Week 7 material Flashcards

(49 cards)

1
Q

what makes up the immune system

A

Innate Immunity + Adaptive Immunity

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2
Q

where do immune cells come from

A

they derive from hematopoietic stem cells in the bone marrow

these stem cells differentiates into different types of blood cells - Hematopoiesis

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3
Q

what are the two types of stem cells hematopoietic stem cells differentiate into

A

myeloid stem cells + lymphoid stem cells

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4
Q

what cells are primarily innate - part of the innate response

A
  • mast cell
  • myeloblast
  • natural killer cell
  • basophil
  • neutrophil
  • eosinophil
  • monocyte
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5
Q

what cells are primarily adaptive - part of the adaptive response

A
  • small lymphocyte
  • t lymphocyte
  • b lymphocyte
  • plasma cell
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6
Q

which cells are antigen presenting (occurs when innate response is presenting antigen to adaptive response)

A
  • macrophage
  • dendritic cell
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7
Q

what are the 2 types of lymphatic organs

A

Primary
- site where leukocytes develop
- red bone marrow = B cells
- thymus gland = T cells

Secondary
- site where the the effector cells get activated
- lymph nodes
- spleen
- appendix

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8
Q

what is innate immunity and adaptive immunity

A

what is innate immunity and adaptive immunity

Innate Immunity
- targets pathogens non-specifically
- responds quickly (0-4 hours)
- recognizes antigens by non-specific effectors
- removes antigen
- presents the antigen to the adaptive immune response + triggers it

Adaptive Immunity
- it attacks antigens specifically
- takes a longer time to attack
- recognizes the microbial-associated molecular patterns

Early Response (4-96 hours):
- inflammation occurs due to recruiting and activating effector cells to the site of infection
- removes antigen

Adaptive Immune Response (more than 96 hours):
- transports antigen to lymphoid organs
- naive B + T cells recognizes antigen
- clonal expansion + differentiation to effector cells
- removes antigen

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9
Q

characteristics of the immune system

A
  • it’s fluid and systemic
  • lymph flows everywhere and is interconnected to blood
  • naive lymphocytes circulate in the blood throughout the body
    naive lymphocytes = B cells + T cells
  • antigen presenting cells gather samples of the antigen in tissues
  • cells then go to the draining lymph nodes and communication here between the APC + lymphocytes allow for activation to occur
  • naive lymphocytes enter lymph nodes from blood
  • antigens from the site of infection are transported to the lymph nodes via lymphatics
  • lymphocytes + lymph return to blood via the thoracic duct
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10
Q

what are the characteristics and key cell types of the innate immune response

A

Characteristics:
- not antigen specific
- does a general attack
- always ready to be initiated quickly (has pre-made cells ready to target pathogen)
- has no memory (doesn’t have the B cells to remember the pathogen incase it infects a 2nd time)

Key Cell Types:
- dendritic cells
- macrophages
- neutrophils
- NK cells

The events in innate response trigger the adaptive response

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11
Q

what are the 1st line innate defenses

A

Mechanical Barriers:
- skin
- tight junctions b/w epithelial cells
- cilia moving fluid

Chemicals:
- fatty acids on skin
- low pH in gut
- enzymes (lysozyme in saliva)
- antibacterial peptides/proteins

Microbiological Protection:
- symbiotic flora (biological organisms have a beneficial relationship with each other)

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12
Q

What is the innate response after the 1st line of defence is not able to prevent the pathogen

A

Chemical Defenses:
- Cytokines + Inflammatory Mediators (Histamine and Bradykinin) are released to recruit immune cells to the site of injury/infection

  • Cytokines are proteins that allow for cells to communicate

Complement Activation:
- Circulating proteins can get activated to attack pathogens

Cellular Defenses:
- Neutrophils, Macrophages, + Natural Killer cells attack the pathogen via Phagocytosis

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13
Q

What is the Complement Cascade

A

The activation of a cascade of proteins

  • includes a group of Plasma Protein Mediators
  • bacteria activates more than 30 protein mediators
  • there are precursors that circulate in the body and become functional when involved in Complement Activation
  • Complement Activation works in 4 ways:

1. Opsonization
2. Inflammation
3. Chemotaxis
4. Cytolysis

  • there are 4 proteins (C6, 7, 8, 9) that come together to form a Membrane Attack Complex
  • the complex creates pores in the Gram-Negative Bacteria’s outer membranes
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14
Q

how do Leukocytes move/where do they go

A
  • Cytokines + Complement get released and attract leukocytes to the site of infection
  • chemical attractants released by pathogens
  • chemical signals released by nearby injured cells
  • leukocytes roll along the blood vessels
  • Extravasation occurs = leukocytes squeeze through the walls of the capillary blood vessels to get to the infected tissue
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15
Q

What are the steps of Phagocytosis

A
  • Chemotaxis = the directed migration of a cell in response to a chemical signal and chemical attractant
  1. Phagocytes go through chemotaxis to get to microbes
  2. Microbes adhere to the chemotaxis
    - chemotaxis create false feet to encapsulate the microbe
  3. Microbes get ingested by phagocytes
  4. Fusion of a series of vesicles (one of them being lysosomes)
    - phagosome + lysosome merge together to make a phagolysosome
  5. microbes get killed by enzymes and other chemicals
  6. elimination/exocytosis
    - degraded proteins can either go through exocytosis OR are important and will be presented elsewhere
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16
Q

how do phagocytes recognize pathogens

A

they recognize the **Pathogen-Associated Molecular Patterns (PAMPs)

  • these are molecular structures that are common to many groups of pathogenic microbes

Examples of PAMPs
- Peptidoglycan
- Flagellin (part of bacterial flagella)
- Lipopolysaccharide (LPS) from outer membrane of gram negative bacteria

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17
Q

what does the complement system involve?

A

serum proteins involved in nonspecific defense

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18
Q

what are antigens

A

means antibody + generator
- a molecule from the body that gets recognized as foreign and worth attacking

  • it triggers an immune response which results in the body creating antibodies
  • they’re unique to the pathogen they’re a part of/all microbes have different antigens
  • important for adaptive immunity that they have a specific response
  • can be a part of bacteria, viruses, fungi, and protozoa
  • ex: capsules, flagella, cell walls, toxins, envelopes, and spike proteins
  • can belong to many molecular classes, carbohydrates, lipids, nucleic acids, + proteins
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19
Q

which antigen works best of which has the highest antigenic potential

A

proteins due to their specific 3D structure

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20
Q

what are epitopes

A
  • smaller exposed regions on the surface of antigen
  • 1 antigen can have many epitopes
  • antibodies bind to a single epitope
21
Q

what are the different types of antigens

A

exogenous - on the surface of microbes

endogenous = when the virus infects a host cell and causes it to have surface antigens

autoantigens - an uninfected cell has antigens on its surface

22
Q

what makes up a well functioning immune system

A

it’s able to tell the difference between a molecule that comes from the body and a molecule that doesn’t belong to or in the body

23
Q

what is the general sequence of immunity

A

INNATE
1. inflammatory response
2. antigen presenting cells brings the antigen to the lymph nodes

ADAPTIVE
3. Helper CD4+ T cells are activated by antigen presenting cells
4. B cells + Cytotoxic CD8+ T-cells are activated

B cells activated
- plasma cells create antibodies
- some become memory cells
- depends on TH2

Cytotoxic CD8+ T cells
- effector cells actively kill infected cells
- some become memory cells
- depends on TH1

24
Q

How do antigen presenting cells present the antigen to T-cells

A
  • dendritic cells + macrophages go from the periphery -> lymph nodes
  • naive T-cells get activated to become effector cells
  • T-cells only recognize the protein fragments that come from antigens so the antigens have to be processed
25
what are examples of **antigen presenting cells**
- dendritic cells - macrophages - B cells
26
how do T-cells receptors recognize antigens
MHC bind to peptide fragments of the antigen and presents them on the cell surface There are 2 types of MHC MHC I = activates **cytotoxic T-cells** MHC II = activates **helper T cells**
27
How does **dendritic cells** present antigens
1. The antigen is engulfed via **phagocytosis** by the dendritic cell. The antigen is now in a **phagosome** 2. **Lysosome** fuses w/ **phagosome** and digests the antigen 3. **Immunodominant epitopes** are presented on the cell surface via **MHC II** The dendritic cells with the epitope/antigen go to the lymph nodes and interact w/ the lymphocytes that enter via the blood - Immature dendritic cells live in the **peripheral tissues** - Dendritic cells go to the lymph nodes via afferent lymphatics (via the lymphatic vessels) - Mature dendritic cells are now in the deep cortex
28
What are other names for the **B cell response** and the **T cell response**
B cell response = **Humoral Immunity** T cell response = **Cell-mediated Immunity**
29
How do **helper T cells/CD4+** get activated
Activation requires 3 signals Signal 1 = T cell receptor recognizes the peptide-MHC Signal 2 = APC have **co-stimulatory molecules**. These molecules interact with the ligands on T cells Signal 3 = Cytokines - these differentiate T cells into different types of **effector T cells**
30
What are the 2 types of CD4+ T cells
**Th1T cell** - Regulates **macrophages** and **cytotoxic T cells** via cell-cell interactions + secreting TH1 cytokines - Macrophages and Cytotoxic T cells are part of the adaptive inflammatory response **Th2 T cell** - Regulates B cells and the class of antibody they create to regulate the antibody response - They regulate B cells and their antibody production via cell-cell interaction ad secreting Th2 cytokines Some of general T cells can turn into **memory T cells**
31
What are the characteristics and key cells involved in **adaptive immune response**
**Characteristics** - antigen specific - forms memory - a longer process to activate or trigger *Key Cells** - B cells - T cells - Th1 + Th2 (CD4+) and cytotoxic (CD8+)
32
What do B cells and T cells use to recognize epitopes
Both cells use receptors that are antigen specific (only binds to 1 epitope). The binding of the epitope to these receptors is one of the signals that activates the B cells and T cells. - B cells use **B cell receptors** - These are antibodies bound to the B cell's membrane - T cells use **T cell receptors** - These recognize epitopes when MHC presents them
33
Why are BCR and TCR antigen specific
Due to **receptor diversity** - There are a lot of different receptors with different antigen-binding sites To create this diversity of receptors: different combinations of gene fragments get pasted together and create a functioning antibody and TCR gene
34
What is the **clonal selection theory**
Explains how the immune response can be triggered by a large variety of antigens + the cell's memory
35
How do lymphocytes develop
- **Pre-T lymphocytes** and **Pre-B lymphocytes** develop in the **bone marrow** ( these are immature lymphocytes) - 1 cell can develop a large number of lymphocytes with different specificity - T cells move to **thymus** - B cells move to **bone marrow** - the mature into **naive lymphocytes** (ready to attack but haven't been activated yet) - Mature naive cells are activated into **effector cells** in the **secondary lymphatic tissue** (lymph nodes, spleen)
36
What is **clonal selection** and **clonal expansion**
Both of these are part of a process where specific immune cells (T cells and B cells) get chosen and replicated to respond to a pathogen **Clonal Selection** - Immune cells (T cells or B cells) that match with the antigen gets chosen **Clonal Expansion** - The selected immune cells rapidly multiply and make a large army to fight the pathogen
37
Steps of the **humoral immunity/ B cells activation**
1. Antigen presented to the T cell activates it 2. T cell differentiates into Th2 cell 3. Clonal Selection - a complementary B cell clone gets chosen 4. Th2 cell activates the B cell clone (B cells have MHC II on their surface) Activation follows **Clonal Selection and Expansion** **COMPLETE ACTIVATION** - Needs 3 signals Signal 1: BCR recognizes the antigen Signal 2: APC have **co-stimulatory molecules**. These molecules interact with the ligands on T cells Signal 3: Cytokines - differentiate the B cells into **antibody secreting cells**(Plasma cells and Memory B cells) 5. B cells differentiate into **plasma cells + memory B cells**/B cell activation and Clonal expansion occurs - B cell gets activated and then will go through expansion of the 2 differentiated cells
38
What are **plasma cells** and **memory cells**
**Plasma Cells** = produces antibodies and secretes large amounts of them **Memory Cells** = circulates and gets reactivated when it gets exposed to the antigen - helps to make the secondary immune response be stronger and faster
39
What are the structure and functions of **antibodies**
AKA immunoglobulins or gamma globulins - Y shaped proteins - Antigen binding sites = variable regions at the ends of the 2 arms - Binds to antigens (microbes, cells, molecules, anything that triggers the production of antibodies) - Binds to antigens via **non-covalent bonds**
40
What are the classes of antibodies
IgM = the first antibody that gets created IgG = most common and long-lasting IgA = associated to body secretions IgE = involved in the response to parasitic infection + allergies IgD = function unknown
41
What are the 5 functions of antibodies
1. neutralization 2. opsonization 3. oxidation 4. agglutination 5. antibody-dependent cellular cytotoxicity (ADCC)
42
How do **cytotoxic T cells/CD8+** get activated
- The **TCR** bind to the MHC-viral peptide complexes - this tells the CD8+ T cell to kill the infected cell with **perforins** and **granzymes** - Activated APC have co-stimulatory molecules on its surface which helps to activate the CD8+ cells 1. APC present antigens to the **T helper cell** to activate it 2. T helper cell differentiates into Th1 cell 3. Cytotoxic T cells are activated by APCs and are differentiated with the help of Th1 **COMPLETE ACTIVATION** - Needs 3 signals Signal 1: TCR recognizes the antigen presented by MHC I Signal 2: APC have **co-stimulatory molecules**. These molecules interact with the ligands on CD8+ T cells Signal 3: Cytokines - differentiates the T cells - Was created by Th1 cells 4. Clonal expansion and differentiation into **memory T cells** and **active Tc cells**
43
How do proteins that come from a virus end up on the MHC I
- Proteins that come from a virus gets created inside of the cell, specifically in the **cytoso**l - These proteins bind to the MHC I in the **ER** and then the MHC I with the bound proteins gets transported out on to the cell surface
44
How do pathogens avoid immune responses
- Using a polysaccharide capsule - Hiding in the macrophage - Antigenic drift - Superantigen production
45
What does a **polysaccharide capsule** do
- Prevents **phagocytosis** done by innate immune cells from occurring - Makes it difficult for APCs to present antigens - Prevents **complement proteins** from doing **opsonization** - Makes it harder for antibodies to bind
46
What happens when TB hides within a macrophage
- Prevents phagosome-lysosome fusion - macrophages can NOT digest TB - Macrophage with the TB hiding in it carries it into the bloodstream - Macrophage squeezes through blood-brain barrier allowing for TB to reach the CNS
47
What is **antigenic drift**
- The host cell develops an immune response to the virus that infected it by creating antibodies that can bind to the virus's antigens - Small mutations to the surface proteins/antigens of the virus can turn the virus into another virus - This makes it unrecognizable to the host cell's antibodies which allows it to infect the host cell
48
What is **superantigenic production**
**Superantigens = exotoxins created by a specific bacteria** - Superantigens avoid the path the antigens take to activate the T cell by binding the TCR to the MHC without any specific antigen bound to it - Causes for a large amount of T cells to be activated and uncontrollably release cytokines
49