CD86 and immunoglobulin G4-related sclerosing disease: In IgG4-RD, the CD19+CD24−CD38hi plasmablasts/plasma cell subset highly expressed the CD86 molecule, suggesting the intriguing possibility that this cell subset may maintain some features of earlier B cells and, by virtue of persistent expression of CD86, chronically stimulate T-cell help and in so doing enhance the likelihood of class-switching recombination to the downstream heavy-chain isotypes IgG4 and IgE.