Regulation of IgE synthesis: from the membrane to the genes
D Vercelli, RS Geha - Springer seminars in immunopathology, 1993 - Springer
D Vercelli, RS Geha
Springer seminars in immunopathology, 1993•SpringerConclusions The data discussed above clearly indicate that the second signal (s) required
for IgE production can be delivered to B cells through different pathways. At the present time,
no unifying explanatory mechanism can reconcile all different observations. Not much is
known about signalling via MHC class II molecules and CD40; the role played by
hydrocortisone is not clear, and other molecules—in addition to CD40 and its ligand—might
be involved in non-cognate TB cell interactions. Signalling via CD21 is not sufficient for IgE …
for IgE production can be delivered to B cells through different pathways. At the present time,
no unifying explanatory mechanism can reconcile all different observations. Not much is
known about signalling via MHC class II molecules and CD40; the role played by
hydrocortisone is not clear, and other molecules—in addition to CD40 and its ligand—might
be involved in non-cognate TB cell interactions. Signalling via CD21 is not sufficient for IgE …
Conclusions
The data discussed above clearly indicate that the second signal(s) required for IgE production can be delivered to B cells through different pathways. At the present time, no unifying explanatory mechanism can reconcile all different observations. Not much is known about signalling via MHC class II molecules and CD40; the role played by hydrocortisone is not clear, and other molecules — in addition to CD40 and its ligand — might be involved in non-cognate T-B cell interactions. Signalling via CD21 is not sufficient for IgE induction, and EBV-induced proteins essential for IgE induction have not been identified. The observation that engagement of CD40 [32] and full expression of latent EBV proteins [21] share the ability to protect human B cells from programmed cell death (apoptosis) is certainly intriguing, but it is unclear whether this effect is in any way related to IgE induction. It seems plausible that the pathways mentioned above may share the ability to activate the switch recombination machinery in B cells in which the ɛ locus has been transcriptionally activated and made accessible by IL-4.
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