Persistent polyclonal B‐cell lymphocytosis is an expansion of functional IgD<sup>+</sup>CD27<sup>+</sup> memory B cells

Himmelmann, Andreas; Gautschi, Oliver; Nawrath, Michael; Bolliger, Ursula; Fehr, Jörg; Stahel, Rolf A.

doi:10.1046/j.1365-2141.2001.02938.x

Cited by 40 publications

(27 citation statements)

References 17 publications

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“…Himmelman et al 34 reported that PPBL could be an accumulation of memory IgD þ CD27 þ B cells, which was confirmed by Loembe et al 35 who showed that these cells were not selected. These data suggest that chronic antigenic stimulation might play an important part in the pathogenesis of this disorder.…”

Section: Cytogenetics Analysismentioning

confidence: 83%

Intravascular bone marrow accumulation in persistent polyclonal lymphocytosis: a misleading feature for B-cell neoplasm

et al. 2004

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Section: Cytogenetics Analysismentioning

confidence: 83%

Intravascular bone marrow accumulation in persistent polyclonal lymphocytosis: a misleading feature for B-cell neoplasm

et al. 2004

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“…Although the bcl-2 gene was first identified at the chromosomal breakpoint of t(14;18) translocation-bearing human follicular Bcell lymphomas [33][34][35] and is found in this NHL type in about 70% to 80% of cases, it may be also found in diffuse lymphoma (about 20% of cases) and in nonmalignant conditions, such as persistent polyclonal B-cell lymphocytosis (PPBL), 7,36,37 which is an expansion of memory B cells without evidence of evolution to a frank lymphoma, as well as in HCV ϩ MCS, a situation which may evolve to malignant B-cell NHL types generally different from follicular lymphoma (lymphoplasmacytoid lymphoma/immuncytoma are the most common lymphomas reported in this subpopulation). 31,38 Despite this, in a large Italian survey, the type of idiopathic NHL more frequently associated with HCV infection was the follicular center type, 31,39 whereas different types were preferentially associated in other studies.…”

Section: Discussionmentioning

confidence: 99%

Effect of antiviral treatment in patients with chronic HCV infection and t(14;18) translocation

Giannelli

Moscarella

Giannini

et al. 2003

Blood

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Hepatitis C virus (HCV) may be associated with the mixed cryoglobulinemia syndrome and other B-cell lymphoproliferative disorders (LPDs). The t(14;18) translocation may play a pathogenetic role. Limited data are available regarding the effects of antiviral therapy on rearranged B-cell clones. We evaluated the effects of interferon and ribavirin on serum, B-lymphocyte HCV RNA, and t(14; 18) in 30 HCV ؉ , t(14;18) ؉ patients without either mixed cryoglobulinemia syndrome or other LPDs. The t(14;18) translocation was analyzed by both bcl-2/J H polymerase chain reaction and bcl-2/J H junction sequencing in peripheral blood mononuclear cells in all patients. Fifteen untreated patients with comparable characteristics served as controls. Throughout the study, the presence or absence of both t(14;18) and HCV RNA sequences were, in most cases, associated in the same cell samples. At the end of treatment, t(14;18) was no longer detected in 15 patients (50%) with complete or partial virologic response, whereas it was persistently detected in nonresponders (P < .05), as well as in 14 of 15 control patients. In 4 responder patients, t(14;18) and HCV RNA sequences were no longer detected in blood cells after treatment, but were again detected after viral relapse; the same B-cell clones were involved in the pretreatment and posttreatment periods. In conclusion, this study suggests that antiviral therapy may induce regression of t(14;18)-bearing Bcell clones in HCV ؉ patients and that this phenomenon may be related, at least in part, to the antiviral effect of therapy. This in turn suggests that antiviral treatment may help prevent or treat HCV-related

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“…The cells have a non-specific B cell immunophenotype without expression of CD5, CD23, CD43 or cyclin D1 but with expression of CD27. The cells are thought to be CD27+, IgD+, IgM+ memory cells with some evidence to suggest that there is a defect in the CD40-induced B-cell activation pathway, which may have a role in the pathogenesis [42,43]. There may be a pathogenetic role for EBV in some cases [44].…”

Section: Sessionmentioning

confidence: 99%

Early lesions in lymphoid neoplasia

et al. 2012

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The increasing use of immunophenotypic and molecular techniques on lymphoid tissue samples without obvious involvement by malignant lymphoma has resulted in the increased detection of “early” lymphoid proliferations, which show some, but not all the criteria necessary for a diagnosis of malignant lymphoma. In most instances, these are incidental findings in asymptomatic individuals, and their biological behaviour is uncertain. In order to better characterize these premalignant conditions and to establish diagnostic criteria, a joint workshop of the European Association for Haematopathology and the Society of Hematopathology was held in Uppsala, Sweden, in September 2010. The panel reviewed and discussed more than 130 submitted cases and reached consensus diagnoses. Cases representing the nodal equivalent of monoclonal B-cell lymphocytosis (MBL) were discussed, as well as the “in situ” counterparts of follicular lymphoma (FL) and mantle cell lymphoma (MCL), topics that also stimulated discussions concerning the best terminology for these lesions. The workshop also addressed the borderland between reactive hyperplasia, and clonal proliferations such as pediatric marginal zone lymphoma and pediatric FL, which may have very limited capacity for progression. Virus-driven lymphoproliferations in the grey zone between reactive lesions and manifest malignant lymphoma were covered. Finally, early manifestations of T-cell lymphoma, both nodal and extranodal, and their mimics were addressed. This workshop report summarizes the most important conclusions concerning diagnostic features, as well as proposals for terminology and classification of early lymphoproliferations and tries to give some practical guidelines for diagnosis and reporting.

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Persistent polyclonal B‐cell lymphocytosis is an expansion of functional IgD⁺CD27⁺ memory B cells

Cited by 40 publications

References 17 publications

Intravascular bone marrow accumulation in persistent polyclonal lymphocytosis: a misleading feature for B-cell neoplasm

Intravascular bone marrow accumulation in persistent polyclonal lymphocytosis: a misleading feature for B-cell neoplasm

Effect of antiviral treatment in patients with chronic HCV infection and t(14;18) translocation

Early lesions in lymphoid neoplasia

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Persistent polyclonal B‐cell lymphocytosis is an expansion of functional IgD+CD27+ memory B cells

Cited by 40 publications

References 17 publications

Intravascular bone marrow accumulation in persistent polyclonal lymphocytosis: a misleading feature for B-cell neoplasm

Intravascular bone marrow accumulation in persistent polyclonal lymphocytosis: a misleading feature for B-cell neoplasm

Effect of antiviral treatment in patients with chronic HCV infection and t(14;18) translocation

Early lesions in lymphoid neoplasia

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Persistent polyclonal B‐cell lymphocytosis is an expansion of functional IgD⁺CD27⁺ memory B cells