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IHO Week 1 > Specific Acquired Immunity > Flashcards

Specific Acquired Immunity Flashcards

1
Q

2 kinds of cells dividing up work of adaptive immune response

A

phagocytes - eat things up that trigger PRRs with PAMPS and DAMPs –> antigen presentation and induction of adaptive immune response
lymphocytes - specialized for recognizing foreignness & enhancing phagocytosis

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2
Q

epitope

A

Epitopes are regions on an antigen that can be recognized by an antibody or by T cell receptors. Epitopes are also called antigenic determinants.

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3
Q

2 kinds adaptive immunity

A

B cell –> release antibodies to protect extracellular = humoral
T cell –> survey surfaces of body’s cells looking for ones w/ damage or parasites = cell-mediated

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4
Q

MHC class 1

A

Antigens synthesized within the cell. Cell antigens of antigens from cell infections. Recognized by CD8+ killer T cells. Expressed on all cells except RBCs.

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5
Q

MHC class 2

A

antigens are products of phagocytosis. Recognized by CD4+ helper T cells. Expressed on monocytes / macrophages, dendritic cells, B cells, and epithelial cells of the thymus.

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6
Q

cytokine to make hsc –> lymphoid progenitor

A

IL-7

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7
Q

lymphoid progenitor goes to make

A

NK cells
dendritic cell
b cell progenitor
t cell progenitor

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8
Q

b cell progenitor goes to

A

mature b cell which makes plasma cells and memory b cells

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9
Q

t cell progenitor goes to

A

cd 8+

cd 4+

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10
Q

cd 8+ t cell goes to

A

effector cd8+

memory cd8+

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11
Q

cd 4+ t cell goes to

A 
memory cd 4+
Th1
Th2
Th17
Th reg
Th FH
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12
Q

cytokine to make Th1 CD4

A

IL-12

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13
Q

cytokine to make Th2 CD4

A

IL-4 (IL-10?)

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14
Q

cytokine to make Th17 CD4

A

IL-6, IL-23

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15
Q

cytokine to make T FH CD4

A

IL-6, IL-21

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16
Q

cytokine to make Treg CD4

A

IL-2, TGFbeta

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17
Q

B and T cells both being production

A

in the bone marrow
B cells are released from the bone marrow as mature cells, while T cells must pass through the thymus to become mature cells.

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18
Q

Mature B cells and T cells can be in the

A

blood or resident in the lymph nodes and spleen

can travel from one lymph node to another and to and from the spleen

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19
Q

Major lymphoid organs and tissues

A

Primary:
Thymus, bone marrow
Secondary:
Tonsils/adenoids, lymph nodes, spleen, lymph nodules, peyer’s patch, urogenital lymphoid tissue

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20
Q

Where do T cells recognize epitopes?

A

Starting in lymphoid tissue

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21
Q

After T cell activated, where do they go

A

proliferates and daughters travel throughout body until they reach place where antigen invaded

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22
Q

What happens when T cells get to infection site

A

Restimulated by local APCs and release short-range lymphokines that attract and activate monocytes and macrophages

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23
Q

All T cells express

A

CD3 and have TCRs created through DNA rearrangement

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24
Q

αβ T cells

A

In αβ T cells the TCR is made up of the variable αβ peptides coupled with the CD3 complex.
These αβ T cells only function by binding to MHC I or MHC II molecules.
They make up all of the CD4+ and CD8+ T cell populations and represent 90-95% of all of the blood T cells in humans.

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25
Q

γδ T cells

A

In γδ T cells the TCR is made up of the variable γδ peptides coupled with the CD3 complex.
Some of these T cells can function by binding directly without the use of a MHC complex.
They protect mucosal surfaces of the body.
Most intraepithelial lymphocytes are CD8+ γδ T cells. Circulating γδ T cells are “double-negative” (CD4- CD8-) T cells.

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26
Q

2 main classes of T cells

A

Helpers and killers

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27
Q

5 specialized subsets of helper T cells

A 
Th1 helper
Th17 
Th2
T follicular helpers
T regulatory
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28
Q

Th1

A

recognize antigen and make a lymphokine that attracts thousands of macrophages, the heavy-duty phagocytes, to the area where antigen has been recognized.

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29
Q

Th17

A

are similar to Th1 in that their main role is to cause focused
inflammation, although they are more powerful than Th1. They have been implicated in many serious forms of autoimmunity

30
Q

Th2

A

stimulate macrophages to become ‘alternatively activated,’ able to function in walling-off pathogens and promoting healing, a process that usually takes place after the pathogen-killing Th1 response. They are very important in parasite immunity.

31
Q

T fh

A

stimulated by antigen and migrate from T cell areas of lymph nodes into the B cell follicles, where they help B cells get activated and make the IgM, IgG, IgE and IgA antibody subclasses.

32
Q

T reg

A

make cytokines that suppress the activation and function of Th1,
Th17, and Th2 cells, so they keep the immune response in check. They are part of the Th family.

33
Q

CTL

A

destroy any body cell they identify as bearing a
foreign or abnormal antigen on its surface.
CD8

34
Q

Activation of αβ T cells

A

Signal 1 - TCR recognition of HLA bound antigen (CD4 to MHC II or CD8 to MHC I)
Signal 2 - CD80/86 on APC to CD28 on T cell (if no CD 80/86 assume autoimmune)
Other signals
Cytokine signals (to tell what to differentiate into)

35
Q

APC –> Th0: IL-12

A

Th1

36
Q

APC –> Th0: IL-6, IL-23

A

Th17

37
Q

APC –> Th0: IL-10

A

Th2 (IL-4?)

38
Q

APC –> Th0: IL-10, TGF-b

A

Treg

39
Q

Activated killer T cell

A

If activated, a clone of the CD8+ T cells gets expanded and the daughters circulate in large numbers throughout the body. When one of the daughters of a stimulated CD8+ T cell binds a cell showing the its “activation” peptide, the T cell delivers a lethal hit to that cell by signaling the target cell to commit suicide through apoptosis. The target cell’s nucleus disintegrates and the cell dies.

40
Q

Killing by killer t cells

A

Kill by FAS – FAS ligand interaction. T cells expressing the FAS ligand bind to FAS, a protein on a target cell to induce caspase activation and apoptosis.

Kill by secreting toxic agents as well. TNF, a cytokine, can also induce apoptosis. Perforin is a pore-forming protein. Granzymes also induce apoptosis.

41
Q

Functions of the thymus

A

Maturation/selection of T cells

42
Q

Positive and negative selection t cells

A

Positive selection – T cells must recognize MHC class I or MHC class II molecules in order to be stimulated to mature (self-restricted).

Negative selection – T cells that recognize self-antigens bound to MHC class II on the thymus epithelial cells are driven to apoptosis (tolerant to self-antigens).

43
Q

CD3

A

all T cells

44
Q

CD4

A

Helper T Cells

45
Q

CD8

A

Cytotoxic T cells

46
Q

CD16, CD56

A

on NK Cells
CD16 - Low affinity receptor for Fc region of IgG
CD56 - Adhesion molecule

47
Q

CD19, CD21

A

B cells
CD19 - signal transduction (Coreceptor CD21)
CD21 - Receptor for complement (C3d and EBV)

48
Q

CD28

A

T cells

Receptor for costimulatory B7 (CD80/96 of APCs)

49
Q

CD40

A

Signal transduction between T cells and APCs and T cells and B cells
On B cells (CD40L on T cells)

50
Q

what markers indicate B cells

A

19,21

51
Q

what markers mean NK cells

A

16,56

52
Q

What markers distinguish t cells

A

4, 8

CD3 on all T cells

53
Q

B cell receptor made of

A

Signal through Ig Alpha and Beta

CD79A and CD79B

54
Q

most abundant antibody in blood.

A

IgG

55
Q

IgG and complement

A

Two adjacent IgG molecules, binding an antigen such as a bacterium, cooperate to activate complement, a system of proteins that enhances inflammation and pathogen destruction.

56
Q

Class of ab that passes through placenta

A

IgG

57
Q

IgM

A

a large polymeric immunoglobulin. It’s even better at activating complement than is IgG and is the first antibody type to appear in the blood after exposure to a new antigen. It is replaced by IgG in a week or two.

58
Q

IgD

A

main form of antibody inserted into B cell membranes as their antigen receptor, which seems to be its only biological role.

59
Q

most important antibody in secretions

A

IgA

60
Q

Ab designed to attach to mast cells in tissues

A

IgE

61
Q

IgE and allergies

A

mast cell to make prostaglandins, leukotrienes, and cytokines, and release its granules which contain powerful mediators of inflammation like histamine.

62
Q

Ab function in disease

A

First time - mucous membrane - IgA (maybe IgE)
Secreted and local immunity from IgA
Antigen then maybe to local lymph nodes or spleen –> IgM then IgG

63
Q

Ab important for combatting what

A

extracellular pathogens like bacteria Staph, strep and hemophilus
neutralizing toxins, block spread of virus in blood (once in cell, need killer t cells)

64
Q

X-linked agammaglobulinemia

A

absence of B lymphocytes

65
Q

CD40 ligan deficiency

A 
Failure of immunoglobulin class switching
B cells can't get T cell help (can't use AID to class switch)
66
Q

Activation-induced cytidine deaminase deficiency

A

Failure of immunoglobulin class switching

67
Q

Common variable immunodeficiency

A

failure to produce Ab against particular antigens

68
Q

Omenn syndrome

A

VDJ recombination failure

Cannot produce BCRs or TCRs

69
Q

X-linked severe combined immunodeficiency

A

failure to produce mature T lymphocytes

70
Q

Digeorge

A

failure of thymus to develop correctly

71
Q

hemophagocytic lymphohistiocytosis

A

failure of CD8+ t cells and NK cells to produce and/or release lytic granules

72
Q

IPEx

A

failure of peripheral tolerance due to defective regulatory T cells

IHO Week 1 (9 decks)

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