In T-cell dependent responses, some activated B cells produce other antibodies besides IgM in this process
Isotype (class) switching
Expressed on the surface of activated T cells and homologous to TNF; required for T-dependent B cell activation
CD40L
Mutations in ATM
Ataxia-telangiectasia
These antibodies are made without class switching
IgM and IgD
Activated B cells produce antibodies that bind to antigens with increasing affinity in this process
Affinity maturation
Mutations in CD40L result in this disease
X-linked hyper-IgM syndrome
Artemis, DNA ligase IV, Cernunnos, Nijmegen breakage syndrome
Radio-sensitive SCIDs
Th2-type cytokines that drive isotype switching from IgM to IgE
IL-4 and IL-13
An example of a stimulus that can activate B cells without T cell assistance
Polysaccharides
True or False: T-cell mediated dendritic cell and macrophage activation involves the interaction of CD40L on activated T cells and CD40 on DCs and macrophages
True
SLAM-associated protein (SAP) signaling stabilizes expression of transcription regulators required for Tfh cell development; mutations in SAP lead to this
X-linked lymphoproliferative syndrome
Key enzyme required for isotype switching and somatic hypermutation
AID
T-independent responses are rapid but simple, consisting mostly of these
Low-affinity IgM antibodies
Activated B cells outside of the follicle induce activated T cells to differentiate into Tfh cells, which express high levels of CXCR5. These are drawn into lymphoid follicles by this ligand
CXCL13
While usually not monogenic, mutations in TACI, BAFF, ICOS, CD19, LRBA can cause this
AID removes an amino group from cytosines in ssDNA templates, converting cytosine to this
deaminated uracil (C-->U)
B cell activation is facilitated by this coreceptor on B cells, which recognizes complement fragments that are covalently attached to the antigen or are part of ICs containing the antigen
CR2
The defining cytokine produced by Tfh cells; required for germinal center development and contributes to the generation of plasma cells
IL-21
This resembles X-linked agammaglobulinemia more than HIGM in that patients are susceptible to bacterial infections only
AID deficiency (also accept UNG deficiency in ddx)
UNG removes U residues to create "abasic" sites for this endonuclease to then create nicks to allow for double-stranded DNA breaks
APE1