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Intro Bio II Exam 3 > Immune System > Flashcards

Immune System Flashcards

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1
Q

Pluripotent

A

Stem cells that can become ANY cell in the body, except for the placenta. This term used to be applied to stem cells in bone marrow but is inaccurate.

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2
Q

Multipotent

A

Cells in the bone marrow. Can become either myeloid stem cells or lymphoid stem cells.

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3
Q

Myeloid Stem Cells become…

A

RBCs
Megakaryocytes
Macrophages (from monocytes)
Granulocytes (types of WBCs)

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4
Q

Lymphoid stem cells become…

A

B cells
Natural Killer cells
T cells (but first go to thymus to mature!)

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5
Q

Functions of the immune system

A
  1. Protect body from pathogens
  2. Remove dead / damaged cells
  3. Remove “non self” cells or cells that have gone down the wrong path
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6
Q

What can go wrong with the immune system?

A 
Autoimmune disease
Overactive response (allergies)
Immunodeficiency
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7
Q

3 Lines of Immune System Defense

A
  1. Integumentary system
  2. Nonspecific immunity (innate)
  3. Specific immunity (adaptive)
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8
Q

Integumentary System

A

Skin, mucous membranes, microbiome

Epidermis, digestive tract, respiratory tract, urogenital tract

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9
Q

Nonspecific Immunity (Innate)

A

Rapid and general response, eliminates pathogens / infected cells

Macrophages, Natural Killer Cells

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10
Q

Specific Immunity (Adaptive)

A

Specific antigens recognized, slower response

B cells, T cells

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11
Q

Toll-Like Receptors (TLRs)

A

A class of PRR (pattern recognition receptor) of the innate immune system that recognizes generally conserved aspects of pathogens, such as bacterial cell wall, viral RNA, outer layer of yeast

We see this specifically on a dendritic cell, which then releases inflammatory cytokines, interferons, and Th1-cytokines to inform adaptive immune system

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12
Q

Physical and Chemical Barriers

A

Part of innate immune system (nonspecific)

  1. Epithelium
  2. Glandular secretion
  3. Stomach acidity
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13
Q

Lymphatic System

A

Tonsil, thymus, lymph nodes, spleen, gut associated lymphoid tissue, bone marrow, lymph vessels

Important processes occur in these places

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14
Q

What is the immune system generally?

A

Mostly cells that travel via blood and lymph

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15
Q

Leukocytes of the Immune System

A

Basophils, mast cells, eosinophils, neutrophils, monocytes, macrophages, lymphocytes, plasma cells, dendritic cells

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16
Q

Phagocytic Leukocytes

A

Neutrophils, monocytes & macrophages

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17
Q

Cytotoxic Leukocytes

A

Eosinophils, some types of lymphocytes and plasma cells (aka cytotoxic T cells and natural killer cells)

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18
Q

Antigen-presenting Leukocytes

A

Macrophages
Lymphocytes and plasma cells (aka B & T cells)
Dendritic cells
Thymus Cells

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19
Q

Which kind of important cell is not a blood leukocyte?

A

Dendritic cells; not found in the blood!

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20
Q

Phagocytosis

A

Pathogens recognized via innate system TLRs / PRRs, or via adaptive system antibodies coating the pathogen

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21
Q

Innate phagocytosis step-by-step

A
  1. Pathogen bind directly to phagocyte receptors
  2. Phagocytosis brings pathogen into phagocyte
  3. Lysosomal enzymes digest, producing antigen fragments
  4. Fragments of antigen displayed on cell surface
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22
Q

Adaptive phagocytosis step-by-step

A
  1. Antibody-coated bacteria recognized by phagocytes
  2. Ingestion of bacteria
  3. Lysosomes digest, producing antigen fragments
  4. Fragments of antigen displayed on cell surface
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23
Q

PAMPs

A

Pathogen-associated molecular patterns. These are recognized by phagocytes to induce phagocytosis.

cell wall of bacteria (Gram +)
cell membrane bacteria (gram -)
ds RNA
basically anything that would never naturally occur in our own bodies

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24
Q

PRRs

A

Pattern recognition receptors. These are on the surface of the phagocyte and bind to PAMPs to induce phagocytosis.

best known is the TLR (toll-like receptor)

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25
Q

Immune response at wound (step by step)

A
  1. Bacteria / pathogens enter wound
  2. Platelets release blood-clotting proteins
  3. Mast cells secrete factors mediating vasodilation and vascular constriction, as well as increased permeability of capillary. This increases blood flow and delivery of nutrients to wound.
  4. Neutrophils secrete factors to kill pathogens.
  5. Neutrophils and macrophages phagocytose pathogens.
  6. Macrophages secrete cytokines to signal to immune system.
  7. Inflammatory response continues until invaders neutralized, wound repaired.
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26
Q

Chemotaxis in immune system

A

Cells of immune system follow cytokines to source; this is an example of chemotaxis

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27
Q

Signs of Infection and Causes

A
  1. Redness and warmth
    Caused by increased blood flow, which increases delivery of proteins and leukocytes
  2. Swelling
    Caused by increased capillary permeability to proteins, allowing proteins to travel to site of injury. Edema is unintended side effect.
28
Q

Inflammation Response

A

Cytokines that relate to inflammation include acute-phase proteins, histamine, interleukins, bradykinin, complement proteins

Inflammation attracts immune cells, produces physical barrier, promotes tissue repair

29
Q

What distinguishes adaptive from innate immune response?

A

Involvement of lymphocytes (T, B cells)

Antigen is recognized in a SPECIFIC, not general, manner. These antigens are diverse and establish immunological memory. Self is distinguished from non-self.

30
Q

Lymphocytes

A

B and T cells

31
Q

Humoral Immunity

A

B cells express antibody molecules on cell surface that recognize specific antigens

Attack invaders OUTSIDE cells

32
Q

Cell-mediated immunity

A

T cells bind antigens already bound on the surface of antigen-presenting cells

Attack invaders INSIDE cells

33
Q

Antibodies

A

‘gamma globulins’, or proteins secreted by plasma cells (aka B cells)

IgG (75% of antibodies)
IgA - breast milk
IgE - target gut parasites, allergies
IgM - primary immune response, blood group antigens
IgD - role unknown
34
Q

Antibody Structure

A

Y shaped

Two Fab (fragment, antigen-binding) regions 
Fc region (constant region, same in all antibodies of a given animal)

The entire structure held together by disulfide bonds

35
Q

Antigen

A

Foreign invader whose surface has many different antigenic sites, or epitopes, that can be recognized by antibodies

36
Q

What can antibodies do?

A

Inactivate the pathogen

  1. Bind to pathogen so they clump and cannot function
  2. Tag antigens for phagocytosis
  3. Trigger cytotoxic attack from NK or eosinophil cell
  4. Complement system… unclear what this is
  5. Activate B lymphocytes to create plasma cells and memory cells, triggering adaptive immune response
37
Q

Primary vs Secondary Immune Response

A

Primary immune response involves low antibody release, takes a long period of time (vaccination)

Secondary immune response has antibody concentration quickly rise (the more vaccine boosters, the faster/stronger this response is)

38
Q

Primary Immune Response

A

Polyclonal response

  1. Exposure to antigen triggers clonal expansion of correct B cells via mitosis.
  2. Short-lived effector B cells carry out immediate response.
  3. Some differentiate into plasma cells, which secrete antibodies.
  4. Some differentiate into memory cells, which are long lived and continue to reproduce.
39
Q

Why do plasma cells have so many lines around the nucleus?

A

Rough ER! Need to secrete tons of proteins (antibodies), so need ribosomes embedded in lipids to do so

40
Q

Secondary Immune Response

A
  1. When memory cells exposed to antigen, clonal response is quicker and stronger.
  2. Creation of many more effector cells and plasma cells to secrete antibodies.
41
Q

Function of the Thymus Gland

A

Two-lobed organ above heart. Produces T lymphocytes and peptides (all beginning in thy-). T cells mature here.

As T cells mature in thymus, self-reactive cells are eliminated. Those that do not attack self-cells are cloned, then released to circulate throughout body.

Reaches greatest size during adolescence, replaced with adipose as you age.

42
Q

T lymphocyte development

A
  1. Multipotent stem cell in bone marrow becomes T cell precursor.
  2. Migrates to thymus gland.
  3. During embryonic development T cell receptors inserted into membrane
  4. Differentiates into cytotoxic T cells and helper T cells.
43
Q

Cytotoxic T Cells (Tc)

A

CD8 protein on cell surface
Eliminate infected/tumor cells
Bind with MHC Class I proteins found on all nucleated cells

44
Q

Helper T cells (Th)

A

CD4 protein on cell surface
Direct immune response rather than attacking cells directly
Bind with MHC Class II proteins found on antigen-presenting cells only

45
Q

MHC Class I

A

Expressed on the surface of ALL NUCLEATED CELLS. The one exception is possibly sperm. MHC I are also found on RBCs, even though those have no nuclei.

All cells in the body are constantly picking up internal peptides and presenting them on their MHC Class I receptors. These talk to cytotoxic T cells.

46
Q

MHC Class II

A

Expressed on the surface of antigen-presenting cells: macrophages, activated B cells, activated T cells, and thymus cells

47
Q

Antigen Presentation via Class I MHC

A

Cytotoxic T cells binds with its T-cell receptor AND CD8 to a Class I MHC protein on infected cell. If it sees a non-self peptide, will destroy the cell.

Peptide fragments created inside of cells via lysosomes, proteosomes.

48
Q

Antigen Presentation via Class II MHC

A

Macrophage / dendritic cell / B cell has internalized antigen and presents it on Class II MHC. Helper T cell uses its receptor and CD4 to read this peptide, then coordinates immune response.

49
Q

Role of helper T cells

A

Once antigen is recognized by helper T cell, this releases cytokines which communicate to B cells and cytotoxic T cells.

50
Q

Complex Immune Response (Innate + Adaptive)

A
  1. Bacteria enter ECF from outside. Skin or mucous membrane penetrated.
  2. Complement system activated. Mast cells secrete chemotaxis and histamine. Phagocytosis.
  3. Antibodies coat pathogen, phagocytose, antigens are presented to helper T cells, which activates B lymphocytes to produce antibodies.
  4. Leukocytes go into circulation.
51
Q

How does immune system recognize and fight viruses?

A
  1. Prexisting antibodies coat viral particles, making them targets for macrophages. Fc region sticks out, and this is identified by macrophage.
  2. Macrophage presents antigen fragments to helper T cell, activating B cells, cytotoxic T cells.
  3. Cytokine release leads to interferons, inflammation.
  4. Cytotoxic T cell lead to apoptosis and “blebbing”, or dissolution of infected cell into blobs.
52
Q

Immunodeficiency Disease

A

Results from weak / under-active immune systems.

SCID (Bubble Boy disease)
Hodgkin’s Disease - cancer of lymphatic system
AIDS (HIV infects helper T cells)

53
Q

HIV infection

A

Viral load early in infection decreases as antibody production increases. However antibody production stays at a high level because of incorporation of viral genome into own genome, constant production of virus.

Eventually CD4 T cell production drops. Opportunistic infections result.

Antibodies can only be used to test for HIV a few months after infection. Need PCR to determine presence of virus.

54
Q

How does HIV target cells?

A

HIV finds cell surface receptor CD4 and CCR5 on helper T cells.

Gp120 on surface of HIV binds to these receptors.

55
Q

Macrophages are derived from what?

A

Monocytes (myeloid stem cells)

56
Q

Plasma cells are derived from what?

A

B cells (lymphoid stem cells)

57
Q

Basophils and Mast Cells…

A

Granulocytes that release chemicals, e.g. cytokines

58
Q

Eosinophils are…

A

Cytotoxic cells that destroy invaders

59
Q

Neutrophils are….

A

Phagocytic cells that ingest invaders

60
Q

Monocytes and macrophages are…

A

Phagocytic cells that ingest invaders

61
Q

Lymphocytes and plasma cells are…

A

Cytotoxic cells - these include B, T, and NK cells. Only cytotoxic T cells and NK cells are cytotoxic.

62
Q

Immunodeficiency vs Autoimmune Disease

A

Autoimmune disease body attacks self: Diabetes I, myasthenia gravis, arthritis.

Immunodeficiency disease body’s immune system not up to par: AIDS, SCID, Hodgkin’s Disease

63
Q

What spikes at the beginning of HIV infection?

A

Viral load and anti HIV-1 antibody

64
Q

What steadily rises over course of months and years during HIV infection? What steadily declines?

A

p24 antigen and plasma viral load rise

CD4 lymphocytes decline

anti HIV antibody stays high and does not change

65
Q

Primary infection (HIV)

A

First few weeks, viral load spikes and helper T cells decline - acute

66
Q

Viral set point (HIV)

A

About ten years - T cells higher than viral load, but problem is chronic

67
Q

HIV Becomes AIDS

A

after prolonged period of time, viral HIV load reasserts itself and T cells rapidly decrease / disappear – this is AIDS, can be diagnosed by opportunistic infections that accompany drop in helper T cells (fungi, viruses, then rare cancers)

Intro Bio II Exam 3 (8 decks)

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