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IHO Week 2 > Diebel-Antibodies II > Flashcards

Diebel-Antibodies II Flashcards

1
Q

What are Abs?

A

Cell surface and soluble proteins that are involved in the recognition, binding and adhesion processes of cells.

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2
Q

Which Ab has the highest number of monomers, highest molecular weight and is the best at fixing complement?

A

IgM

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3
Q

Why does IgD, the monomer expressed on every B cell, have a low serum conc?

A

It is always membrane bound or associated w/ a B cell.

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4
Q

Which is the only Ab that can cross the placenta?

A

IgG

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5
Q

Which Ab isotype has the lowest serum conc and is responsible for mast cell and basophil degranulation?

A

IgE

It is not expressed at high levels and when it is expressed it gets picked up by mast cells and basophils through an Fc receptor.

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6
Q

Which Ab isotype is

A

IgE

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7
Q

Elevated levels of IgM reflect…

A

Recent infection/exposure to antigen.

Fights viruses and bacteria and serves as a BCR but is not useful in protecting immunocomp pts. Can be present in bodily secretions.

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8
Q

Which isotype can be used to protect immmunocomp individuals, block Ab to TNF production (RA) and block antibody to block allergens?

A

IgG

Good for virus, toxins, bacteria.

Present in interstitial fluids.

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9
Q

Which Ab mediates hemolytic disease of the newborn?

A

IgG

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10
Q

Daily production of what Ab is greater than any other and why?

A

IgA

B cells that produce IgA migrate to the subepithelial tissue so that the IgA secreted lines the mucosal epithelium.

Good for virus, toxin, bacteria

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11
Q

Which Ab is present in bodily secretions (breast milk and clostrum)?

A

IgA

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12
Q

What are the two major roles of IgE and how does it work?

A
  1. Combat parasite infections
  2. Combat pulmonary fungal infections

Crosslinking of IgE on a mast cell or basophil causes the release of histamine and syntehsis of inflammatory mediators.

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13
Q

What causes allergies?

A

The overproduction of IgE to allergy inducing antigens.

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14
Q

What is the clonal selection theory?

A

T cells make only ONE antibody. The choice of which antibody to make is not random. The entire population of T cells exists in an individual before it has had contact w/ an antigen. The best fitting T cells are selected by the antigen.

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15
Q

What is the difference between an isotype and an allotype?

A

Isotype: IgA, IgE, IgD

Allotypes: genetic variations between people, specifically between h and l chains of Ab. We have two copies of H and L (from mom and dad) only one H chain and one L chains is synthesized in a B cell (allotypic exclusion)

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16
Q

What is recombination?

A

Changing the relative positions of 2 pieces of DNA

17
Q

How do you make a heavy chain?

A

The developing B cell brings one random D segment close to one J. Cutting and joining occurs. It then brings a V segment up to DJ. More cutting and joining occurs. Then the entire region from the assembled VDJ unit to the end of IgD constant region gene is transcribed to RNA. Primary RNA transcripts are then processed using alternative polyA sites and splicing first to make IgM and then to make IgM and IgD.

18
Q

How do you make light chains?

A

Pretty much the same way as you’d make a heavy chain, but w/ only V and J segments, no D and only 1 C domain gene (for kappa or lambda).

19
Q

What do RAG1/2 do and how do they work?

A

These are the recombinases responsible for the recombination of antibodies.

  1. Recombinases bind splice signals (12/23 bp sequences) to the right of a D segment and left of a J segment. Pulls them together, cuts and splice.
  2. Then they look for a splice seq to the right of a V seg and do it again.
20
Q

What is Omenn Syndrome?

A

A very rare disease that occurs if recombinases are knocked out. If RAGs are knocked out you can’t make B and T cells.

21
Q

What is somatic variation?

A

RAG cells are kinda messy so the VD and DJ joints are sloppy. Exonucleases can chew away nucleotides before joining or Tdt can ADD nucleotides but you can’t predict the sequence of the joining area. (N region)

Somatic variation comes from when you pull VDJ segments together and their are MISTAKES.

22
Q

What are the pros and cons of the N region?

A

It produces A LOT of random diversity.

BUT 2/3 times the N region creates a frame shift mut that leads to a nonsense codon that terminates trxn.

23
Q

What is receptor editing?

A

If sloppy recombination leads to termination you can try again w/ another allele if RAG is still active.

24
Q

Why do mature B cells initially express IgD and IgM?

A

These are b cell receptors that are selected for when mRNA is processed.

25
Q

Where does the switching of membrane bound IgD and IgM to secretory IgM occur?

A

Level of processing mRNA transcripts.

26
Q

When does additional class switching occur from IgM to IgG, or IgE or IgA?

A

Level of rearrangements of DNA

27
Q

What is somatic hypermutation?

A

Before you class switch you can make recptors better. B cell binding antigen can make it better.

Selection of the best fitting mutatns after antigenic stimulation allows for an increase in affinity during an IR (affinity maturation).

28
Q

What is the role of AID in Somatic Hypermutation?

A

When a B cell binds a particular antigen AID is induced. AID makes base mutations in genes. At the end of cell division the daughter cells makes a different antigen that could have better/worse binding.

29
Q

How does class switching work? What part of the antibody stays the same and what changes?

A

A mature B cell starts by making both IgM and IgD (through differential splicing) which it puts into its membrane as receptors.

Later it can switch to making IgG, IgE or IgA (dna rearrangement).

L chain and VH domain stay the same.
C region of the H chain changes.

30
Q

How is it possible to get 10^14 antibodies?

A
  1. 2 chain receptors from H and L chain. Each chain provides half of recognition site for epitope
  2. Recombination from germ line segments
  3. Optional diversity- B cell chooses kappa or lambda.
  4. Somatic mutation- N region diversity (nucleotides randomly subtracted/added)
  5. Somatic hypermutation- AID (intentional mutation to get different cells)
31
Q

What are the proliferation cytokines?

A

IL2,4,5

32
Q

What are differentiation cytokines?

A

IL 2,4,5 IFNy, TGFB

33
Q

What are the class switching cytokines?

A

IFNy–> IgG2a (blocks switching to IgE)
IL4–> IgG1, IgE
IL5–> IgE

34
Q

What is Burkitt’s Lymphoma?

A

Cancer of B lymphocytes
Adolescents/young adults
T (8;14)—translocation of c-myc 8 and heavy chain Ig (14)
Associated w/ EBV
Jaw lesion in endemic form; pelvis/abdominal lesion in sporadic form
Tx: Chemo ( rituxan shows an 8 year survival rate)

35
Q

What is Acute lymphocytic Leukemia?

A

Most common in children
Disorder in B/T cell lymphocyte progenitor–> proliferation of blasts in marrow–> suppression of hematopoiesis
Anemia, thrombocytopenia, anemia, neutropenia
Tdt+ (marker of pre-T and pre B cells), CALLA+.
Most responsive to therapy.
May spread to CNS and testes.
T(12;123)→ better prognosis

36
Q

What is Acute myelogenous Leukemia?

A

Cancer of the myeloid line of blood cells, most common acute leukemia affecting adults
Age: median onset 65 years
Somatic mutations in multipotent hematopoietic cell–> abnormal blast cells–> impaired production of normal cells–> anemia and thrombocytopenia

37
Q

What is chronic lymphocytic leukemia?

A

Age > 60 yrs, M>F
Often asymptomatic
Accumulation of monoclonal pop of small mature-appearing CD5B lymphocytes
Autoimmune hemolytic anemia
SLL same as CLL except CLL has an increase in peripheral blood lymphocytosis or bone marrow involvement

38
Q

What is chronic myelogenous leukemia?

A

15% all leukemias
Age: highest incidence at 30-60 yrs
Philadelphia chromosome (t [9-22],bcr-abl)–> bone marrow makes tyrosine kinase–> too many stem blood cells triggered to become WBC
Splenomegaly; may accelerate and transform to AML or ALL (blast crisis)
Very low leukocyte alkaline phosphatase as a result of immature granulocytes

39
Q

What are the diseases associated with Ig gene expression?

A

Burkitt’s Lymphoma

Acute Lymphocytic Leukemia

Acute Myelogenous Leukemia

Chronic Lymphocytic Leukemia

Chronic Myelogenous Leukemia

IHO Week 2 (11 decks)

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