Humoral Immune System

Front 1

Are the heavy and light chains of Abs coded by the same genes?

Back 1

No. separate

Front 2

What types of antigens to Abs recognize?

Back 2

"native" (unprocessed) antigens

Front 3

Which T cells help in Ab production?

Back 3

CD4-->Th2 (humoral)

Front 4

Which surface Ig do mature, naive B cells express?

Back 4

"MD" IgM and IgD

Front 5

* What process, following activation, do B cells undergo to produce IgA, G, E?

Back 5

class switching

Front 6

* What are the "two steps" in B cell activation?

Back 6

1. mature, naive B cell encounters antigen --> internalizes, processes, and presents to T cell in MHC
2. **Upon interaction with T cell --> B cell becomes activated to differentiate (plasma cell or memory cell)

Front 7

what is the source of all blood cells (red and white)?

Back 7

bone marrow

Front 8

In B cell maturation, what occurs in the Pre-B stage and the Immature B?

Back 8

Pre-B = Rearrangement of heavy chain

Immature B = Rearrangement of light chain

Front 9

What generates Ab diversity?

Back 9

Gene Rearrangement

Front 10

What are the resulting heavy chains in the gene rearrangement of Abs?

Back 10

mu heavy chain or sigma

(IgM or IgD)

Front 11

What is the process of "gene" rearrangement in Ab production? What is the structure/components of the gene at the Primary RNA transcript stage (post DNA translation)?

Back 11

VDJ (DJ first, then V joins) in DNA --> transcription --> primary RNA --> mRNA --> polypeptide

* at Primary RNA transcript, both mu and delta constant regions are present (splicing then occurs)

Front 12

What are the sites where immune cells are generated? activated?

Back 12

Primary (bone marrow and thymus)

Secondary (spleen , lymph nodes, MALT, lymphatic vessels)

Front 13

Which primary lymphoid organ undergoes age-related atrophy?

Back 13

thymus

Front 14

What is the source of pro-T cells?

Back 14

Bone marrow --> migrate to thymus

Front 15

Which secondary lymphoid organ has the most Ab-secreting plasma cells?

Back 15

MALT (more than spleen, lymph nodes and bone marrow combined)

Front 16

Which secondary lymphoid organ filters Ag in fluid from tissues? from blood?

what are the sites of B cell proliferation in secondary lymphoid organs (general)?

Back 16

Lymph nodes (tissue via lymphatic vessels)
Spleen (filters Ag via blood)

germinal centers in lymphoid follicles (post Ag-exposure)

Front 17

Can B cells activate without involving T cells?

Back 17

Yes, Thymus-independent (TI) antigens can induce Ab response without T cells --> much less common

DO NOT involve: isotope switching, affinity maturation or memory (less complex without T cell help)

Front 18

Which type of antigens/b cell activations involve isotope switching, affinity maturation and memory cells?

Back 18

Thymus-dependent (T cells involved)

Front 19

What is the structure/set up of Ig's that bind antigen receptor mediated transduction pathways?

Back 19

Cross-linking (two surface Ig's bind one Ag); or co-receptor CR2 can bind complement, which is bound to Ag

Front 20

* what binds complement that is bound to an Ag? what role does this play?

Back 20

B cell co-receptor (along with Ig that binds Ag directly) --> dual binding leading signal cascade and B cell activaiton

Front 21

What are the functional consequences of Ig-mediated B cell activation (prior to T cell meeting)?

Back 21

Increased expression of B7 co-stimulators (activate T's) and receptors for T cell cytokines

(* improving overall ability of the B cell to then interact with the helper T)

Front 22

What types of antigens require an Ab response with the participation of T cells?

Back 22

protein antigens (thymus-dependent)

Front 23

** What type of T cell meets with a naive mature B cell? what is "unique" about this interaction?

where/how does this take place?

Back 23

Effector CD4 Helper T: that has previously been presented with THE SAME ANTIGEN that the naive B cell has encountered

In the lymphoid tissue, the T cell migrates toward the lymphoid follicle and the B cell exits the lymphoid follicle and meets the T cell in the parafollicular cortex

Front 24

* What are the specifics of the Helper T and naive B cell interaction?

Back 24

B cell presents protein Ag in MHC II, B7(on b cell) + CD28 (on t cell) bind also

** then CD40 ligand expressed on T cell and cytokines secreted --> this completes the B cell activation

Front 25

* What is the process through which C regions of H chain genes are rearranged, leading to a variety of activated B cells (B*) expressing a new Ig isotype (IgG, IgA, IgE)?

Does this affect the V region (Ab specificity)?

Back 25

Isotype (class) switching

NO!

Front 26

What directs isotope (class) switching of activated B cells?

Back 26

cytokines from Th cells

Front 27

What region of the Ab is affected by isotype (class) switching? by affinity maturation?

Back 27

Constant region

Variable region (Ab specificity)

Front 28

What process is associated with somatic hypermutation? Where is this occurring (specific to the molecule)?

Back 28

affinity maturation (increasing affinity of memory b cells)

--> Variable region

Front 29

How does the secondary Ab response to T-dependent antigens vary from the initial response?

Back 29

faster, stronger, better

Front 30

What do the Fc receptors bind to?

Back 30

they bind to an the Fc region of an Ab which is already bound to an Ag

Front 31

What are the Effector Functions of Abs?

Back 31

Neutralization
Agglutination
Opsonization
Complement-dependent lysis
Antibody-dependent Cell-mediated Cytotoxicity (targeting cells with "Fc" receptors)

Front 32

In Antibody-dependent Cell-mediated Cytotoxicity (ADCC), what do the Ab bind to on the effector cells?

Back 32

Fc receptor binds to Ab

Front 33

* What is the primary effector function of each of these Abs?
IgG, A, M, E

Back 33

G: 1st (most predominant), Gut/Placenta
A: Mucosal Immunity
M: Complement activation
E: Immediate Hypersensitivity and Parasites

D: unclear

Front 34

In general terms, what is happening when an Ab "neutralizes" a pathogen?

Back 34

Ab binds pathogen and "blocks" or prevents that pathogen from then binding to other cells and entering

e.g. stopped before entering adjacent cell or before entering intestinal epithelium

Front 35

* Which Ab passes through the mucosal epithelium? How does this occur?

Back 35

IgA (mucosal immunity) (GI and respiratory epithelium)

IgA binds a 'Poly-Ig receptor' and is endocytosed through the epithelial cell, into the lumen where it can bind and block entry of antigens

Front 36

Which Ab has the "J-chain", what role does this play?

Back 36

IgA (J-chain links dimer)

J-chain is the secretory component

Front 37

What are the two "methods" that opsonization can occur?

Back 37

Ab dependent

or

via complement activation

Front 38

Which two Abs mediate ADCC?

Back 38

IgG --> induce cytotoxic cells

IgE --> induce eosinophils (helminth and inflammatory allergies)

Front 39

What are the three complement system pathways?

Back 39

Classical, Alternative, Lectin

Front 40

* What are the important pathway factors for activation of the Alternative and Classical complement pathways?

Back 40

Alt: C3

Class: C1, C2, C4 (& C3)

*Lectin also uses C2 and C4

Front 41

Which components of the complement system form the terminal MAC complex?

Back 41

C5-C9 (poly)

Front 42

* What three functions does the Complement system have in Ag regulation?

Back 42

1. Opsonization
2. Cytolysis (MAC)
3. stimulates Inflammatory rxn

Front 43

Which Ig most stimulates the Complement system?

Back 43

IgM

Front 44

Why is regulation of the Complement system so important?

Back 44

To protect host cells from being attacked

Front 45

Is it easier to regulate the Complement system early in the activation process or later?

What is C1 INH?

Back 45

Earlier

Key inhibitory/regulatory protein of complement system

Front 46

What are antigenic variation, inhibition of complement, and resistance to phagocytosis examples of?

Back 46

Evasion of humoral immunity by Microbes

Front 47

* What is a conjugate vaccine? How/when is it useful?

Back 47

Combining bacterial polysaccaride with a protein carrier --> generates a T-dependent Ab response (more powerful) :. Using a protein carrier to generate a T-dependent response to another antigen that otherwise would have generated a lesser Ab response.

--> especially helpful in children where immune system is not yet fully developed (HIB - Influenza B)

Front 48

* What is the difference in response of a Conjugated Polysaccharide and an Unconjugated Polysaccharide?

Back 48

Conjugated --> invokes T cell help --> greater response

Non-conjugated is B cell only --> lesser response

Front 49

What is the difference between Natural and Artificial Immunization?

Back 49

both are Passive Immunization (Ab transferred, no memory):

Natural: mother to child (IgG or IgA (breast milk))

Artificial: Injected

Front 50

What is happening in Erythrobastosis Fetalis? which pregnancy does this impact? What drug treats this?

Back 50

Mother forms Rh-Abs --> attack Rh-Ag of the fetus (killing RBCs)

Second (first required to generate Rh-Abs)

Rhogam

Front 51

Which Complement system is Ab-dependent? Which are not?

Back 51

The complement system may be activated by antibody-dependent (classical pathway)

antibody-independent (alternative and lectin pathways) mechanisms