Study your flashcards anywhere!

Download the official Cram app for free >

  • Shuffle
    Toggle On
    Toggle Off
  • Alphabetize
    Toggle On
    Toggle Off
  • Front First
    Toggle On
    Toggle Off
  • Both Sides
    Toggle On
    Toggle Off
  • Read
    Toggle On
    Toggle Off

How to study your flashcards.

Right/Left arrow keys: Navigate between flashcards.right arrow keyleft arrow key

Up/Down arrow keys: Flip the card between the front and back.down keyup key

H key: Show hint (3rd side).h key

A key: Read text to speech.a key


Play button


Play button




Click to flip

60 Cards in this Set

  • Front
  • Back
Unproductive light gene rearrange can be replaced
1) using V & J gene segments not used in prev. rear.
2) Further rear can result in a fnx gene.
3) When 2nd joint made->DNA w/ 1st joint excised
Surrogate light chain contains
1) A 2 protiens
a) /\5 protien > constant region
b) VpreB > variable region
Pre-B-cell receptor
1) On cell surface > short time.
What does the expression of the pre-B-cell receptor generate
1) Positive signal allowing B cell =/ apoptosis > proceeds to next stage of maturation.
2) u, Iga, and IgB > synth. & retained in E.R
What happens when the RAG genes are turned back on?
(i) Light chain gene rearang. Proceeds
When fnxal light chain gene is formed?
1) Light chains are made & assemb. w/ u to form IgM.
What happens to the IgM
1) Iga & IgB join it > form mature B-cell receptor
2) Which moves to cell surface
The appearance of a fnxal b cell receptor leads to ?
1) Light chain gene rearrangement
Cell division initiated by signal through the preBcell receptor results?
1) In a clone of 30-70 small preB cell
2) All have same H gene
3) Potential to have diff L gene
1) Terminal deoxynucleotidyl transferase
a) Enzyme that adds N nucleotides at the jnx b/t rear. Gene segments
b) expressed in proB cells
When is TdT expressed?
1) When the H chain gene begin to rearrng
When is TdT not expressed?
1) In small pre-B cells when light chain gene begin to rearrange
What is the signifigance of TdT expression
1) N nucleotides are found in all VD and DJ joints of rearranged human H chain genes
2) But only in half the VJ joint of human L chains
when is synthesis of Iga & IgB polypeptides is turned on
1) pro-B cell stage & continues thru life of B cell
What is the period “ON” for Iga and IgB consitent with
1) With the polypeptides being necessary for the cell surface expression of immunoglobulin
2) & for the transduction of signals from pre-B cell and B-cell receptors to the interior of the cell
when is Iga and IgB genes turned off?
1) when An stimulated B cells diff into Ab-secreting plasma cells,
2) and their An receptors are no longer required,
a) Ig ceases to apprear on cell surface
1) Brutons tyrosine kinase
a) Another signal transduction molecule
b) Encoded by a gene on the X chrom
c) Essential for B cell maturation
Patients who lack a fnx Btk gene have?
1) Almost no circulating Ab b/c tgheir B cells are blocked at the pre-B cell stagge
2) Results in X-linked agammaglobulinemia
X-linked agammaglobulinemia?
1) Leads to recurrent infections
many B cell tumors carry?
1) Chromos translocations > join Ig genes to genes regulating cell growth.’
transformation of a normal cell into a tumor cell involves?
1) Series of mutations that release the cell from the normal restraints on its growth.
1) events that fuse part of a chromosome with another
a) in B cell tumorsthe Ig gene has often b/c joined to a gene involved in the control of cell growth
1) Genes that cause cancer when their fnx or expression is perturbed.
1) The viral gnes responsible for transformation
Two examples of protooncognes?
1) Burkitt’s lymphoma
2) BCL2
Burkitt's Lymphoma?
1) The MYC protooncogne
a) On chromosome 8
(i) translocation to either
(a) an Ig heavy-chain gene on chrom 14
(b) a k L chain gene on chrom 2
(c) a /\ L chain gne on chrom 22
1) Translocation found in b cell tumors
2) Normally prevent premature apoptosis
3) In tumors enable B cells to live longer
a) So they accumulate additional mustations that can lead to malignant transformation
B-1 Cells?
1) Subset of human Bcells
2) Arise in early embryonic development
a) From stem cell
3) Expresses CD5 (a gp) on cell surface
1) Gp on cell surface
2) Otherwise considered a marker for the human T cell lineage
Specific characteristics of B-1 Cells?
1) Little or no IgD on surface
2) Distinctive repertoire of antigen receptors
3) A.k.a CD5 B cells
B-1 vs. B-2

When first produced?
1) Fetus VS after birth
B-1 vs. B-2

N-regions in VDJ junctions?
1) Few VS extensive
B-1 vs. B-2

V-region repertoire?
1) Restricted VS diverse
B-1 vs. B-2

Primary location?
1) Peritoneal & pleural cavities VS 2nd lymph organs
B-1 vs. B-2

mode of renewal?
1) self renewing(IL-10) VS replaced from bone marrow
B-1 vs. B-2

spontaneous production of Ig?
1) High VS low
B-1 vs. B-2

isotypes secreted?
1) IgM>>IgG VS IgG> IgM
B-1 vs. B-2

response to carbohydrate antigen?
1) Yes VS Maybe
B-1 vs. B-2

response to protein antigen?
1) maybe VS Yes
B-1 vs. B-2

requirement for Tcell help?
1) No VS yes
B-1 vs. B-2

somatic hypermutation?
1) Low-none VS High
B-1 vs. B-2

Memory development?
1) Little or none VS yes
B-1 cell Tumor?
1) Chronic lymphocytic leukemia (CLL)
a) A bone marrow transplant from identical sibling is successful treatment
Self-reactive immature B cells are altered, eliminated or inactivated by?
1) Contact with self antigens
when is a B cell 1st described as an immature B cell?
1) when it first expresses IgM on its surface.
Becoming a mature B cell involves?
1) Emigration from the bone marrow
2) Use of alternative splicing of H chaim mRNA
a) To place IgD, as well a IgM on the cell surface.
1) Quality control mechanisms
a) Prevent maturation of B cells whose receptors bind to normal components of the human body
If B cells whose receptors bind to normal compoenets of the human body were allowed to mature?
1) They could make potentially disease-causing antibodies
kinds of self antigens?
1) Multivalent
2) Soluble
immature B cells that do not encounter a stimulatory self-An?
1) leave the bone marrow and enter the peripheral circulation, expressing both IgM & IgD on their surfaces
Multivalent self antigens?
1) Consists of gp,proteoglycans and glycolipids
2) Go through clonal selection >apoptosis
Soluble self anitigen?
1) Soluble proteins & gp
2) When surface IgM of an immature B cell binds to a soluble self-antigen, > Bcell inactive > Does Not Die
3) Becomes anergic
1) The state in which the B cel matures but does not respond to subsequent exposure to antigen
2) Migrate to periphery > where they express IgD > but remain anergic.
Receptor Editing?
1) A process of assessing the compatibility of receptors produced from successive gene rearrang.
Steps of receptor Editing?
1) Ligation of IgM on self-antigen
2) Arrest of B cell development
3) New receptor specifity is now expressed
a) If new receptor is still self- reactive > apotosis
b) If new receptor is no longer self reac> imm B cell migrates to periphery and matures
Clonal deletion?
1) Apoptosis in receptor editing
a) Occurs within the bone marrow or shortly after cell enters peripheral circulation
Ligation of IgM on self antigen?
1) When dev. B cell produces antigen receptors htat are strongly X linked by multivalent self antigen
2) B cell undergoes develop arrest.
Arrest of B development?
1) and cont. L chain rearran.: low cell surface IgM
2) Amount of IgM on the surface is reduced
a) RAG genes are not turned off.
new receptor specificity?
1) cont synthesis of RAG proteins allows the cell to cont L chain gene rear.
a) Leads to a new productive rear. & expression of a new L chain
(i) Which combines w/ the previous H chain to form new receptor
Primary lymphoid follicles?
1) Within 2nd lymphoid tiss, B cells congregate in organized structures