Monoclonal B-cell lymphocytosis: what hematologists should know—a narrative review

Introduction

Background

Monoclonal B-cell lymphocytosis (MBL) is a hematologic condition characterized by the presence of a small population of clonal B-cells in otherwise healthy individuals. Since its initial identification more than 20 years ago (1), MBL has attracted considerable interest because of its potential role as a precursor to chronic lymphocytic leukemia (CLL) and other B-cell lymphoproliferative disorders (B-LPDs) (2,3).

Rationale and knowledge gap

Despite significant advances in the detection and characterization of MBL since its initial proposal as a distinct clinical entity (4), uncertainties remain regarding its prognostic stratification and clinical outcomes. More importantly, in addition to its role as a precursor state of CLL, emerging evidence indicates that MBL is associated with immune dysfunction and increased risk of developing malignant neoplasms (2,5-8). This shift in understanding has transformed the clinical perspective of MBL, which was viewed, in the early 2000s, primarily as an “incidental immunophenotyping finding”, into that of a condition that, in some cases, warrants careful clinical evaluation, extensive laboratory investigation, and continuous follow-up.

Objective

This narrative review aims to provide hematologists with a comprehensive and practical overview of MBL, addressing its epidemiology, biological features, and natural history, as well as current approaches to diagnostic evaluation and clinical management. By synthesizing the available evidence, this article highlights key concepts that hematologists should understand to appropriately recognize, monitor, and counsel individuals with MBL. We present this article in accordance with the Narrative Review reporting checklist (available at https://aob.amegroups.com/article/view/10.21037/aob-2025-1-56/rc).

Methods

A literature search was conducted in PubMed covering the period from June 2000 to October 2025, using the search term “Monoclonal B-Cell Lymphocytosis” and limited to articles published in English. Case reports and conference abstracts were excluded, and no meta-analysis or statistical analysis was planned. As this narrative review was based exclusively on previously published literature, approval from a human research ethics committee was not required. Details of the search strategy are provided in Table 1.

Diagnosis

According to the 2025 World Health Organization (WHO) Classification of Haematolymphoid Tumours (5th edition), MBL is defined as an asymptomatic condition characterized by the presence of small numbers of clonal B-cells in the peripheral blood (specifically, fewer than 5.0×10⁹ cells/L), in the absence of lymphadenopathy, organomegaly, or features diagnostic of another B-LPDs (3). In current clinical practice, the diagnosis of MBL relies almost exclusively on multiparametric flow cytometry, which allows the identification of the monoclonal B-cell population through light-chain restriction—defined by an abnormal kappa-to-lambda ratio (>3:1 or <0.3:1)—together with characteristic immunophenotypic features, most commonly resembling CLL. Molecular methods for the detection of immunoglobulin gene rearrangements are rarely required for diagnosis and are generally reserved for selected cases in which flow cytometric assessment is inconclusive (3,5,9,10).

MBL is classified according to immunophenotype and the number of clonal B-cells into three categories:

• Low-count MBL (LC-MBL), also referred to as clonal B-cell expansion. It is defined by a clonal B-cell count less than 0.5×10⁹/L and typically exhibits the immunophenotype of classical CLL, namely, coexpression of CD5 and CD23 in clonal CD19⁺ B-cells, with weak or absent expression of CD20, CD79, and surface immunoglobulin. Clonal B-cells in LC-MBL usually express CD43, CD81, CD200, and ROR1 and are negative for CD10 and CD103. LC-MBL is characteristically detected in population screening studies (2,3,8,9,11-17).
• CLL-type MBL, also referred to as high-count MBL (HC-MBL). It is defined by the presence of abnormal B-cells with an immunophenotype similar to that observed in LC-MBL but with a clonal B-cell count equal to or greater than 0.5×10⁹ cells/L and less than 5.0×10⁹ cells/L. HC-MBL is typically identified during the clinical investigation of lymphocytosis (2,3,8,9,11-17).
• Non-CLL-type MBL. It is defined by the presence of abnormal B-cells with an immunophenotype distinct from that of CLL. These cases are typically negative for CD5 and CD10, and the majority exhibit immunophenotypic features consistent with marginal zone lymphoma or lymphoplasmacytic lymphoma (2,3,17-20). In this subtype, B-cell count thresholds have not been formally set up (3,20).

The numerical cutoffs used to define LC‑MBL, HCMBL, and CLL were traditionally established by expert consensus and prognostic observations, as the risk of progression to CLL increases with higher clonal B-cell counts (3-5,21-23). Objectively, the cut‑off of 0.5×10⁹/L separates LC‑MBL from HC‑MBL, and the upper limit of 5.0×10⁹/L corresponds to the classical B-lymphocytosis threshold used to diagnose CLL (3,12). Importantly, these criteria are based on the absolute count of clonal B-cells obtained by flow cytometry rather than the total lymphocyte count, which may introduce uncertainty in cases of reactive lymphocytosis and does not reliably reflect clonal burden (22,23).

Of note, following the 2022 divergence between the WHO and the International Consensus Classification (ICC) in the classification of hematolymphoid neoplasms (24), the ICC currently recognizes an “atypical” CLL-type MBL, characterized by CD5⁺ B-cells with bright CD20 expression and variable CD23 expression (11,16,25).

Epidemiology and natural history

The prevalence of MBL and its natural history vary according to age and population characteristics, with reported rates in the general population ranging from 0.14% to 17% (2,9,11,26-33). The male-to-female ratio approaches parity with near-equal distribution between sexes (1,15,17).

Overall, MBL is estimated to be at least 100 times more common than CLL (9). A clear age-related increase in MBL prevalence has been documented, with rates rising from approximately 2% among individuals aged 40–60 years to 5–10% in those older than 60 years (9,14). Some studies have reported substantially higher prevalence in very elderly individuals, including rates exceeding 20% and even 40% among those aged over 80–90 years (2,9,14,29,34-36). Notwithstanding, in the study by Soosapilla and colleagues, after an initial age-related increase, the prevalence of MBL reached a plateau at approximately 8–12% from the sixth decade onward, without a marked rise even among individuals aged 90–100 years (37). These discrepancies likely reflect differences in study design, population structure, and methodological sensitivity (4,8,37).

Many studies have shown that MBL and CLL exhibit strong familial clustering (26,38-41). Indeed, both in “sporadic CLL” families (defined as families with only one member diagnosed with CLL) and in “familial CLL” families (defined as families with two or more members diagnosed with CLL), the prevalence of MBL is higher than in the general population. Reported prevalence rates range from 4.1% to 24% in sporadic CLL families (42-44) and from 13.5% to 22% in familial CLL families (26,39-41).

The natural history of MBL has been elucidated in recent years, establishing it as an early stage within a biological continuum that may culminate in CLL. Yet the risk of progression differs among MBL subtypes (2,8,41,45-48). Significantly, the vast majority of MBL cases (approximately 90–95%) correspond to LC-MBL (2,5,36,49). This subtype typically remains stable over time, with a minimal risk of progression to HC-MBL or CLL (36,49-51). In contrast, HC-MBL carries an annual risk of progression to CLL estimated at 1–2% (2,5,13,21,35,52-54).

In recent years, several studies have challenged the classical notion according to which LC-MBL represents merely an age-related finding rather than a preleukemic condition. Notably, data from a prospective study that followed 139 individuals with LC-MBL and a family history of CLL estimated a progression rate to CLL of 1.1% per year, with a median follow-up of 5.8 years (41). These preliminary data are important because they suggest that individuals with LC-MBL who have a family history of CLL likely harbor an inherent genetic component that is not present in subjects with LC-MBL who do not belong to CLL families. In a subsequent study, Slager and colleagues showed that, compared with controls, individuals with HC-MBL had a 75-fold increased risk of progression to lymphoid malignancies (including CLL, diffuse large B-cell lymphoma, and mantle cell lymphoma), whereas individuals with LC-MBL had a 4.3-fold increased risk (36).

Of note, the absolute B-cell count consistently emerges as the most reliable predictor of progression, showing a strong association with the risk of subsequent clinical evolution (3,55-58). In this respect, recent genomic studies indicate that progression along the LC-MBL/HC-MBL/CLL continuum reflects dynamic clonal behavior of the abnormal B-cells rather than a purely quantitative expansion (5,59). Thus, two non-mutually exclusive models have been proposed. In the first, progression is associated with increasing genomic complexity, including cytogenetic lesions such as del(13q), trisomy 12, del(11q), del(17p), and lesions enriched in CLL such as NOTCH1, TP53, and SF3B1, consistent with stepwise molecular evolution (5,8,23,48). Alternatively, longitudinal analyses demonstrate that many LC-MBL clones remain genomically stable over time, suggesting that progression may result from the selection and expansion of a pre-existing subclone without major qualitative shifts in the mutational landscape (36,49). Together, these data support a model in which LC-MBL, HC-MBL, and CLL represent biologically connected phases of a single B-cell disorder rather than discrete entities (5,23,36).

Biology

In general, cytogenetic aberrations detected by fluorescence in situ hybridization (FISH) are largely similar between LC-MBL and HC-MBL, except for a lower frequency of trisomy 12 in LC-MBL (17,60,61). In HC-MBL, the most frequent chromosomal abnormalities are deletions at 13q14 and trisomy 12, which occur at frequencies comparable to those observed in CLL (13,62,63). Biallelic del(13q14) as a sole abnormality, as well as concurrent monoallelic and biallelic del(13q14), have been identified exclusively in HC-MBL cases, whereas t(11;14) occurs only in atypical MBL and del(7q31) only in non-CLL-type MBL (48,64,65). Interestingly, del(17p), which is classically associated with a worse prognosis in CLL, has also been identified in both LC-MBL and HC-MBL (49,60). More recent data obtained by single nucleotide polymorphism (SNP) array indicate that mosaic chromosomal alterations (mCAs)—acquired structural genetic changes involving large DNA segments, including gains, losses, or copy-neutral loss-of-heterozygosity events—are more common in HC-MBL than in LC-MBL, with frequencies comparable to those observed in CLL (66,67). Significantly, mCAs appear to represent early clonal events and are frequently detected among somatic alterations that precede the diagnosis of CLL, consistent with large-scale sequencing studies demonstrating that chromosomal lesions act as early initiators of CLL pathogenesis (68,69).

Immunoglobulin heavy-chain variable region (IGHV) mutation status, an important prognostic marker in CLL, also differs between MBL subtypes: approximately 70%–80% of HC-MBL cases harbor mutated IGHV, which correlates with a more indolent disease course in CLL. Importantly, an unmutated IGHV status may represent a risk factor for progression from MBL to CLL (22). The IGHV gene usage repertoire also differs between HC-MBL and LC-MBL, with HC-MBL showing an overrepresentation of genes such as IGHV3-23 and IGHV4-59/61 and an underrepresentation of IGHV1-69, which has been associated with aggressive CLL. In contrast, LC-MBL frequently expresses IGHV4-59 and IGHV4-61 genes, which are rarely observed in CLL, and shows an underrepresentation of IGHV1 family genes (17,28,35,60). Collectively, these findings indicate that HC-MBL and CLL are closely related at the immunogenetic level, whereas LC-MBL exhibits a more distinct IGHV repertoire.

Gene mutation analysis shows that alterations in genes such as NOTCH1, which are frequently associated with poor prognosis in CLL, occur less often and at lower variant allele frequencies across all MBL subtypes (60,70). Likewise, mutations in SF3B1 and BIRC3 are detected at particularly low frequencies in HC-MBL, mirroring their rarity in CLL at the time of diagnosis (16,35).

MicroRNAs (miRNAs) play a key role in the regulation of gene expression and have been implicated in the pathogenesis of several malignant neoplasms (71). The first indication of miRNAs deregulation in cancer emerged from the discovery that miR-15a and miR-16-1 are downregulated in patients with CLL, particularly in those harboring del(13q14) (72,73). In this context, accumulating evidence suggests that miRNAs abnormalities may also be present in MBL, where they may contribute to early B-cell clonal expansion (74). Indeed, several miRNAs that are aberrantly expressed in CLL appear to also play a role in MBL pathogenesis. Among these, miR-155 is consistently overexpressed in CLL compared with HC-MBL and normal controls, suggesting its potential utility as a marker of disease progression (75). In addition, miR-181a and miR-181b are downregulated in both CLL and MBL (76). Notably, low miR-181b expression has been associated with a worse prognosis in CLL (77).

Finally, analyses of telomere length (TL) also differ among CLL, HC-MBL, and LC-MBL (78,79). When TL was compared across CLL Binet stage A, HC-MBL, LC-MBL, and normal controls, all three study groups exhibited similar TL, which was shorter than that observed in controls. However, after adjustment for age, TL in LC-MBL was comparable to that of controls (78). The presence of short telomeres within the small abnormal B-cell clone of HC-MBL supports the hypothesis that telomere erosion may represent an early leukemogenic event in CLL (78).

Clinical implications

Malignant neoplasms

HC-MBL is consistently associated with an increased incidence of both hematologic and nonhematologic malignancies (2,5,6,19). Recognized as an established precursor of CLL and non-Hodgkin lymphomas (NHLs) (80-82), HC-MBL is also linked to a higher incidence of solid tumors, particularly those of the breast, lung, and gastrointestinal tract (6,19). Interestingly, LC-MBL, despite its negligible risk of progression to CLL, has also been associated with a higher incidence of cancers (2,36,51), including a 4.3-fold increased risk of lymphoid malignancies (36) and approximately twofold increased risk of melanoma, when compared with the general population (83). In consonance with these findings, Shen and colleagues reported that, among 53 patients diagnosed with MBL, nearly 32% developed at least one malignant neoplasm. Skin cancer was the most frequent and included cases of melanoma. Prostate, bladder, breast, papillary thyroid, pancreatic, and colon cancers were also diagnosed. Additionally, two patients with MBL were diagnosed with diffuse large B-cell lymphoma, consistent with Richter’s syndrome (80).

In this setting, individuals with MBL should adhere to age-appropriate cancer screening programs, including, but not limited to, mammography and colonoscopy (5,19,82,84). Ultimately, the diagnosis of MBL not only identifies a precursor state of CLL but also signals a broader predisposition to other malignant neoplasms (6,13,36,85), underscoring the need for continuous clinical monitoring and preventive strategies (2,17,86).

Immune impairment, infection risk and thrombosis risk

Individuals with LC-MBL and HC-MBL experience higher rates of hospitalization for severe infections than the general population, likely as a result of significant alterations in both the humoral and cellular arms of the immune system (2,7,8,87-92). In line with these findings, Shanafelt and colleagues demonstrated a higher cumulative incidence of hospitalization for MBL over an 8-year period, affecting 23% of individuals compared to 11% of controls. Indeed, severe complications such as pneumonia and bloodstream infections occurred in 9% of LC-MBL, whereas these were observed in only 2% of the control group (91). Additionally, unrecognized MBL may probably account for a substantial proportion of the increased coronavirus disease 2019 (COVID-19) hospitalization risk observed in individuals older than 65 years, including greater need for oxygen therapy, intensive care, and longer hospital stays (93).

Regarding humoral immunity, individuals with LC-MBL and HC-MBL exhibit a progressive decline in B-cell responsiveness to newly encountered antigens, with dysfunction becoming more pronounced from LC-MBL to HC-MBL (7). With respect to cellular immunity, expansions of T-cells have been reported across multiple subsets in LC-MBL, including CD4⁺ and CD8⁺ T-cells (2,42,59,94,95), as well as increased number of regulatory T-cells (2,96) and CD20⁺ T-cells (95). HC-MBL also exhibits early features of T-cell dysfunction, including expansions of regulatory T-cells (96), abnormalities in CD20⁺ T-cell subsets (95), reduced levels of circulating CD4⁺CD8⁺ double-positive T-cells (2,97), and the presence of exhausted CD8⁺ phenotypes (CD8⁺PD-1⁺, CD8⁺CD160⁺, CD8⁺CD244⁺) (54). Collectively, these immune abnormalities are likely to contribute to the higher incidence of infections observed in individuals with LC-MBL and HC-MBL (2,52). Consistently, population-based data demonstrate that future CLL and MBL subjects exhibit increased antimicrobial use beginning years before diagnosis, with higher exposure to macrolides, antivirals, and antifungals for up to two decades, suggesting long-standing infection susceptibility preceding overt disease (98).

In light of this scenario, preventive strategies such as vaccination are strongly recommended for individuals with MBL, although live-attenuated vaccines should be avoided (2,5,17,84). Yet, it is important to emphasize that post-infection and post-vaccination immune responses to influenza, pneumococcal, herpes zoster, and COVID-19 vaccines in individuals with HC-MBL are substantially impaired (99-101). In any event, given their intrinsically increased risk of life-threatening infections, any degree of protection conferred by vaccination remains important, even when immune responses are suboptimal (19,102,103).

An association between MBL and autoimmune disorders has been reported. Clonal B-cell populations consistent with MBL have been identified in up to 20% of cases of immune thrombocytopenic purpura (ITP) or autoimmune hemolytic anemia (AIHA) (5,8,104).

Finally, an increased risk of venous thromboembolism has been described in individuals with MBL, estimated to be approximately six-fold higher than in age- and sex-matched controls, with minimal differences observed between patients with MBL and those with CLL. However, it remains unclear whether this elevated risk is directly attributable to MBL itself (2,105).

Clinical evaluation, monitoring, management, and special scenarios

General management principles

The management of individuals with MBL begins with accurate diagnosis and classification. Indeed, distinguishing MBL from CLL is crucial, as this distinction directly influences follow-up strategies (4,5,8,9,16,17,19,82). In addition, emerging data suggest that the CLL International Prognostic Index (CLL-IPI), a prognostic tool originally developed to stratify patients with CLL, may also have potential prognostic value in this setting by identifying individuals with MBL who may be at higher risk of eventually requiring therapy (36,106). However, these observations derive from single-center studies and remain insufficiently validated. Consequently, these findings should be interpreted with caution and should not be directly extrapolated to routine clinical practice. In fact, at present, the CLL-IPI—as well as other biological markers—should not be used in subjects with MBL to estimate the individual risk of progression to CLL or to guide clinical management.

After an accurate diagnosis, subsequent management of MBL should be tailored according to the risk associated with each subtype (5,8,17,105). LC-MBL is widely regarded as a highly stable condition, with a low or negligible risk of progression to CLL (2,8,13,17,49). Consequently, LC-MBL does not require specialized hematologic follow-up outside of research settings (2,5,8,82). For individuals with LC-MBL, routine physical examination and complete blood count (CBC) are considered sufficient, and follow-up may be conducted by a general practitioner (9,82,84,107).

In contrast, individuals with HC-MBL, as a premalignant condition with a small but non-negligible risk of progression to CLL, require lifelong clinical monitoring by a hematologist (2,8,9,82). The initial assessment should include a complete medical history, physical examination, a comprehensive review of systems, and family history, given the possibility of familial CLL. This should be followed by annual evaluations that include physical examination, CBC, and immunophenotyping (5,8,9,17,82). Individuals should be advised to promptly report signs of disease progression, such as lymphadenopathy, fever, or weight loss (8,9,108).

Individuals with non-CLL-type MBL require a more extensive initial clinical and laboratory evaluation to exclude underlying NHL. Computed tomography (CT) scans of the chest, abdomen, and pelvis, bone marrow biopsy, and FISH analysis are usually recommended. Subsequent follow-up should be tailored to the subtype and risk associated with the identified clone, with monitoring intervals ranging from every 3 to 12 months. Shorter intervals (approximately 3–6 months) are suggested for higher-risk clones, including those with 17p deletion or indolent mantle cell lymphoma (when treatment is not required), whereas longer intervals (approximately 6–12 months) are considered appropriate for lower-risk or more indolent entities, such as marginal zone or follicular lymphomas (8,9,17,20,56,82,84) (Table 2).

In general, it is crucial to reassure individuals about the low risk of progression, particularly in LC-MBL, and to advise them to remain alert for the emergence of new clinical signs (13,50,82,107). Management should aim to balance active surveillance with minimizing unnecessary interventions (109,110). Preventive strategies, including vaccination and strict adherence to cancer screening protocols, are essential for all individuals with MBL, given the increased risk of severe infections and malignant neoplasm (6,17,19,51,87,91). An overview of MBL diagnosis and management is illustrated in Figure 1.

Figure 1 Management algorithm for MBL. B-LPD, B-cell lymphoproliferative disorder; CBC, complete blood count; CLL, chronic lymphocytic leukemia; CT, computed tomography; FISH, fluorescence in situ hybridization; MBL, monoclonal B-cell lymphocytosis; NHL, non-Hodgkin lymphoma.

The psychological impact of MBL diagnosis can be considerable, as the term “MBL” itself may cause confusion and anxiety. Individuals often become “patients-in-waiting,” living in a liminal state between health and disease (111). Although it is important to emphasize that the risk of progression to CLL requiring treatment is low, particularly in cases of LC-MBL, many individuals nonetheless experience distress, anxiety, and depression (112). These feelings are frequently exacerbated by prognostic uncertainty and the stigma associated with a condition linked to leukemia (21,111).

Special scenarios

The prevalence of both HC-MBL and LC-MBL among healthy blood donors has been reported to be approximately 7.1% (5,19,30). Despite this relatively frequent detection in donor populations, current evidence indicates that blood transfusion poses a negligible risk for the acquisition of MBL (8,19,113).

Documented cases of MBL or CLL B-cell clone transfer have been reported in the context of allogeneic hematopoietic stem cell transplantation (HSCT) (5,114-116). In this setting, the risk is particularly relevant when donors are family members, as a higher frequency of MBL has been observed among first-degree relatives of patients with CLL, both in familial cases (28,40) and in sporadic cases (9,42,44). These data support the recommendation of the American Society for Blood and Marrow Transplantation (ASBMT) that such individuals should be screened when considered as potential related HSCT donors in the context of CLL treatment (117,118).

A tissue-based form of MBL has been recognized (3,5,48,119). This entity is defined by small clonal B-cell populations identified in lymph nodes or extranodal tissues rather than in peripheral blood and is typically detected incidentally by flow cytometry studies (5,48,119). In tissue MBL, the affected lymph nodes are characteristically small (<1.5 cm), preserve normal architecture, and lack proliferation centers—features that help distinguish this entity from minimal CLL nodal involvement. Immunohistochemistry may identify the clonal population in some cases, although not consistently (10,48,119). A similar phenomenon has also been described in bone marrow, usually representing less than 20% of marrow cellularity (47). Overall, tissue MBL appears indolent, and peripheral blood evaluation frequently reveals HC-MBL (10,48,119).

Conclusions

MBL is an asymptomatic condition characterized by the presence of a small population of clonal B-cells in the peripheral blood, without clinical or laboratory evidence of overt B-LPDs. Advances in immunophenotyping and genetic analyses have defined three main subtypes—LC-MBL, HC-MBL (CLL-type MBL), and non-CLL-type MBL—each with distinct clinical implications. LC-MBL is typically stable and carries a minimal risk of progression, requiring only periodic clinical monitoring. In turn, HC-MBL is a premalignant state with an annual 1–2% risk of progression to CLL, warranting lifelong hematologic follow-up. Immune dysfunction and the increased risk of infections and cancers underscore the importance of vaccination, preventive care, and patient education. Management should remain individualized and clear communication may help reduce the psychological burden associated with the diagnosis.

Acknowledgments

None.

Footnote

Reporting Checklist: The authors have completed the Narrative Review reporting checklist. Available at https://aob.amegroups.com/article/view/10.21037/aob-2025-1-56/rc

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