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Memory B Cell Markers

Lucas Baumard, PhD | 4th August 2025

Memory B (MB) cells have an important role in protecting against repeated infections and, along with long-lived plasma cells, are a key part of the humoral immune system. The continued sensitivity of MB cells to a specific antigen enables them to quickly differentiate into antibody-secreting cells upon antigen re-exposure in order to mount a fast and powerful immune response.1

Both MB cells and plasma cells develop from naïve B cells that have been exposed to a specific antigen. Plasma cells constantly secrete antibodies against the specific antigen but do not respond well to re-infection due to low expression of membrane-bound immunoglobulin for antigen detection.2 This contrasts to MB cells, which, through somatic hypermutation, are able to generate a broad repertoire of antibodies to previously encountered infectious agents. After reinfection, pre-existing antigen-reactive clones in the MB cell compartment are positively selected and differentiate into plasma cells. MB cells therefore do not represent a terminally differentiated population.

Explore allSee Memory B Cell Marker Antibodies

Table of Contents

Memory B Cell Developmental Markers

Memory B cells are one of a number of developmental stages of B cells and plasma cells. A summary of these stages and some markers that are commonly used to identify each stage are depicted in Figure 1.

H+E staining of the B cell zone in the human spleen

Figure 1: Markers of B cell developmental stages

B cells can be divided into two populations: B2 or B1. B2 cells are the major population found in the spleen, lymph nodes and peripheral blood and derive from germinal center (GC) Figure 1) interactions to produce high-affinity antibodies. B1 B cells are found in the peritoneum and pleural cavities and produce IgM antibodies in response to self and common bacterial antigens 3. Originally it was thought that MB cells could only derive from B2 cells, but recent studies have shown that some B1 B cells can differentiate into cells with memory-like potential in response to antigen into MB cells 4 5. However, this process is not well understood and on this page we will focus on B2 cell development into MB cells.

H+E staining of the B cell zone in the human spleen

Figure 2: Hematoxilyn-eosin staining of human spleen at 100 μm (A) and 50 μm (B) to reveal the structure of a B cell zone. Red pulp (RP); periarteriolar lymphocyte sheath (P); germinal center (GC); mantle region (M); marginal zone (MZ). Edited and reproduced under Creative Commons 4.0 CC-BY from 7.

B Cell Differentiation Pathways

B cells can differentiate into MB cells via a GC-dependent or GC-independent pathway, but both are reliant on T cell interactions in and around GCs. Neither of these pathways, nor the expression of specific markers across B cell precursors, are well studied or understood.

Naïve B cells can encounter antigens in secondary lymphoid tissues which bind to B cell receptors (BCR). These now activated cells upregulate the chemoattractant receptors CCR7 and EB12 which drive them towards the B cell follicle T cell zone with EB12 subsequently downregulated in GC B cells.8,9 In combination with co-stimulation from helper T cells (themselves activated by antigen presenting dendritic cells), B cells proliferate and these cells then choose one of the aforementioned pathways. T cell help is vital to the survival of activated B cells – without it, BCR-activated B cells undergo apoptosis.10

Germinal Center-Dependent and -Independent Pathways

Activated B cells can differentiate by two pathways:

  • GC-independent pathway: Without entering the GC, they differentiate into short-lived plasma cells or GC-independent MB cells (Figure 3 ‘Phase 1’).11
  • GC-dependent pathway: They enter the light zone of newly forming GCs to become long-lived plasma cells or (GC-dependent) MB cells (Figure 3 ‘Phase 2’).12,13
    • .

Whether a B cell is destined for an MB or plasma cell fate during Phase 1 (Figure 3) seems to be partially determined by T follicular helper cell signaling14 and the affinity of BCRs, with high affinity antigen-BCR interactions leading to a plasma cell fate.15

GC-dependent and GC-independent MB populations, as well as GC B cells, have been shown to arise from CD38+GL7+ precursors.16 This same study showed that strong CD40 signals from helper T cells can push CD38+GL7+ B cells to become MB cells via the GC-independent pathway. Similarly, through inhibition of GC formation, weak CD40 signals might push cells into becoming GC B cells and swIg+ (switched Immunoglobulin) MB cells.16 Immunoglobulin switching is the process where naïve B cells proliferate and switch Ig isotypes from IgM and IgD to IgA, IgG or IgE in order to improve antibody responses.17 However, this model is complicated by the existence of IgM+ MB cells,2 and this likely represents a population of GC-independent CD73- MB cells.16

Diagram of B cell maturation in lymphoid tissue

Figure 3: Memory B cell maturation in lymphoid tissue. Naïve B cells encounter antigen presented by follicular dendritic cells (FDCs) and travel to the T-B border driving differentiation (Phase 1). GC B cells form GCs, undergo proliferation and somatic hypermutation in GC dark zones, and exit into the light zone where they meet FDCs and T follicular helper cells to drive further differentiation (Phase 2).

B cells destined to enter and form GCs and to become GC-dependent MB cells (Phase 2 route) highly express the G-protein-coupled receptor sphingosine 1-phosphate receptor 2 (S1P2). This receptor for S1P is important in regulating cell growth and viability in growing GCs and inhibiting chemoattractant signals, keeping cells within GCs.19

Within GCs, B cells undergo affinity selection for antigen before being selected for an MB or plasma cell fate. Through this process, B cells engage antigen through their BCR, with higher affinity interactions leading to better internalization of the antigen for presentation to TFH cells.20 GC B cells have 100-fold higher capacity to signal through BCR and internalize antigen than naïve B cells.21 B cells in GC light zones are identifiable by CCR6 expression and these cells have been shown to become memory B cells.22,23

Overall the process of B cell maturation into memory B cells is complex and not well understood, with differences between murine models and human biology making their study more complicated.

Markers of Differentiated Memory B Cells

CD27

CD27 is a transmembrane glycoprotein of the TNF-R superfamily24 and the most canonically described memory B cell marker in humans. CD27 is upregulated during germinal center maturation of B cells.25 CD27 is also expressed on GC B cells, plasma cells (highly), NK cells, CD4+ and CD8+ T cells.26,27 Expression of CD27 in MB cells may differ between organs, with MB cells in the spleen shown to express lower levels than in the peripheral blood.28 CD70 is the only ligand for CD27 and their interaction has been shown to increase Ig production.29 This interaction has been shown to be crucial for B and T activation with defective receptor:ligand signaling in humans leading to reduced memory B cells and increased susceptibility to viral infection.30

There does exist a (small) CD27-IgD- MB cell population that share common characteristics and genealogy with their CD27+ counterparts, differing mainly by the expression of the CDR-H3 repertoire at the variable regions of the BCR.31

IHC - Anti-CD27 Antibody [LPFS2/4177] (A250621)

Figure 4: IHC of human tonsil stained with Anti-CD27 Antibody [LPFS2/4177] (A250621).

Flow cytometry - Recombinant Anti-CD27 Antibody [DM57] - BSA and Azide free (A318640)

Figure 5: Flow cytometry analysis of Expi293 cells stained with irrelevant protein (A) or human CD27 (B) stained with Recombinant Anti-CD27 Antibody [DM57] - BSA and Azide free (A318640).

Other MB Cell Markers

CD80 and programmed death ligand 2 (PD-L2) are both members of the B7 family of immune-regulatory ligands and are expressed at higher levels in murine memory B cells compared to naïve B cells.32 These markers are expressed in a heterogeneous fashion and define subsets of MB cells (see Memory B Cell Subsets).

CD80 is upregulated on activated murine and human B cells 33 and is also expressed on antigen-presenting cells like macrophages, monocytes and dendritic cells as well as activated T cells.33,34 CD4+ T cell co-stimulation has been shown to be dependent on CD80 expression on (IgM, swIg) MB cells.35

PD-L2 is a ligand of programmed cell death protein 1 (PD-1) and is also expressed on B-1 cells, macrophages and dendritic cells and overexpressed on human cancer cells.36,37 PD-L2 exerts immunosuppressive effects on T cells,38 but its ability to affect MB cell activity is not fully understood.

Antigen-specific (murine) MB cells have been shown to have increased expression of CCR6 and increased chemotactic responses to its ligand CCL20.39 CCR6 is not essential for MB cell expansion and maintenance, but is essential for recall responses to antigen.39 CCR6 is also expressed on Th1, Treg and dendritic cells.40

IF - Anti-PD-L2 Antibody [PDL2/2676] (A250390)

Figure 6: IF of Jurkat cells stained with Anti-PD-L2 Antibody [PDL2/2676] (A250390).

Flow cytometry - Anti-CD80 Antibody [MEM-233] (PE) (A85961)

Figure 7: Flow cytometry analysis of Expi293 cells stained with irrelevant protein (A) or human CD27 (B) stained with Anti-CD80 Antibody [MEM-233] (PE) (A85961).

Memory B Cell Subsets

There are numerous MB cell subsets based upon their expression of various surface markers such as CD80, PDL2 and CD73 (mouse) / CD27 (human) (see Murine vs Human Memory B Cell Markers), yet most are poorly explored and understood. These subsets may reflect differentiation potential in MB cells after re-activation of antigen.

The expression of CD80 and PDL2 can define MB cell subsets. Upon re-exposure to antigen, CD80+PDL2+ MB cells differentiate into plasma cells and have a large number of mutations, whereas CD80-PDL2- MB cells differentiate into GC B cells and have few mutations in the immunoglobulin variable region.33,41 MB cell populations positive for only one of these markers have intermediate mutation counts.42 All subsets express IgM/ swIg, however the double-negative population are predominantly IgM+ whereas the single- and double-positive cells express more IgG and swIg.32,43 This double-positive (CD80+PDL2+) population is associated more with memory-like features compared with the more naïve-like double negative (Figure 8), with the former differentiating more quickly into antibody-forming cells compared to GC B cells.43

Memory B subsets defined by CD80, PD-L2, CD73

Figure 8: Memory B cell subsets, defined by the markers CD80, PD-L2 and CD73. Adapted from Bergmann, B. et al. Memory B Cells in Mouse Models. Scand. J. Immunol. 78, 149–156 (2013).

CD45RB and CD69 expression can be used to divide splenic CD27+ MB cell populations. CD45RB is found on most peripheral blood MB cells and is a glycoepitope of CD45 and CD69 is a type II C-lectin receptor classically seen as a marker of activation.44,45 In a study of human splenic samples, ~20% of CD27+ B cells were CD45RB-CD69- whereas ~60% were CD45RB+ and/or CD69+. This expression could change in other sites, for instance CD69 was almost completely absent in peripheral blood and bone marrow.46 The authors postulated that CD45RB+CD69+ cells were tissue or gut-resident MB cells.

cells.40

IF - Recombinant Anti-CD45RB Antibody [PTPRC/2877R] (A249819)

Figure 9: IF of Raji cells stained with Recombinant Anti-CD45RB Antibody [PTPRC/2877R] (A249819) (green), counterstained with phalloidin (red).

Flow cytometry - Anti-CD69 Antibody [FN50] (PE) (A86795)

Figure 10: Flow cytometry analysis of human PHA-activated peripheral blood stained with Anti-CD69 Antibody [FN50] (PE) (A86795).

Memory B Cell Subsets by Immunoglobulin Expression

As previously described (see Germinal Center-Dependent and -Independent Pathways, immunoglobulin expression is typically a poor marker as not all MB cells undergo somatic hypermutation or isotype switching. CD27+ peripheral blood MB cells are divided into: swIg (40%); IgM+IgD+ (40%); IgM+ (20%); IgD+ (low) subsets.47,48 The roles of these subsets remain to be fully understood, but some characteristics of these populations are described below.

  • CD27+swIg+ MB are one of the main GC-dependent B cell descendants. Activation of CD27 by CD70 in response to re-infection has been shown to induce differentiation of these cells into plasma cells,49 allowing them to quickly produce antibody in response to re-infection.
  • It is unclear whether CD27+IgM+IgD+ are true MB cells or another subset of B cell that develops along a different developmental pathway.50,51 The origin of these cells is not currently understood, with studies pointing to a GC-independent or GC-dependent source.35,52-54
  • CD27+IgM+ MB cells most likely represent a population of GC-dependent B cells, though there is some debate over their heterogeneity.55
  • CD27+IgD+ MB cells are very rare in peripheral blood of humans (0.1-0.5%)25 but seem to derive from the tonsils before migrating to other mucosal sites.56
  • The majority of murine IgM+ MB cells are CD80-CD73- and are capable of differentiating back into GC B cells upon antigen re-exposure, whereas CD80+CD73+IgG1+ MB cells differentiate into mostly plasma cells.57,58
  • CD23+IgG+ MB cells are posited to differentiate into IgE-producing plasma cells, which themselves are associated with pathogenesis in chronic allergy.59
    • These IgG MB cells are increased in asthma/ atopic dermatitis patients and positively correlate with plasma levels of IgE.59
    • CD23 is a receptor for the cytokines IL-4 and IL-13 produced by T cells in type 2 responses.59
  • IgA+ memory cells are a relatively small population (10% in plasma) that are mostly CD27+ and associated with intestinal, mucosal lymphatic tissues.60

Murine vs Human Memory B Cell Markers

There are several differences between human and murine MB cells, in terms of expression patterns but also biological prevalence. In humans, ~40% of peripheral blood B cells are MB cells whereas in mice this number is only ~5%, with this difference ascribed to the longer life span of human MB cells.61,62

In the mouse, most GC-independent MB cells have been shown to be CD73-IgM+, though there is a small subset of CD73+IgM+.63 However, in humans, most IgM+ cells are GC-dependent.64 It is postulated that this is due to the differing species role of CD73 and CD27, with CD27 used to define MB cells in humans. CD27+IgM+ cells undergo somatic hypermutation whereas CD27-IgM+ do not, leading to the original classification of this latter population as non-MB cell,61 whereas later studies have identified this CD27- population as likely being GC-independent MB cells.64 From this data, it seems that CD27 fulfills the same role as CD73 in the mouse in identifying GC-independent/dependent (-/+) MB cells and indeed, only a minor portion of murine MB cells express CD27.27

In murine models, MB cells are IgM- and IgD-, in contrast to human MB cells that express both together or independently.47,48,61

Methods for the Examination of Memory B Cell Markers

Memory B cells are best characterized by the expression of surface markers, rather than intra-cellular proteins such as cytokines. This is because memory cells are not effector/ producing cells, instead, upon activation, they differentiate into antibody-producing plasma cells. For this reason, techniques such as flow cytometry or IHC will be the most powerful tools to examine MB cells. Because MB cells make up a large, nebulous family of subsets, a combination of markers and techniques might be best to accurately characterize these populations.

Memory B Cell Marker Antibodies

CCR6 Antibodies
CD19 Antibodies
CD20 Antibodies
CD27 Antibodies
CD45RB Antibodies
CD69 Antibodies
CD73 Antibodies
CD80 Antibodies
PD-L2 Antibodies

References

Diagrams created with BioRender.com.

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