We show that cHL is less often associated with MF and primary cutaneous CD30-T-LPD than previously thought and that the coexpression of CD30 and CD15 in these TCLs may lead to a mistaken diagnosis of cHL.
As upregulation of CD99 led to a decrease in cHL diagnosis marker CD30 and CD15 and an increase in plasma-cell differentiation marker CD38 and the restoration of B-cell makers PAX5, CD79α and CD19, we suggest that downregulated CD99 leads to the prevention of plasma-cell differentiation in Hodgkin/Reed-Sternberg (H/RS) cells.
All ptHL expressed CD15, CD30 and LMP-1 of EBV; the B-cell markers BOB-1, Oct2, CD79a and CD20 were more commonly expressed in ptHL versus cHL (100%, 86%, 50% and 38% in ptHL compared to 6%, 14%, 10% and 33% in cHL, respectively); all ptHL expressed phosphoinositide 3-kinase (PI3K) versus 81% of cHL; 2/6 (33%) ptHL displayed gains at 9p24 that were similar to cHL (32%).
Immunohistochemical studies revealed that the large atypical cells were CD30 (+), CD15 (weakly +), CD20 (-), CD45 (-), Pax5 (weakly +), BOB.1 (-), and Oct2 (-), indicating the coexistence of SMZL with cHL.