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D & T 1 - Exam 1 > Immunology - Exam 1 > Flashcards

Immunology - Exam 1 Flashcards

1
Q

Antigen def. Give 4 examples. How many antigens are on a microbe?

A

ANY substance that induces a specific immune response (ex. proteins, nucleic acids, polysaccharides, metals). Each microbe has a LOT of different antigens.

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2
Q

Pathogen: def and (5) types

A

pathogen = infectious organism. Includes:

1. virus, 2. bacteria, 3. fungi, 4. protozoa, 5. helminths (worms)

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3
Q

(2) categories of leukocytes and sub-categories of each

A

Lymphoids (3) and Myeloids (4).
LYMPHOIDS = T lymphocytes, B lymphocytes, and Natural Killer (NK) cells

MYELOIDS = Monocytes/Macrophages; Dendritic cells; Mast cells; and PMNs/Granulocytes (3)
-(3) PMNs = Neutrophils, Basophils, and Eosinophils

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4
Q

(5) differences in Innate v. Adaptive Immunity

A
  1. Innate is primitive host defense and adaptive is specific or acquired
  2. Innate is effective immediately and adaptive takes time to develop/the secondary defense
  3. Adaptive is antigen-specific, but innate is not
  4. Adaptive increases in magnitude and effectiveness after successive exposure to infectious agent, but innate does not
  5. Innate is mediated by NON-antigen specific immune cells, while adaptive IS mediated by antigen-specific lymphocytes and their products
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5
Q

What cells are the 2 mediators of the adaptive immune response? Which cells are part of the innate immune response?

A
  • B and T lymphocytes are 2 mediators of Adaptive.

- ALL of the myeloids + Natural Killer cells = Innate. (So innate is phagocytes (macrophages, neutrophils) and NK cells)

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6
Q

(2) types of adaptive immunity and their functions. Which targets extracellular v. intracellular microbes?

A
  • Humoral immunity = defense where our B lymphocytes make antibodies. These secreted antibodies block infections and aid in elimination (phagocytosis) of EXTRAcellular microbes.
  • Cell-mediated Immunity = both helper T cells and cytotoxic T cells that, respectively, activate macrophages to kill phagocytosed microbes or directly kill infected cells. Protects again INTRAcellular microbes.
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7
Q

Antibodies: definition and function

A
  • Made by B lymphocytes in the Humoral type of adaptive immunity. Antibodies are proteins in the blood and body fluids that bind to specific antigens (or other structures) on the surface of microbes.
  • Antibodies can neutralize toxins or microbes OR aid in phagocytosis of microbes
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8
Q

(2) types of T lymphocytes

A

Helper T cells = CD4+ cells. Make cytokines that ACTIVATE macrophages that have phagocytosed, but have not yet killed microbes. Their cytokines also activate neutrophils to cause inflammation. Also help B cells make antibodies and T cells to proliferate (get it on)
-Cytotoxic T cells = CD8+ cells. Directly kill cells infected w/ virus or some other intracellular pathogen

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9
Q

3rd type of T cell and its function

A

Regulatory T cells: job is to regulate the overall immune response–both innate and adaptive–by suppressing other immune cells

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10
Q

Clonal expansion

A

After exposure to specific antigen, a crap ton of lymphocytes specific for that antigen are cloned in order to keep up with the proliferating microbes. Since microbes express many different antigens, an infection of one type of microbe can lead to several different clones with different antigen-specificities; yet they will all attack the same microbe.

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11
Q

(7) features of adaptive immunity

A
  1. Specificity = each lymphocyte responds to 1 specific antigen
  2. Diversity = a billion diff antigen specificities
  3. Memory = after initial antigen exposure, get bigger, more potent response to next exposure
  4. Clonal expansion = cloning antigen-specific lymphocytes to attack the microbe
  5. Specialization = antibodies target EXTRAcellular pathogens, while CD8+ target virally-infected/INTRAcellular pathogens
  6. Contraction and homeostasis
  7. Non-reactivity to self = prevents injury to the host during response to foreign antigens
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12
Q

(4) steps of clonal hypothesis

A
  1. Lymphocyte precursors turn into mature lymphocytes in lymphoid organs (Bone marrow = B and Thymus = T)
  2. Mature lymphocytes specific for diff antigens enter lymphoid tissues
  3. There, antigen-specific clones are activated by their antigens
  4. Travel to site of infection/injury for immune response
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13
Q

Immunological memory

A

the final phase of the adaptive immune response following the Contraction & Restoration of homeostasis phase. Most lymphocytes undergo regulated apoptosis or inactivation. But some lymphocytes stick around and become memory cells in order to provide a faster, more potent response to the next antigen exposure.

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14
Q

1st phase of the adaptive immune response

A

capture and display of microbial antigens. Done by antigen-presenting cells, e.g. Dendritic cells that present the antigen to NAIVE T-cells

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15
Q

Effector lymphocytes. Which phase of adaptive immunity?

A

functional lymphocytes. They differentiate (and clone) into this after exposure and recognition of their specific antigen. This occurs during the Lymphocyte Activation phase (3 of 6)

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16
Q

(3) actions included in the Antigen Elimination (Effector) phase of adaptive immunity

A

eliminate pathogens by 1. production of cytokines that activate cells of BOTH innate and adaptive immunity; 2. direct killing of infected cells (cell-mediated immun); and 3. production of antibodies (humoral immun)

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17
Q

(4) Myeloid cells

A

Myeloids are mostly phagocytes. Include:

  1. Monocytes/Macrophages (phag)
  2. PMN cells (phago) = neutrophils, basophils, and eosinophils
  3. Dendritic cells (phag)
  4. Mast cells
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18
Q

Lymphoid cells

A

Lymphoids = the (3) lymphocytes. T cells, B cell,s and NK cells

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19
Q

Monocytes/Macrophages. Look, location, and function

A

Mononuclear phagocytic cells in tissue

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20
Q

PMNs. Look and function. 3 subtypes.

A

PMNs = Polymorphonuclear cells. MULTI-lobed nuclei with cytoplasmic granules. Phagocytic cells, include:

  • Neutrophils: phagocytosis and activation of bactericidal mechanisms
  • Basophils: unknown, but appear similar to mast cells
  • Eosinophils: kill antibody-coated parasites and involved in allergy
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21
Q

Dendritic cells. Look and function

A

mononuclear cells with dendrites. Antigen uptake in peripheral sites and present antigens to T cells

22
Q

Mast cells. Location and function. Ex of sx mast cell can cause

A

located in mucous membrane and connective tissue. release granules containing histamine (and active agents). Major effector cell in allergy, but can also protect against intestinal worms. Mast cells cause bronchiospasms

23
Q

Natural Killer cells.

A

NON-antigen specific lymphocyte. Release lytic granules that can kill virus or other INTRAcellular parasite-infected cells (or tumor cells) directly. Innate Immunity.

24
Q

(2) functions of CD4+ cells and which type of immunity that is

A
  • B cell differentiation (humoral immunity)

- Macrophage activation (cell-mediated immunity)

25
Q

Bone marrow

A

Site of virtually all immune cell precursors (generation) AND site of B cell maturation

26
Q

Ratio of CD4 to CD8 in blood

A

Usually 2:1 (twice as many CD4). Ex. One indicator of HIV is a decrease in that ratio.

27
Q

Maturation site of B and T cells

A

B cells in bone marrow. T cells in Thymus

28
Q

What happens in primary v. secondary lymphoid organs. Name (2) primary and (3) secondary.

A

Primary = lymphocyte development and maturation. (2) primary are bone marrow and thymus.

Secondary = lymphocyte activation (where first meet pathogens or their components), proliferation, and differentiation into effector/memory cells.
(3) are spleen, lymph nodes, and intestinal mucosa

29
Q

Thymus cortex v. medulla populations. Direction of migration.

A

Thymus cortex is densely populated with all the BABY thymocytes. They undergo positive selection and then migrate into medulla.

Medulla filled w/ developing/mature thymocytes. Mature thymocytes then dump into blood stream and travel to secondary lymphoid organs

30
Q

Naive lymphocytes: definition and circulation pathway. HEV?

A

has never seen an antigen before. Circulate between blood, lymph, and lymph nodes (enter lymph nodes via HEV). But overall congregate in lymph nodes (B cell and T cell zones) where FIRST encounter antigens from pathogens

31
Q

Location of B and T cell zones in lymph node

A

B cells on outside and T cells are inner

32
Q

(2) functions of spleen and location of each

A
  1. RED pulp = remove damaged or old RBCs

2. WHITE pulp = activate lymphocytes against blood borne pathogens (e.g. polysaccharide encapsulated bacteria)

33
Q

(3) traits of naive lymphocytes. (v. effector lymphocytes)

A
  1. just come out of the thymus
  2. never encountered its antigen or been stimulated. Thus, has NO effector function
  3. has receptors that allow it to enter the lymph node from the blood (v. effectors, which express surface markers that allow them to leave lymph nodes and stick to vascular endothelium at site of infection)
34
Q

What if a naive T or B lymphocyte doesn’t encounter their specific antigen in a lymph node?

A

They will eventually migrate out of the lymph node via efferent lymphatic vessels, into the lymph, and then go to ANOTHER lymph node

35
Q

(2) ways naive lymphocytes can enter lymph nodes

A
  1. from blood circulation through HEV

2. from another lymph node via afferent lymphatic vessel

36
Q

Defense mechanism for extracellular infection: interstitial spaces/blood/lymph v. epithelial surfaces

A
  • Interstitial spaces, blood, lymph = complement, macrophages, and neutrophils; whereas
  • epithelial surfaces = antimicrobial proteins
37
Q

Defense mechanism for intracellular infection: cytoplasmic v. vesicular

A
  • Cytoplasmic, such as viruses = NK cells

- Vesicular, such as mycobacteria = Activated Macrophages

38
Q

(3) characteristics unique to innate immunity

A
  1. recognizes structures SHARED by diff microbes, but not present on normal host cells
  2. Pattern-recognition receptors (PRR), such as TLR have limited diversity
  3. PRR distrubtion is nonclonal, meaning there are identical receptors on all cells of the same lineage
39
Q

PRRs

A

PRRs recognize PAMPs.
PRR = pattern recognition receptor; on surface and in cytosol of innate immune cells (e.g. macrophages, DC, neutrophils)
Include TLRs in plasma membrane, and NOD-like receptors and RIG-like receptors in cytosol. These all recognize similar types of ligands = REDUDANCY

40
Q

TLR-4 and TLR-3. Location and molecule recognition

A
  • TLR-4 is on surface of innate immune cells (plasma membrane). Recognizes LPS (lipopolysaccharides)
  • TLR-3 is internal in plasma membrane of an ENDOSOME. It recognizes double-stranded RNA (dsRNA)
41
Q

PAMPs

A

PAMP = Pathogen-associated Molecule Patterns. These are things expressed ONLY by microbes and recognized by PRRs of innate immune cells. Ex. Lipopolysaccharides (TLR-4) and dsRNA (TLR-3)

42
Q

TLR Signal Transduction. (2) adaptor proteins and different outcomes

A

TLR signals to either MyD88 or TRIF (adaptor proteins).

  • MyD88 leads to cytokine production = acute inflammation and stimulation of ADAPTIVE immunity
  • TRIF leads to IFN-alpha/beta production = antiviral state
43
Q

NLRP3 inflammasome

A

multi-protein complexes that are assembled based on sensing the microbial produce or other cell damage. The inflammasome assembly leads to ACTIVATED Caspase-1 and resulting cleavage of pro-IL1 and secretion of IL-1 = ACUTE INFLAMMATION. (erego “inflammasme”)

44
Q

Name 2 antimicrobial peptide categories

A

Defensins and Cathelicidins. These are involved in the chemical barrier protection on skin (epithelial barriers) and act as peptide antibiotics!

45
Q

Name (4) tissue-specific macrophages. Where does differentiation and proliferation happen?

A

Differentiate in blood and divide in the tissue.

  • Brain: Microglial cells
  • Liver: Kuppfer cells
  • Lung: Alveolar macrophages
  • Spleen: Sinusoidal macrophages
46
Q

Which cells mediate the later stages of the innate immune infection (1-2 days after infection)?

A

macrophages. they persist at the inflammation site and are long-lived

47
Q

Which components of activation of classic M1 macrophages leads to inflammation and which lead to killing of microbes? (Hint 3 different component to receptor actions)

A

Microbe + TLR = cytokines TNF, IL-1, IL-6, and IL-12. These lead to inflammation and enhanced adaptive immunity

Cytokine (e.g. IFN-gamma) + cytokine receptor = ROS = killing of microbes

Complement fragment + complement receptor = iNOS and phagocytosis of microbe into phagosome, also = killing of microbe!

48
Q

Which cell links the innate and adaptive immune responses?

A

DC b/c they capture and display microbial antigens to naive T lymphocytes AND tune the the T cell repsonse

49
Q

How do NK cells work? How do they affect macrophages?

A

NK cells are NON-phagocytic and kill virus-infected cells via Perforin and Granzyme.
NK cells produce IFN-gamma, which ACTIVATES macrophages, leading to killing of phagocytosed microbes

50
Q

How is activation of NK cells controlled?

A

there is a separate inhibiting and activating receptor. Once the inhibitory receptor is engaged, it will block the signal coming from the activating receptor (if that one is also engaged).

51
Q

How does innate immunity stimulate adaptive immunity (both B and T cells)?

A

Innate immunity provides SECOND signals:
B cells: ex. IL-6 and C3d ACTIVATE B-cell proliferation and differentiation
T cells: ex. DC make cytokines, such as IL-6, IL-1, and IL-23, that make T cells differentiate

D & T 1 - Exam 1 (3 decks)

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