Expression of follicular helper T cell markers in nodal peripheral T cell lymphomas: a tissue microarray analysis of 162 cases

Abstract

AimsTo evaluate the role of the follicular helper T (TFH) cell markers, CD10, BCL6, programmed death-1 (PD-1) and CXCL13, in the differential diagnosis of nodal peripheral T cell lymphomas (PTCLs) and to determine whether PTCL subtypes other than angioimmunoblastic T cell lymphoma (AITL) express TFH cell markers.Methods162 nodal PTCL specimens and 53 other lymphoid pathology specimens were collected. Immunohistochemistry for CD10, BCL6, PD-1 and CXCL13 was performed on tissue microarray sections. Morphological feature analysis and double labelling assay were also performed.ResultsFor AITL cases, the rate of CD10, BCL6, PD-1 and CXCL13 expression was 75.0% (36/48), 66.7% (32/48), 93.8% (45/48) and 97.9% (47/48), respectively. Expression of CD10, PD-1 and CXCL13 in the AITL group was significantly higher than in other nodal PTCLs and the control group (p<0.05). The rate of coexpression of three or four (≥3) markers was 83.3% for AITL cases, which was significantly higher than that for any of the non-AITL cases (0–4.9%; p<0.05). The rate of coexpression of PD-1 and CXCL13 (91.7%, 44/48) was significantly higher than that of CD10 and BCL6 (56.3%, 27/48) (p=0.000) in the AITL group. Seventeen cases of PTCL not otherwise specified (PTCL, NOS) expressed CXCL13, including both cases of the follicular variant of PTCL, NOS (FVPTCL, NOS), three of the four cases of the lymphoepithelioid variant of PTCL, NOS (LVPTCL, NOS), and the remaining 12 cases which displayed one or more features of AITL.ConclusionsThe combined detection of CD10, BCL6, PD-1 and CXCL13 has high specificity and sensitivity for the differential diagnosis of AITL. PD-1 and CXCL13 are more sensitive, superior diagnostic markers for AITL than CD10 and BCL6. Currently, TFH cell markers are the only available markers that show high specificity for AITL. LVPTCL, NOS and/or FVPTCL, NOS may also arise from TFH cells and fall within the spectrum of AITL.