Comparison of A and B-type lamin expression in reactive lymph nodes and nodular sclerosing Hodgkin's disease

• Published in: Histopathology Vol. 31; no. 4; pp. 304 - 312
• Main Authors: JANSEN, M.P.H.M., MACHIELS, B.M., HOPMAN, A.H.N., BROERS, J.L.V., BOT, F.J., ARENDS, J.W., RAMAEKERS, F.C.S., SCHOUTEN, H.C.
• Format: Journal Article
• Language: English
• Published: Oxford, UK Blackwell Science Ltd 01-10-1997; Blackwell
• Subjects: Biological and medical sciences; Fluorescent Antibody Technique, Indirect; Hematologic and hematopoietic diseases; Hodgkin Disease - immunology; Hodgkin's disease; Humans; immunocytochemistry; Immunophenotyping; Ki-1 Antigen - analysis; Ki-67 Antigen - analysis; Lamin Type A; Lamin Type B; Lamins; Leukemias. Malignant lymphomas. Malignant reticulosis. Myelofibrosis; Lymph Nodes - immunology; Medical sciences; nodular sclerosing Hodgkin's disease; nuclear lamins; Nuclear Proteins - metabolism; reactive lymph node; Reed-Sternberg cells; Reed-Sternberg Cells - metabolism; Human; Immunohistochemistry; Cell proliferation; Lymph node; Benign lymphoid hyperplasia; Hodgkin disease; Malignant hemopathy; Nodular sclerosing Hodgkin's disease; Lymphoma; Intermediate filament; Proteins; Pathology; Lymphoproliferative syndrome; Immunofluorescence; Comparative study
• ISSN: 0309-0167; 1365-2559
• DOI: 10.1046/j.1365-2559.1997.2820881.x

Aims:
In order to clarify the differentiation and proliferation status of the Reed–Sternberg and Hodgkin cells we studied A and B‐type lamin expression with specific monoclonal antibodies in nodular sclerosing Hodgkin's disease. Its normal counterpart, the reactive lymph node, was also examined for lamin subtype expression.
Methods and results:
The CD20 positive centrocytes and centroblasts of the follicle centre in the reactive lymph nodes expressed lamin B1, but were not or only very weakly positive for lamin B2 or A‐type lamin antibodies. Mantle zone lymphocytes displayed lamins B1 and B2, but were negative for A‐type lamins. Furthermore, CD3‐ and CD20‐positive lymphocytes in the medulla and paracortex lacked A‐type lamins, but were positive for both B‐type lamins. Finally, the proliferation marker Ki67 was mainly detected in the centroblasts, but also in a fraction of the A‐type lamin negative cells in the paracortex and medulla. In Hodgkin's disease, all cells expressed lamins B1 and B2, whereas A‐type lamins were primarily observed in CD30‐positive Reed–Sternberg and Hodgkin cells. About 20% of the Reed–Sternberg and Hodgkin cells expressed Ki67, with co‐expression of lamin A in most of these cells.
Conclusions:
Ki67 and A‐type lamin staining were in general mutually exclusive in lymph nodes, indicating that A‐type lamin positive cells are not proliferative. This suggests also that the A‐type lamin expression in Reed–Sternberg and Hodgkin cells is correlated with a relatively mature phenotype of these malignant cells. However, some of these differentiated malignant cells still have a capacity to proliferate as indicated by Ki67 positivity. Our observation that lamin B2 expression in the follicle centre cells of the reactive lymph node is low or absent indicates that this lamin subtype is not always expressed in nucleated cells, which is in clear contrast to the results obtained in previous studies in other diseases and in normal tissues. Absence of lamin B2 expression may be associated with the follicle centre stage of B‐cells.