Immunology I - Mclean Flashcards

1
Q

Innate immune system cells:

A

Macrophage
Dendritic cell
Mast Cell
Natural Killer cell
Granulocytes (basophil eosinophil neutrophil)
complement proteins
(fast response)

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2
Q

Adaptive immune system cells:

A

B & T cells
(slow response)

B cells -> antibodies
T cells -> CD4+ T cell / CD8+ T cell

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3
Q

Pus forming terminologies:

“need to know”

A

Suppurative
pyogenic
purulent

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4
Q

Immunity -> branches into…

potential question

A

Immunity -> adaptive / innate
adaptive -> natural / artificial
natural (deliberate) -> passive (maternal)/ active (infection)
artificial (not deliberate) -> passive (antibody transfer) / active (immunization)

passive: getting antibodies
active: making antibodies

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5
Q

How does innate system recognize pathogens?

know 2 terms involving recognition*** target

A

First step: recognition:

Pathogen associated molecular patterns (PAMPs) are on pathogens
Pattern recognition receptors (PRRs) on host cells

second step: recruitment:

Effector cells can come and kill pathogen
Complement proteins can be recruited via blood and assist in phagocytosis. Can lyse it too.

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6
Q

Innate immune response to infection:

A

Causes inflammation.
Vasodilation, increased vascular permeability, infected tissue becomes inflamed causing pain, swelling, heat.

bacteria engulfed from effector cells, cytokine release, causes the vasodilation / inflammation.

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7
Q

Types of innate immune responses:

A

acute inflammation
chronic inflammation
Granulomatous inflammation: (cant get rid of pathogen, so u just wall it off). Granulomas wall off.

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8
Q

Mediators of innate immune response:

A

Cytokines: increase vasodilation, attract WBCs
Acute phase proteins: activate complement system, cell lysis. (C-reactive protein)
Bradykinins: Responsible in pain and itching.*****

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9
Q

Mediators: Kinins (Bradykinin)
What is the function?

potential question

A

plays an important role in pain and itching
increase vasodilation
increase vascular permeability

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10
Q

First line of defense:

what happens when it fails:

A

Innate: first line

acquired / adaptive / protective immunity: happens when fails

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11
Q

Speed of innate vs adaptive:

A

innate: primary and secondary immune response same speed. Rapid initial response time.
Also: antigen nonspecific
adaptive: secondary immune response way faster than primary. Slow initial response time.
Also: antigen specific.

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12
Q

Function:

B lymphocytes:

T lymphocytes:

A

B: synthesize / secrete specific antibodies. mediate HUMORAL immunity. (fluids of body used to be called humor, thus humoral. antibodies go around in fluids of body.)

T: recognize antigens presented by antigen presenting cells (APCs). Mediate cellular immunity.

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13
Q

HIV selectively infects which type of cell?

A

CD4 T cells. results in loss of adaptive immune response.

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14
Q

Progenitor cell of all the cells of the blood:

gives rise to:

A

Hematopoietic stem cell (HSC)
gives rise to:
1.) common lymphoid progenitor -> B / T cells / NK cells
2.) common myeloid progenitor
3.) common erythroid megakaryocyte progenitor -> megakaryocyte / erythroblast

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15
Q

Myeloid cells: give rise to:

A

Granulocytes:
Neutrophils: phagocytosis
Eosinophils: provides defense against parasites such as worms
Basophils: allergic reactions

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16
Q

B cells differentiate into…. which make…

A

B cells -> plasma cells -> make antibodies: soluble forms of Igs that are released into the blood and body fluids

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17
Q

Primary lymphoid tissues:

Secondary lymphoid tissues:

A

primary: This is where lymphocytes develop and reach maturity. Examples:
B cells develop in bone marrow
T cells develop in thymus
secondary: where mature lymphocytes become stimulated to respond to pathogens. examples:
spleen, tonsils, adenoids, appendix, lymph nodes, peyer’s patches

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18
Q

Draining lymph node:

Spleen:

A

lymph node receiving fluid from an infected site. afferent lymph vessels: deliver pathogens to the lymph node
efferent: lymph leaves lymph node

Spleen: The spleen is the only secondary lymphoid organ that filters damaged cells from blood.

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19
Q

Lymphocyte mechanism: activation in secondary lymphoid tissue:

A

Dendritic cell carries engulfed bacterium (or bacterium just travels there).
Activates B cells to convert into plasma cells -> secrete antibodies
Naive T cells -> either helper T cells which help other cells, or cytotoxic T cells which kill cells

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20
Q

antigen
immunogen
antigenicity
immunogenicity

define

A

antigen: an agent that can bind to components of immune system
immunogen: any agent capable of inducing an immune response.

Therefore, all immunogens are antigens, but not all antigens are immunogens.

antigenicity: ability to be antigenic
immunogenicity: ability to be immunogenic. Proteins are the best

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21
Q

adjuvant:

epitope:

A

substance that u mix with an antigen or immunogen to make it more immunogenic.

epitope: part of an antigen to which an antibody would bind. on the antigen. (T cell receptor)
paratope: on the antibody. small region of antibodies which bind to epitopes. (MHC)

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22
Q

T-independent antigen:
T-dependent antigen:

A

T-independent antigen: antigen binds to B cell. antibodies produced.
T-dependent antigen: requires presence of helper T cells to stimulate antibody production by B cells.

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23
Q

tolerization
autoimmunity

definition:

A

tolerization: During development, pre B and T cells learn to differentiate between self / non self

autoimmunity: failure to differentiate between self / non self.

24
Q

Mature B cell (naive B cell): whats on surface

what about plasma cell:

A

IgD and IgM on surface

plasma cell: secreting the antibodies. IgM, IgG, IgA, IgE. Not so much IgD

25
Q

Which one of these antibodies, IgM, IgG, IgA, IgE, IgD, which one is more specific for protecting the mucosal surfaces of the oral cavity?

A

IgA, Dimeric form. U find this in saliva.

26
Q

MHC class I and MHC class II present itself to which T cells?

A

MHC class I - CD8 : killer
MHC class II - CD4 : helper

27
Q

2 major types of CD4 T cells: what they do?

A

TH1 cells: secrete cytokines at site of infection and activate macrophages. CELL MEDIATED RESPONSE.
viruses / bacteria favor th1 (much smaller, so phagocytosis)

TH2 cells: secrete cytokines in secondary lymphoid organs that primarily stimulate B cells to make antibodies to bind to extracellular pathogens and virus particles. HUMORAL IMMUNE RESPONSE

allergens / parasites favor th2

28
Q

What does the invariant chain protein do?

A

Prevents MHC class II from binding peptides in the ER.

Why is antigen not binding itself to MHC class II when both antigens are in ER?
MHC II binding groove blocked by invariant chain.

29
Q

Bare Lymphocyte syndrome:

A

rare disease characterized by defective TAP protein resulting in

poor cd8 t cell responses to viruses
mhc class I retention in ER. never received peptide antigen.

30
Q

What does the invariant chain protein do?

A

prevents MHC class II from binding peptides in the ER.

31
Q

Autograft
Isograft
Allograft
Xenograft

A

transplant from same individual.
transplant from twin
transplant from allogenic person (not identical)
transplant from different species

32
Q

Langerhans cells:

A

Macrophages of the skin that act like dendritic cells.

33
Q

IL-2

A

important cytokine for proliferation of T cells

T cells can produce IL2 for itself, stimulate itself.

34
Q

basic antibody structure:
Hinge region:
Fab:
F(ab’)2:
Fc region:

A

Hinge region: flexible region
Fab: antigen binding site, obtained by papain digestion
F(ab’)2 - obtained by pepsin digestion
Fc region: portion of the constant region that forms the “stem” of the Y shaped Ig molecule.

Pepsin: digests Fc region but makes F(ab’)2. the Fabs are still in tact
Papain: separates stem and 2 top parts (Fab)

35
Q

adjuvant:

A

substance that when mixed with an immunogen, enhances the immune response of the immunogen.

36
Q

Epitope vs paratope:

A

epitope on antigen
paratope on antibody

37
Q

which Ig can form polymers?

A

IgM and IgA.

IgM : can form pentamer
IgA: can form dimer

both linked to a J chain that can facilitate this polymerization.

38
Q

abundancies of 5 different isotypes of heavy chains:

A

Example: IgG1, IG2, IgG3, IgG4.

Lower the number, the more abundant it is.

39
Q

Are MHC peptide binding sites specific?

A

no. They have degenerate binding specificity - ability to bind several different sequences. (meanwhile TCRs are specific)

40
Q

MHC class I molecules vs MHC class II molecules:

A

MHC Class I: Present antigens of intracellular origins to CD8 T cells.
expressed by all cell types except erythrocytes. Meets mhc class I in ER.
“When a cell is infected, it shows itself via MHC 1”

MHC class II molecules: present antigens of extracellular origins to CD4 T cells.
expressed by antigen presenting cells (APC). Macrophages/B cells) Meets MHC class II in endocytic vesicle.

“When a cell deliberately takes up and phagocytosis a pathogen, it presents via MHC class II”

41
Q

Mature B cell (naive B cell): whats on surface

what about plasma cell:

A

IgD and IgM on surface

plasma cell: secreting the antibodies. IgM, IgG, IgA, IgE. Not so much IgD

42
Q

Variable region:

Constant region:

A

variable (V): responsible for binding pathogens. Differences here that accounts for different isotypes. The antigen-binding sites, the tips of the Fab regions.

constant (C): contains binding sites for receptors on phagocytes / complement proteins. The Fc region and half of the Fab regions.

43
Q

Light chains / Heavy chains in Igs:

A

2 identical H chains
2 identical L chains -> but theres 2 types. either 2 Lambda L chains or 2 kappa L chains.

44
Q

Hypervariable regions:
Framework Regions:

A

Hypervariable regions: high variability on antigen binding site. Sometimes called complementarity determining regions. This forms antigen binding site.
Framework Regions: relatively invariant regions.

45
Q

Neutralization
Opsonization:

A

neutralization: neutralizing antibodies directly inactivate pathogen / toxin by binding to it and preventing it from interacting with human cells. can endocytosis the toxin.

opsonization: some antibodies are opsonins, they function in opsonization, the coating of a pathogen. facilitates phagocytosis.

46
Q

IgM:
IgG:
IgA:
IgD:
IgE:

A

IgM: first antibody made. Good in agglutination
IgG: can pass through placenta. 80% of total Ig. **
IgA: Protects mucosal surfaces of oral cavity. Dimeric form does this. **

- monomeric form predominantly in serum.
IgD: little known activity
IgE: present on mast cells / basophils, protects against worms.

47
Q

Primary immune response: antibody content
Secondary immune response:

A

primary: first IgM released. Majority of it here. Some IgG.
secondary: Majority IgG. Some IgM.

48
Q

Somatic recombination:

Light chain:
Heavy chain:

types of segments in genome

A

Light: V and J segments
Heavy: VDJ segmenets

Somatic recombination: mixing of these different V’s, D’s, J’s can make billions of different antibodies.

49
Q

Allelic exclusion:

A

process of using genes from only one parental chromosome which assures that each B cell expresses only one type of heavy chain and one type of light chain. therefore, antibody of a single specificity.

50
Q

how to go from membrane to secretary form of Igs:

A

Alternate pattern of Heavy chain mRNA processing.

basically u just choose either the secretory codon (SC region) or membrane codon (MC region) in the genome.

51
Q

Somatic hypermutation:

Isotype switching:

A

Mutations occur in V genes of heavy / light chains. This leads to affinity maturation (more specificity for antigen).

Isotype switching: after encountering an antigen, can swap from IgG to IgA or IgE, etc. Thus, effector functions are different, but antigen specificity is the same.

Note: its the T cells that can do this isotype switching. (in T-dependent antigens, flashcard number 22).

52
Q

Mechanism of isotype switching:

A

Constant region that is closest to the VDJ region determines the Ig type. To swap to a different one, you loop out that region. Cannot go back.

Goes from IgM -> IgA
No switch regions between IgM and IgD. thats why u have them together from start.

53
Q

Development of T lymphocytes:

A

Goes from no receptors -> 2 receptors -> end up with 1 receptor (CD4 / CD8).

First you have positive selection of cells whose receptor binds to MHC molecules, then you have negative selection and death of cells that react too much with these MHC molecules or dont react at all.

1.) initially, its just a T cell. no CD4 or CD8
2.) Then you have a double positive. T cells have both CD4 and CD8
3.) Positive selection of cells whose receptor binds to MHC molecules. AKA: the cells that have a receptor will be selected.
4.) Therefore you end up both CD4s and CD8s.
5.) The T cells that failed to have a receptor to MHC will die.
6.) Later on, you will have death of cells that react too strongly with MHC.

SO: Initially, you wanna select cells that can interact with MHC I or MHC II. Then you wanna kill the ones that can’t interact. Then you want to kill the ones that react too much. (The ones that react too strongly can lead to autoimmunity)

54
Q

TCRs vs Igs:

A

TCRs:

TCRs only have one antigen binding site
TCRs are always surface receptors
no somatic hypermutation
no isotype class switching
can only interact with antigen via antigen presenting cells. not directly.

55
Q

Graft vs host disease

alloreaction

A

alloreaction: transplant rejection. kidney comes in, body rejects kidney

graft vs host disease: bone marrow transplant. new bone marrow attacks body.

56
Q

Professional antigen Presenting Cells:

A

Dendritic cells
Macrophages
B cells

57
Q

SUMMARY SLIDE:

Infection on foot. What happens after if innate response doesn’t solve the problem?

A

Infection causes innate response, if this doesn’t fix problem, dendritic cells / macrophages (APCs) will go to closest lymph node

when it enters afferent lymph vessel, B cells / T cells proliferate. These naive B / T cells can either:

form cytotoxic T cells
form helper T cells
B cells -> plasma cells, secrete antibodies.

Helper T cell can either become TH1, TH2.

TH1 -> help macrophages
TH2 -> help B cells

When CD4 TH2 cells bind with B cells, this is an advantage because they can undergo Isotype Switching.