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Microbiology > Ch. 15 > Flashcards

Ch. 15 Flashcards

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1
Q

Physical Barriers

A

Prevent approach and deny access to pathogen
- hair, secretions, epithelium

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2
Q

Phagocytes

A

Removes debris and pathogens
- fixed macrophage, neutrophil, free macrophages, eosinophil, monocyte

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3
Q

Extracellular Killing

A

Destroys abnormal cells by NK Cell attacks abnormal cell, resulting in a lyses abnormal cell

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4
Q

Effects of an inflammatory response

A
  1. Increased Blood Flown
  2. Phagocytes Activated
  3. Capillary permeability increased
  4. Complement activated
  5. Clotting reaction walls off region
  6. Regional temperature increase
  7. Specific Defenses activated
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5
Q

Fever

A

Mobilizes defensens, accelerates repairs, inhibits pathogens
- body temperature rises above 37) degrees Celsius

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6
Q

Interferons

A

Increase resistance of cells to infection, slow spread of disease
- released by activated lymphocytes and by macrophages and by virus-infected cells

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7
Q

Complement system

A

Attacks and breaks down cell walls, attacks phagocytes, stimulates inflammation

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8
Q

Acquired

A

Requires training and is developed/refined over time - more specific - not born with
- third line of defense

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9
Q

Third Line of Defense

A

Adaptive or acquired immunity
- product of B and T lymphocytes
- immunocompetence: ability of the body to interact with a wide variety of foreign substances
- uses Antigens: molecules that stimulate response by T and B cells - specific to recognizing a a particular molecule or pathogen - one antigen can have many epitomes (antigenic determinant sites - sites on antigen that can be recognized)

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10
Q

Acquired Responses

A

Two features that characterize specific immunity
1. specificity: antibodies produced, function only against the antigen that they were produced in response to
2. Memory: lymphocytes are programmed to “recall” their first encounter with an antigen and respond rapidly to subsequent encounters
Other Characteristics
3. Discrimination: self vs. non-self - done through clonal selection, resulting in tolerance for self
4. Diversity/Adaptiveness: recognize and respond to never before seen antigens

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11
Q

Antigen Independent Period

A

The period where lymphocytes are being created to recognize specific antigens - if they recognize self, they will be destroyed

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12
Q

Colonial Selection

A

Each lymphocyte (B and T cells) has the capacity to recognize a unique shape (antigen - epitope on antigen) - they are called either a B or T cell receptor - when these lymphocytes are being made (either in the thymus or bone marrow), they are being exposed to self antigens so they know what we look like - we don’t want immature lymphocytes to recognize self so we get rid of them. If they recognize self, they will destroy self. - lymphocyte clones that carry a specificity for self molecules are eliminated from the pool of diversity to achieve immune tolerance

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13
Q

Antigen Dependent Period

A

Lymphocytes in lymphatic organs are situated to respond to specific antigens that carry a matching surface receptor to the ones they are programmed for - if it matches to the foreign antigen, it will triggers an immune response

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14
Q

Specificity resulting in cross-reactivity

A

Breakdown of specificity between similar antigens can result in cross-reactivity
Good: immunity to strain A will also protect against strain B and C
Bad: immunity to an antigen causes cross-reactivity to recognizing host antigens - can result in breaking down discrimination

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15
Q

Diversity

A

The ability to produce an immune response to a wide range of antigens (sugars, fats, proteins, DNA, etc.)

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16
Q

Adaptiveness

A

The ability to respond to antigens never seen as well as refined previous responses to make them better

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17
Q

Genie paradox

A

We have tremendous antibody diversity, but a small genome - so we generate that diversity despite us having a small antibody region within our entire genome - we can do this through elegant genetic mechanisms: VDJ rearrangement -different segments of antibody gene in V, D, and J regions and within each of those regions there are more regions, meaning there are many unique combinations to produce an antibody. To make an antibody, it takes one of the subset regions from each V, D, and J regions.
- heavy chain: VDJ combo
- light chain: V, J, combo
Heavy chain and light chain pair resulting in the overall combination that creates its unique shape to be able respond to a particular pathogen

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18
Q

Memory

A

Anamnistic Response: ability to respond more quickly and stronger the second, third, fourth time you encounter the same antigen
- primary responses: takes 10-14 days to find a combination to form an antibody to get it to respond - first types of antibodies made are IgM and a few weeks later, you get IgG antibodies
- secondary response: if you see exposed to same antigen again, it utilizes antibodies that were previously created, allowing you to respond much more efficiently, strongly, and with typically more IgG

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19
Q

Characteristics of Antigens and Immunogens

A

Antigen (Ag) - substance that has potential to elicits immune response in specific lymphocytes
- antigenicity: property of behaving as an antigen (foreignness, size, shape, and accessibility)
- antigens have many antigenic determinants (epitopes) - small molecular group recognized by lymphocytes
- sometimes we encourage the immune system to respond to an antigen - by adding substances t
Immunogen: actually does elicit a response

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20
Q

What makes a good antigen that provokes our body to respond to it?

A
  1. Forgiveness: less like self the easier to distinguish it from self
  2. High molecular weight: the bigger the better
  3. Complexity: more potential epitopes
  4. Degradability: antigens often must proceed
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21
Q

Common Types of Antigens

A

Proteins, lipoproteins/lipopolysaccharides, nuceloproteins (DNA and protein complexes), polysaccharide (some), and glycolipids

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22
Q

Other functional categories of antigens

A
  1. Alloantigens: specific surface markers on cells
    - blood markers
  2. Superantigens: more like a toxin than an antigen - strategy for confusing our immune system - bypasses the need for an antigen to non-specifically illicit an immune response - produced by some bacteria to avoid immune system by overstimulating, and thus, confusing it - also attacks host by turning own immune system against itself
  3. Allergens: recognized by IgE antibodies
  4. Auto antigens: molecules of self - reaction that cross reacts with one of our own molecules
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23
Q

How do we acquire immunity?

A
  1. Active Immunity: your own body generates that response, which creates immunological immunity
  2. Passive Immunity: something else is producing response - and you are taking advantage of that response because you don’t have immunity - but you are taking the antibodies that something else produced
24
Q

Natural vs. Artificial Immunity

A

Natural: active and passive immunity
- ex of passive: mother passing on antibodies to baby through placenta - only passes on antibodies and not cells that produce it so it’s short-term immunity
Artificial Immunity: produced purposefully through medical procedures ‘
- active: through vaccinations
- passive: results when a person is given selected immune substances made by another individual

25
Q

Separate but related activities of the specific immune response

A
  • development snd differentiation of the immune system
  • lymphocytes and antigen processing
  • the cooperation between lymphocytes during antigen presentation
  • b lymphocytes and the production of antibodies
  • T lymphocytes response
26
Q

Development of the lymphocyte system

A
  • lymphocytes arise from same stem cells but differentiate into two distinct cell types: T and B cells
  • once released after maturation, they settle in lymphoid organs and serve as an attack force for infectious agents
  • antigens are recognized and engulfed by antigen-presenting-cells like dendritic cells, which take them in and process them
  • T helper cells first receive the processed antigen from APC and activate B and other T cells
  • T cell response: once T cell recognizes the specific antigen, the T cell will proliferate to create memory cells and then differentiate into helper cells or cytotoxic cells - T cell immunity is cell-mediated because the whole T cell acts directly to destroy microbes instead of secreting molecules into the body
  • B cell response: B cells are activated by T helper cells and will undergo cell division to produce memory cells that can recall an antigen - plasma cells will also be created, which secrete proteins, called antibodies
  • Humoral immunity (through B cells):antibodies that circulate in fluids provide humoral immunity - antibodies react specifically with the antigen and mark it for enhanced response
27
Q

Cell-Mediated Immunity

A

T Cells
- T cells are trained (colonal selection) in the Thymus
- thymus positively selects for functional T cells
- negatively selects for self-reactive T cells
- directed by chemical signal, cytokines ‘
- do NOT make antibodies
- require that antigens be processed and presented to them before activation - must be presented on MHC (major histocompatibility complex) platter
- T cells come with different functions
- T cells recognize antigens by using unique T-cell receptors (TCR) on their surface - each T cell expresses one type of TCR, but expresses many copies of it on its own surface - the diversity of these TCR is generated in a similar fashion as the genie paradox - TCR are able to recognize antigens that have been processed and placed into a MHC molecule on another cell
- T cells contain co receptors that are MHC that help stabilize the interaction between immature T cell and APC (antigen presenting cell) to activate T cell
- After activation by APC, two major events take place - both of them are driven by cytokines
1. Proliferation: cell begins to divide rapidly
2. Differentiation: nature or functions of the cell is altered - differentiated into memory T cell, helper T cell, and Cytotoxic T cells

28
Q

What is difference between helper T cells and Cytotoxic cells

A
  • the cells have different co-receptors
  • each T cell has one type of T cell receptor AND will either have CD4 or CD8 co-receptor
  • CD stands for cluster differentiation and they help recognize MHC
  • MHC platters come in two types
    1. MHC Class 1: platters on all nucleated cells - everything but RBCs - platter presents small pieces of Proteins 8-12aa and presents it to things that are interacting to the outside of it
    2. MHC Class 2: not found on all cells - only B cells and APCs - present larger prices of proteins (bigger epitope) for proteins 14-24aa
    *CD4 interacts with MHC Class 2
    *CD8 interacts with MHC Class 1
29
Q

CD8 positive T cells: Cytotoxic T cells

A

Killer cels, that look for cells expressing MHC Class 1 molecules with a specific foreign antigen fragment being presented
- types of cells doing this: viral infected cells, cancer cells, transplanted cells
Kills the cells by releasing Perforin/Granzyme

30
Q

CD4 Positive T Cells - Helper T cells:

A

Help activate B cells and regulate immune system
Type 1. Activate B cells to produce antibodies
Type 2. Activate other immune cells (CD8 positive T cells and macrophages) by secreting TNF and interferons
- Interact with MHC Class II molecules

31
Q

Superantigens

A

Produced by some bacteria to avoid the immune system by overstimulation (confusion) as well as attack the host by turning the host immune system against itself
- works by binding both MHC class II and TCR - this brings them together and activated them without an antigen - activates CD4 cells in absence of the particular antigen - causes many T cells to be activated that don’t have specificity - secreting a lot of cytokines so now you have an overwhelming production of chemical signals - cytokine storm - overdose on these potent chemical signals
- ex: of a Superantigens: toxic shock syndrome - tampons produce and secrete Superantigens

32
Q

Immunoglobulin (Ig) - Antibodies

A

Molecule with 4 polypeptide chains connected by disulfide bonds
- all antibodies have two functionally distinct segments (fragments)
1. Antigen Binding Fragments (Fabs): “arms” with their amino-terminal end (variable regions of heavy and light chains) as antigen-binding sites
2. Crystallizable Fragment (FC) binds to various cells and molecules of the immune system

33
Q

What happens when. Knifing occurs and you get the structural change from an antibody binding to an Antigen?

A

Principle Activity of antibodies: unite with, immobilize, call attention to, or neutralize Ag for which it was formed
‘’NOCAP”
N: neutralization: antibodies fill the surface receptors on a virus or the active site on a microbial enzyme to prevent it from attaching - coats viral particle so it can no longer get into a cell
O: opsonization: process of coating microorganisms or other particles with specific antibodies so they are more readily recognized by phagocytes. Carried out antibodies called “opsonins”
C: complement fixation: activation of the classical complement pathway can result in the specific rupturing of cells and some viruses
A: Agglutination: Ab aggregation; cross-linking cells or particles into large clumps- sequestering antigens do they can’t move away and immune system can eliminate the large clumps
P: Precipitation: aggregation of particulate antigen - precipitate out

34
Q

Different classes (isotopes) of antibodies (immunoglobulins)

A

Different constant regions can be swapped in without losing the specificity of the variable region - can change how/where the antibody functions
5 Functional Classes:
1. IgD: monomer, serves as a receptor for antigen in B cells
2. IgG: monomer, produced by plasma cells (primary response) and memory cells (secondary), most prevalent
3. IgA: monomer circulates in blood, dimer in mucous and serous secretions
4. IgM: five monomers, first class synthesized following Ag encounter
5. IgE: involved in allergic responses and a parasitic worm infections
*The differences in these classes are due primarily to variations in the Fc

35
Q

IgG

A
  • Number of antigen binding sites: 2 monomers
  • % of Total antibody in serum: 80%
  • average life on serum: 23 days
  • crosses placenta
  • fixes compliment
  • binds to phagocytes
    *long-term immunity; memory antibodies; neutralizes toxins, viruses
36
Q

IgA (dimer/secretory version)

A
  • Number of antigen binding sites: 2 or 4 dimers/monomers
  • % of total antibody in serum: 13%
  • average life in serum: 6 days
  • does Not cross placenta
  • does NOT fix complement
  • binds to epithelial cells
    *secretory antibody; on mucous membranes
37
Q

IgM

A
  • number of binding sites: 10 pentamers
  • % of total antibody in serum 6%
  • average life in serum: 5 days
  • does Not cross placenta
  • fixes complement
  • binds to: NA
  • produced at first response to antigen; can serve as B-cell receptor
38
Q

IgD

A

-number of antigen binding sites: 2 monomers
- % of total antibody serum: 0.001%
- average life in serum: 3 days
- does NOT cross placenta
- does Not fix complement
- binds to NA
*receptor on B cells for antigen; can serve as B-cell receptor

39
Q

IgE

A
  • number of antigen binding sites: 2 monomers
  • % of total antibody in serum: 0.002%
  • does NOT cross placenta
  • does NOT fix complement
  • binds to mast cells and basophils
    *antibody of allergy; worm infections
40
Q

B-Cell Activation & Antibody Production

A
  • Once B cells process Ag, interact with T helper cells, and are stimulated by growth and differentiation factors, they enter the cell cycle in preparation for mitosis and clonal expansion
  • divisions give rise to plasma cells that secrete antibodies and memory cells that can react to the same antigen later
41
Q

The main events involved in B cell responses are:

A
  1. Colonial selection and binding antigen
  2. Induction by chemical mediators
  3. B-cell/T helper cell cooperation and recognition
  4. B cell activation
  5. Clonal expansion
  6. Antibody production and secretions
42
Q

Clonal Selection and antigen Binding B cells

A

Can independently recognize microbes and their foreign antigens, and can bind the, with their Ig receptors. This is how the initial selection of the antigen-specific B-cell clone occurs

43
Q

Antigen Processing and Presentation

A

Once the microbe is attached, the B cell endocytose it processes it into smaller protein units, and displays these on the MHC-II complex (similar to other APCs). This event readies the antigen got presentation of the specific T helper cell

44
Q

B-cell/T helper cell cooperation and recognition

A

For most B cells to become functional, they must interact with a T helper cell that bears receptors for antigen from the same microbe. The T cell may have been activated by an APC. The two cells engage in a linked recognition, in which the MHC-II receptor bearing antigen on the B cell binds to both the T-cell antigen receptor and the CD4 molecule on the T cell (inset)

45
Q

B-Cell activation

A

The T cell gives off additional signals in the form of interleukins and B-cell growth factors. The linked receptors and the chemical stimuli serve to activate the B-cell. Such activation signals an increase in cell metabolism, leading to cell enlargement, proliferation, and differentiation

46
Q

Clonal Expansion/Memory cells

A

The activated B cell undergoes numerous mitotic divisions , which expand the clone of cells bearing this specificity and produce memory cells and plasma cells. Memory cells are persistent, long term cells that can react with the same antigen on future exposures

47
Q

Artificial Active Immunity

A
  • can be conferred artificially by vaccination - deliberately exposing a person to material that is antigenic but not pathogenic
  • principle is to stimulate a primary and secondary anamnestic response to -relate the immune system for future exposure to a virulent pathogen
  • response to a future exposure will be immediate, powerful, and sustained
48
Q

Effective Vaccine Requirements

A
  • It should have a low level of adverse side effects or toxicity and not cause serious harm
  • It should protect against exposure to natural, wild forms of pathogen.
  • it should stimulate both antibody (B cell) response and cell-mediated (T cell) response
  • It should have long-term, lasting effects (produce memory cells)
  • It should work with minimal doses or boosters
  • It should be inexpensive, have a relatively long shelf life, and easy to administer
49
Q

Most vaccines are prepared from:

A
  • killed whole cells or inactivated viruses
  • live, attenuated cells or viruses
    -antigenic molecules derived from bacterial cells or viruses
  • genetically engineered microbes or microbial agents
50
Q

Advantages of live preparations:

A
  • organisms can multiply and produce infection (but not disease) like the natural organism
  • they confer long-lasting protection
  • usually require fewer doses and boosters
51
Q

Disadvantages of live vaccines

A
  • require special storage, can be transmitted to other people, can conceivably mutate back to virulent strain
52
Q

Vaccines from microbe parts

A

Exact antigenic determinants can be used when known:
- capsules: pneumococcus, meningococcus
- surface protein: anthrax, hep B
- exotoxins: diphtheria, tetanus
Antigen can be taken from cultures, produced by genetic engineering, or synthesized

53
Q

Recombinant Vaccine

A

Insert genes for pathogen’s antigen into plasmid vector, and clone them in an appropriate host
- stimulated clone host to synthesize and secrete a protein product (antigen), harvest and purify the protein - hepatitis
“Trojan Horse” vaccine - genetic material from a pathogen is inserted into a live carrier non-pathogen; the recombinant express the foreign genes
- experimental vaccines for aids, herpes simplex 2, leprosy, tuberculosis

54
Q

Genetically Engineered Vaccines

A
  • DNA vaccines: create recombination by inserting microbial DNA into plasmid vector
  • human cells pick up the plasmid and express the microbial DNA as proteins causing B and T cells to respond, be sensitized, and form memory cells
  • experimental vaccines for Lyme disease, hep C, herpes simplex, flu, tuberculosis, malaria
55
Q

Genetically Engineered Vaccine Process

A
  1. DNA that codes for protein antigen is extracted from pathogens genome
  2. Genomic DNA is inserted into plasmid vector; plasmid is amplified and prepared as a vaccine
  3. DNA vaccine is injected into subset
  4. Cells of subject accept plasmid with pathogens DNA. DNA is transcribed and translated into various proteins
  5. Foreign protein of pathogen is inserted into cell membrane, where it will stimulate immune response

Microbiology (8 decks)

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