Stimulation of angiogenesis

Endothelial cell activation

Stimulation of antigen presentation

Stimulation of IL-6 production

The GC is a site of intense immune activity, so the normal mechanisms of cell death can’t work there.

A failure to switch off AID in unselected B cells allows them to accumulate excess mutations, which contribute to cancer.

GC are sites of intense cellular proliferation

Targeting AID activity is imprecise which can result in mutations in genes that control the cell cycle

SHM and CSR are untargeted events, occurring at random within immunoglobulin loci

SHM and CSR require different activities of activation induced cytidine deaminase (AID)

Activation induced cytidine deaminase (AID) is required for both SHM and CSR

IgM antibodies are always higher affinity than IgG antibodies recognising the same antigen because each secreted IgM antibody is a pentamer

That they were concentrated in the complementarity determining regions (CDRs) of the V segments

That they were concentrated in the framework regions (FWR) of the V gene

That they were evenly distributed along the V segment

That they reflected the distribution as first introduced by the enzyme AID

Somatic mutations are never found in the V genes of IgM B cells because they are already high avidity

Secreted IgM can enter any tissue

IgG is used for long-term immunity because it has a lesser energy cost to synthesise and secrete

Secreted IgM can bind to antigens with an affinity lower than IgG

alters the constant region of the heavy chain

switches from the membrane to secreted form of immunoglobulin

alters the variable region

selects for high affinity antigen B cell receptors during an immune response

B and T cells alter migration within their respective zones, increasing the probability of encountering each other

B and T cells arrest on dendritic cells as they encounter antigen, increasing the probability of encountering each other

Binding to the same antigen brings them into physical contact

T cells gain expression of CXCR5 and enter B cell follicles to find their cognate B cells

pre-existed prior to the appearance of the antigen

is activated, which triggers the B-cell to undergo proliferation

changes to fit the antigen

undergoes class-switch recombination in response to the antigen binding

B cells gain a single specificity after encountering an antigen

Every B cell has a unique specificity

Every antigen induces a response from one B cell

Each B cell clone targets a different part of the antigen

Many mutations in the gene that codes for the spike protein allowed the virus to more effectively infect lung cells by interacting with both the ACE2 receptor & the TMPRSS2 protease

T cell-based immunity gained against other COVID-19 variants did not provide any protection against the Omicron variant

T and B cell-based immunity gained against other COVID-19 variants did not provide any protection against the Omicron variant

Many mutations in the gene that codes for the spike protein allowed the virus to more effectively infect lung cells by interacting with the ACE2 receptor but NOT the TMPRSS2 protease