BIO 343 Lecture Notes - Lecture 4: Fetus, Memory T Cell, Mutation Rate
Immunology Chapter 4: Adaptive Immunity (Test 2)
Hayden Casassa
• Diversification of antibodies after naïve B cells encounter Ag
o Antibodies can actually change Initial antibody to something else in response to infection
o Differentiate into plasma cells
• Once a B cell is activated by antigen it differentiates in plasma cells that begin to make secreted antibody
o How do they switch to making secreted antibody?
o An identical RNA is alternatively processed and spliced so that the mRNA contains either a hydrophobic
exon that anchors the Ab in the membrane or a hydrophilic exon that allows it to pass through the
membrane
▪ When we want it secreted, through alternative splicing hydrophilic membrane allows it to slip
through membrane to be free floating Ab
o Due to this we have multiple Poly adenylation sites depending on the type of antibody
• Why is the secondary immune response more powerful than the primary immune response?
o Memory B/T cells are more numerous than naïve lymphocytes that respond to primary response
o Memory cells are more quickly activated than naïve cells
o Memory T cells can patrol non-lymphoid tissue and thus respond faster to infection
o Memory B cells make better/ higher quality antibodies
▪ They have higher affinity binding sites due to somatic hypermutation
▪ They make different, more appropriate Ab isotypes (other than IgM)
o Memory cells are that much better that there is a mechanism that shuts down naïve cells to not even
respond at start of infection
• What is somatic hypermutation?
o DNA point mutations that occur in V regions of H and L chains in activated B cells after they have
already been rearranged.
o This only occurs once B cells have been stimulated by Ag and mutation rate is a million higher
o Some mutants generated have higher affinity and others have lower affinity
▪ This leads to affinity maturation
o Affinity maturation is continued clonal expansion of only mutated B cells that make Ab with higher
affinity than the original
▪ This is responsible for increase in Ab affinity observed during immune response
• Somatic hypermutation drives affinity maturation
• IgM is the first Ab made and secreted in a primary response
o Secreted as a pentamer--- bound by J chain and disulfide bonds
o Binds strongly to Ag because it has 10 Ag binding sites
▪ Avidity—overall strength of binding at multiple sites is high
o Lacks some effector functions common to certain other Abs
▪ No Fc receptors on phagocytes which can bind IgM
o Therefore, B cells need to be able to switch to making different Ab isotypes that have different effector
functions but are able to retain the same ag specificity
o Every B cell has the ability to express classes/subclasses of antibodies
o IgM is good but there are better antibodies
• Because of constant regions no Fc receptors on phagocytes which bind IgM
• B cells that make IgM must have ability to switch to other isotypes having the same
specificity
find more resources at oneclass.com
find more resources at oneclass.com
Document Summary
Igm is good but there are better antibodies: because of constant regions no fc receptors on phagocytes which bind igm, b cells that make igm must have ability to switch to other isotypes having the same specificity. Ige is the least prevalent: 5 classes of antibodies traits. Iga is best for mucosal surface transportation: maternal igg crosses the placenta. Igg readily escapes blood vessels and enters tissues. Igg characteristics: 4 subclasses most abundant ab in internal body fluids/lymph, good at neutralization/opsonization, only ab that can cross placenta to fetus and present in mother"s milk (due to ch region, high levels made during secondary immune response. Iga characteristics: monomeric iga is found in blood and dimeric in secretions, found in mother"s milk, tears, sweat, saliva, respiratory tracts. In total, more iga is made than any other isotype: example of impact of somatic hypermutation, affinity maturation, and isotype switching, remember, phagocytes lack receptors for igm.
