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Lange's med micro & immuno review book and BRS seem to be at odds with each other 😕
BRS- Dendritic cells of lymphoid tissue (I'm making assumption that they mean Follicular dendritic cells) are APCs and they express lots of MHC II.
Lange- Follicular dendritic cells are not APCs, and they don't produce MHC II. These cells basically catch immune complexes that come their way (via FC receptor). They then proceed to secrete chemokines to attract B cells to them, some sort of interaction occurs between B and FDC and ultimately B cells produce Ab thru affinity maturation b/c of this interaction.
Can someone also explain to me when somatic hypermutation occurs? I'm under the belief that it occurs during affinity maturation. Meaning somatic hypermutation is the 'what' when it comes to why the Ab now is able to form a better bond with its antigen, and that affinity maturation is the 'process'.
Thanks for any insight into my jumbled knowledge 😳
BRS- Dendritic cells of lymphoid tissue (I'm making assumption that they mean Follicular dendritic cells) are APCs and they express lots of MHC II.
Lange- Follicular dendritic cells are not APCs, and they don't produce MHC II. These cells basically catch immune complexes that come their way (via FC receptor). They then proceed to secrete chemokines to attract B cells to them, some sort of interaction occurs between B and FDC and ultimately B cells produce Ab thru affinity maturation b/c of this interaction.
Can someone also explain to me when somatic hypermutation occurs? I'm under the belief that it occurs during affinity maturation. Meaning somatic hypermutation is the 'what' when it comes to why the Ab now is able to form a better bond with its antigen, and that affinity maturation is the 'process'.
Thanks for any insight into my jumbled knowledge 😳