The Plasmablasts in Castleman Disease

To the EditorIn their article, Hsi et al1 described the broad spectrum of histopathologic features of Castleman disease (CD). We would like to report one additional peculiar case, rich in human herpesvirus-8 (HHV-8)-infected plasmablasts (PBs), which we recently observed in our institution. The normal PB is a short-lived, very mobile B cell that can secrete antibodies but retains characteristics of an activated and proliferating cell.2 The PB could be considered the precursor of the more mature noncycling plasma cell (PC). Both naive and memory B cells can differentiate into PBs when activated with or without T-cell help, with or without antigen.3 The maturation of PBs in PCs is characterized by the cessation of proliferation and loss of mobility. B-lymphocyte-induced maturation protein 1 (Blimp-1)/PR domain zinc finger protein (PRdm-1) is essential for PC maturation, repressing the expression of genes that m aintain B-cell identity (Pax5) and others that promote B-cell proliferation, such as Bcl6 and MYC.3 The PB is characterized by the following phenotype: CD19+, CD27++, CD38−/+, CD20−/+, cIgM+.4 The PBs are rare in normal lymph nodes; they probably live around the mantle zone of the germinal centers, and then they exit into peripheral blood and may survive for a short period only unless they are recruited into mucosa or bone marrow niches by chemokine receptor expression.5,6 In pathology, PBs characterize only rare human disorders, most notably the multicentric, HHV-8-related variant of CD. HHV-8, which uses host cell division as a means of propagation, targets the rapidly proliferating, antibody-secreting PBs.7 …