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BCL-6 Mutations in Pulmonary Lymphoproliferative Disorders: Demonstration of an Aberrant Immunological Reaction in HIV-Related Lymphoid Interstitial Pneumonia¹

Katsushi Kurosu^2,*, Michael D. Weiden, Yuichi Takiguchi^*, William N. Rom, Norio Yumoto, Jagirdar Jaishree, Koh Nakata, Yasunori Kasahara^*, Nobuhiro Tanabe^*, Koichiro Tatsumi^*, Atsuo Mikata and Takayuki Kuriyama^*

^* Department of Respirology (B2) and Department of Pathology, School of Medicine, Chiba University, Chiba, Japan; Division of Pulmonary and Critical Care Medicine and Bellevue Chest Service and Department of Pathology, New York University Medical Center, New York, NY 10016

We used a PCR and sequence procedure to analyze the Ig V_H gene and the mutations in the 5' regulatory regions of BCL-6 genes in pulmonary lymphoproliferative disorders (mucosa-associated lymphoid tissue (MALT) lymphoma, HIV-related, EBV-related, and virus-negative lymphocytic interstitial pneumonia (LIP)). Eight of 20 (40%) pulmonary MALT lymphoma and 10 of 20 LIP (5 of 5 (100%) HIV-related, 2 of 5 (40%) EBV-related, and 3 of 10 (30%) virus-negative LIP) cases showed BCL-6 gene mutations. Intraclonal heterogeneity of the BCL-6 mutations was observed only in pulmonary MALT lymphoma cases whose Ig V_H genes also showed intraclonal heterogeneity. Ongoing BCL-6 mutations might reflect re-entry into a germinal center pathway to further mutations. BCL-6 mutations in pulmonary MALT lymphoma and HIV-negative LIP showed some features (high transition to transversion ratio, standard polarity, and RGYW/WRCY bias) of Ig V_H gene hypermutation, leading to the view that pulmonary MALT lymphomas and HIV-negative LIP are under the influence of germinal center hypermutation mechanisms. Because BCL-6 mutations in HIV-related LIP cases did not demonstrate features of Ig V_H gene hypermutation, immunological reactions in HIV-related LIP are the result of a process different from that found in HIV-negative pulmonary lymphoproliferative disorders.