Phenotypic analysis by flow cytometry of surface immunoglobulin light chains and B and T cell antigens in lymph nodes involved with non-Hodgkin's lymphoma
“…As in the report of Glassman et al (12), a variety of benign lymph node histologies could not be categorized by FCI. In contrast to the report of Liendo et al (13), there were no cases in which there was a monoclonal B‐cell population by FCI and benign lymph node histology. There was 100% concordance between the cases negative by FCI and benign by histology (category A).…”
“…As in the report of Glassman et al (12), a variety of benign lymph node histologies could not be categorized by FCI. In contrast to the report of Liendo et al (13), there were no cases in which there was a monoclonal B‐cell population by FCI and benign lymph node histology. There was 100% concordance between the cases negative by FCI and benign by histology (category A).…”
“…Normally, either kappa or lambda light chains are expressed, and the great majority of B cell lymphomas show skewing of the normal kappa/lambda ratio or an otherwise obvious light chain-restricted population. [1][2][3][4][5][6][7][8] The absence of SIg light chain expression has been observed in about one third of B-cell non-Hodgkin lymphomas using immunohistochemical stain on frozen tissues; about 30% to 40% of these SIg-negative cases were diffuse large B-cell lymphoma and follicular lymphoma. 1 Subsequent studies using the relatively more sensitive FCI technique demonstrated that lack of SIg light chain expression in B-cell non-Hodgkin lymphoma was a rare phenomenon.…”
Section: Discussionmentioning
confidence: 99%
“…1 Subsequent studies using the relatively more sensitive FCI technique demonstrated that lack of SIg light chain expression in B-cell non-Hodgkin lymphoma was a rare phenomenon. [2][3][4][5][6][7][8] In the earliest study using FCI, Liendo et al 2 reported that 4 of 47 cases of B-cell non-Hodgkin lymphoma lacked SIg light chains, but the criteria for SIg negativity was not described. In a subsequent study by de Martini et al, 3 the absence of SIg was defined as B cells expressing less than 15% kappa and less than 10% lambda immunoglobulin light chains.…”
We determined the prevalence and significance of finding B cells without surface immunoglobulin (SIg) light chain expression. The flow cytometry database at Johns Hopkins Medical Institutions was searched for cases in which immunoglobulin light chain staining was performed to rule out a B-cell malignant neoplasm between January 1994 and February 2000. We excluded plasma cell dyscrasias, precursor B-cell acute lymphoblastic leukemia/lymphomas, and hematogones. Cases with more than 25% of B cells lacking SIg light chain expression were retrieved. Polymerase chain reaction assays for immunoglobulin heavy chain gene rearrangements were performed in SIg-negative cases with available tissue blocks. We identified 36 cases; all represented lymphoma. Their diagnoses included diffuse large B-cell lymphoma (20), HIV-related lymphoma (5), follicular lymphoma (5), Burkitt lymphoma (2), monomorphic posttransplant lymphoproliferative disorder (1), chronic lymphocytic leukemia/small lymphocytic lymphoma (1), marginal zone B-cell lymphoma (1), and low grade B-cell lymphoma (1). Of the 17 SIg-negative cases with amplifiable DNAs, 12 (71%) showed a clonal immunoglobulin heavy chain gene rearrangement. SIg-negative B-cell lymphomas are rare. Complete absence of SIg light chain expression in a mature B cell proliferation can be used as a surrogate marker to help diagnose peripheral B-cell lymphoma.
“…Tumor cells were isolated with B cell negative isolation kit from Miltenyi Biotech, Inc., sorted out with anti-Lambda or anti-Kappa antibodies and labeled as tumor Ig light chain (C) B cells. 10,11 The normal B cells were sorted as the tumor Ig light chain (¡) B cells at same time. Monocytes were isolated with CD14 and MHC class II antibody.…”
Section: Normal Donors and Patient Samplesmentioning
The B-cell receptor (BCR) expressed by a clonal B cell tumor is a tumor specific antigen (idiotype). However, the T-cell epitopes within human BCRs which stimulate protective immunity still lack detailed characterization. In this study, we identified 17 BCR peptide-specific CD4 C T-cell epitopes derived from BCR heavy and light chain variable region sequences. Detailed analysis revealed these CD4 C T-cell epitopes stimulated normal donors' and patients' Th1 CD4C T cells to directly recognize the autologous tumors by secretion of IFNg, indicating the epitopes are processed and presented by tumor cells. One BCR peptide-specific CD4 C T cell line was also cytotoxic and lysed autologous tumor cells through the perforin pathway. Sequence analysis of the epitopes revealed that 10 were shared by multiple primary patients' tumors, and 16 had the capacity to bind to more than one HLA DRB1 allele. T cells stimulated by shared epitopes recognized primary tumors expressing the same sequences on multiple HLA DRB1 alleles. In conclusion, we identified 17 BCR-derived CD4C T-cell epitopes with promiscuous HLA DRB1 binding affinity that are shared by up to 36% of patients, suggesting a strategy to overcome the requirement for individual preparation of therapeutic agents targeting idiotype.
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