
  2. MHC molecules are “billboards” that provide a snapshot of what is going on inside infected cells and phagocytic cells
19
Q

what happens after activation of CD4+ t lymphocytes?

A

Differentiates into various subsets based on the cytokines they produce

20
Q

how do CD8+ t lymphocytes kill? 2

A

activated by antigen peptides presented by MHC class I

CD8+ T cells kill viruses and intracellular bacteria/tumours via two mechanisms. Both mechanisms require cell-cell contact.

  1. Granzyme-mediated killing
  2. Fas-FasL-mediated killing
21
Q

difference between CD4+ AND cd8+

A

cd4
-helpers of adaptive immune response
-differentiate into subsets based on cytokine production
-requires antigen presentation via MCH class II for activation

cd8
-fas-fasl mediated killing
-requires antigen presentation via MHC class I for activation
-cytotoxic
-granzyme mediated killing
-directly attack virus infected cells

22
Q

what is Primary immunodeficiency

A

when part of the immune system is functioning abnormally as a result of a genetic change.

23
Q

what is Secondary immunodeficiency and examples

A

when the immune dysfunction occurs as a result of exposure to infectious agents, toxins or drugs.

occurs in response to acquired infections like HIV, diabetes, anti inflammatory/immunosuppressive drugs and host physiology (young age/etc)

24
Q

types of vaccines 4

A

1 Inactivated or killed -(does not replicate in host but stimulates immunity). E.g. polio, influenza A and hepatitis A vaccines

2 Live attenuated -(replicates in host and stimulates immunity but does not cause disease). E.g. chickenpox, tuberculosis (BCG) and measles, mumps, rubella (MMR) vaccines

3 Subunit -(contains parts of a microorganism that are known to stimulate immunity. E.g. Hepatitis B and Haemophilus influenzae type B (Hib) vaccines

4 Toxoid- (inactivated bacterial toxin that does not cause disease but stimulates immunity). E.g. diphtheria and tetanus vaccines

25
Q

which out of inactive/killed and attenuated is more effective for protection

A

attenuated

26
Q

4 types of hypersensitivity

A

immediate hypersensitivity (type I)
antibody-mediated hypersensitivity (type II)
immune complex disease (type III)
delayed hypersensitivity (Type IV)

27
Q

what is immediate hypersensitivity (type i)

A

is mediated via mast cell degranulation and eosinophils in the innate immune system and IgE in the adaptive immune system. The onset of Type I hypersensitivity is immediate.

Type I hypersensitivity reactions cause atopic diseases including eczema and asthma.

Type I hypersensitivity reactions leads to inflammation including hyperaemia and oedema associated with vasodilation.

28
Q

what is antibody mediated hypersensitivity (type II)

A

cell-bound antigen, is mediated via complement and phagocytic cells in the innate immune system and IgG in the adaptive immune system. The onset of Type II hypersensitivity is immediate.

Type II hypersensitivity reactions cause targeted destruction of cells such as blood transfusion reactions or rheumatic heart disease.

29
Q

Immune complex disease (type III)

A

immune complex hypersensitivity, is mediated via complement and neutrophils in the innate immune system and IgG in the adaptive immune system. The onset of Type III hypersensitivity occurs within hours of exposure.

Type III hypersensitivity reactions cause large, globular immune complexes (antigen-antibody complexes) to deposit in tissues causing inflammation. Post-streptococcal glomerulonephritis is an example of Type III hypersensitivity.

30
Q

what is delayed hypersensitivity (type IV)

A

delayed hypersensitivity, is mediated via macrophages in the innate immune system and T-lymphocytes in the adaptive immune system. The onset of Type IV hypersensitivity days (2-3) after exposure.

Type IV hypersensitivity reactions cause CD4+ T-lymphocytes to secrete cytokines and CD8+ T-lymphocytes to destroy cells (self or non-self) displaying the target antigen. Examples of diseases associated with Type IV hypersensitivity reactions include rheumatoid arthritis, Type I diabetes and tuberculosis.

31
Q

auto immunity define and what is autoimmune disease

A

the immune system produces antibodies that attack the body’s own healthy cells, tissues and organs, resulting in prolonged inflammation and damage.

In autoimmune disease, antibodies mistakenly target self-antigens. Autoimmunity may be a consequence of genetics, environmental factors or infectious diseases.

32
Q

examples of autoimmune diseases

A

multiple sclerosis
type 1 diabetes
thyroiditis
eczema

33
Q

primary cause of autoimmune disease

A

specificity for self antigens

34
Q

MHC stands for and does what

A

major histocompatibility complex bind to t cell recetors presenting antigens

LQB201- MICROBIOLOGY (13 decks)

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