EFB Dengue Literature Review

Age-Associated B Cell

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Age-Associated B Cell

This page is the canonical entry for the age-associated B cell (ABC) named population specifically. For the field-level synonymy map across “atypical,” “ABC,” “T-bet⁺,” “CD11c⁺,” “DN,” and “alternative lineage” labels — and how they route to precise sub-populations — see the umbrella Atypical B Cell. For the human IgD⁻CD27⁻ effector that the IgD⁻CD27⁻ ABC subset maps onto, see DN2 B Cell.

Overview

Age-associated B cells (ABCs; also “T-bet⁺ B cells,” “age/autoimmunity-associated B cells”) were first defined in aged mice as CD19⁺CD21⁻CD23⁻ B cells expressing the transcription factor T-bet and the integrin CD11c (Hao 2011). They are rare in the young and accumulate with age; they also expand prematurely in autoimmunity and chronic infection. “ABC” is, in current usage, primarily a murine term, with the human “DN2” subset regarded as its closest counterpart — but the equation is only partial (see Contradictions).

ABC is a heterogeneous superset, not a single cell. Per Tangye (2023) the ABC population comprises CD27⁺ B cells, IgD⁺ B cells, and — predominantly — IgD⁻CD27⁻ (DN) cells. Only this IgD⁻CD27⁻ fraction corresponds to DN2; the CD27⁺ and IgD⁺ members fall outside the DN definition. This is the central distinction that separates the ABC label from the DN label (see Lamprinou2026 - ABCs and DN B Cells).

Key Points from Literature

  • Phenotype and aging. ABCs are CD19⁺CD21⁻CD23⁻T-bet⁺CD11c⁺, rare in young healthy individuals and steadily increasing with age; a subset shows reduced BCR-mediated antibody production consistent with immunosenescence while retaining other functions (see Lamprinou2026 - ABCs and DN B Cells, opinion, citing Hao 2011 / Cancro 2020).

  • Differentiation programme. ABCs are hyper-responsive to endosomal TLR7 and TLR9 and differentiate under TLR stimulation combined with IFN-γ and/or IL-21: IL-21 robustly induces CD11c; IFN-γ primarily promotes T-bet. BCR signalling contributes (with TLR/IFN-γ/IL-21/CD40) but is insufficient alone (see Lamprinou2026 - ABCs and DN B Cells, opinion, citing Cancro 2020 / Liu 2024 / Naradikian 2016 / Rubtsov 2017 / Imabayashi 2025). TLR7 is X-linked — a proposed partial basis for the female autoimmunity bias.

  • Heterogeneous isotype/marker composition. Most ABCs are class-switched (IgG or IgA), but the population also contains unswitched IgD⁺ cells by scRNA-seq, and some ABCs express the memory marker CD27 (see Lamprinou2026 - ABCs and DN B Cells, opinion, citing Ambegaonkar 2022 / Rubtsov 2011 / Tangye 2023).

  • IgD⁺ ABCs are not naive. They carry somatic hypermutation and are clonally related to IgD⁻ cells, indicating prior antigen experience (see Lamprinou2026 - ABCs and DN B Cells, opinion, citing Maul 2021; see Somatic Hypermutation).

  • Transcriptomics (murine). ABCs are discrete from B1 and follicular B cells; they highly express CD11c and T-bet with Ig-heavy-chain and CD138 transcripts and intermediate plasma-cell-differentiation TFs, interpreted as probable plasma-cell precursors; IL-21-inducible and cell-adhesion genes are upregulated in autoimmunity (see Lamprinou2026 - ABCs and DN B Cells, opinion, citing Rubtsov 2011 / Wang 2018).

  • Effector functions beyond antibody. Pro-inflammatory cytokine/chemokine production, antigen presentation with strong phagocytic capacity, and T-cell activation (see Lamprinou2026 - ABCs and DN B Cells, opinion, citing Xie 2025).

  • Origin debated. A GC-experienced origin is proposed for at least a subset (diverse Ig repertoire, SHM, antigen-driven activation), but homeostatic proliferation and GC-independent/extrafollicular routes are not excluded (see Lamprinou2026 - ABCs and DN B Cells, opinion, citing Cancro 2020). This contrasts with DN cells, which are more strongly tied to extrafollicular differentiation.

  • Disease associations. Premature expansion in SLE, RA, Sjögren’s, SSc, and MS — in some cases correlating with disease activity, autoantibody titres, and organ involvement (e.g., T-bet⁺ B cells track SLE activity and lupus nephritis as a candidate biomarker); also induced by chronic HIV, hepatitis C, and malaria (see Lamprinou2026 - ABCs and DN B Cells, opinion, citing Sachinidis 2020/2025 / Kourkouni 2024 / SoRelle 2025 / Portugal 2017 / Knox 2017).

  • Therapeutic targeting. BAFF inhibition (belimumab) and CD20 depletion (rituximab) reduce ABC frequencies in SLE blood; a broader portfolio includes IRF5 inhibitors, JAK inhibitors (baricitinib), adenosine A2a agonists, TNF inhibitors, tocilizumab (anti-IL-6R), and ROCK inhibitors (fasudil) (see Lamprinou2026 - ABCs and DN B Cells, opinion, citing Sachinidis 2024/2025 / Ramsköld 2019).

  • Cross-reference — transcriptomic correlate. The “alternative lineage” defined by scRNA-seq/CITE-seq (atBC1–3 + MBC1; T-bet/CD11c/FCRL5⁺) is the high-dimensional transcriptomic correlate of the ABC/atypical cluster, present at ~20% of B cells even in non-exposed donors, with CD11c the best single surface marker (see Sutton2021 - Alternative Lineage B Cells in Vaccination and Infection, n=4 CITE-seq).

  • Cross-reference — nomenclature caution. The “ABC”/“atypical” label conflates ≥5 populations and its identity/function depend on context; precise DN nomenclature is preferred (see Sanz2025 - Human Atypical B Cells Overview, review).

  • ★ ZEB2 is a key ABC transcription factor in both mice and humans, proposed as the factor imposing the conserved cross-context ABC programme. Functionally dual-edged: B-cell-specific Zeb2 deletion improved disease in a lupus mouse model, yet reduced GCBC numbers during persistent Plasmodium infection — the same population is pathogenic in autoimmunity and supportive of humoral immunity in persistent infection (see Glaros2025 - Multilayered Identity of B Cell Memory, review, citing Dai 2024 Science + Gao 2024 Sci Immunol, mouse and human). Adds a second, independent TF axis to the T-bet-centric account above.

  • ★ T-bet is not strictly required for ABC formation. Although T-bet was long “believed to be essential,” CD11c⁺ ABCs still arise in both infection and autoimmune models in the absence of T-bet (see Glaros2025 - Multilayered Identity of B Cell Memory, review, citing Du 2019 + Levack 2020, mouse conditional-KO). The murine ABC definition above (T-bet⁺CD11c⁺) therefore describes the dominant state, not a requirement.

  • Conserved transcriptional programme across malaria, HIV, and autoimmunity. ABCs from these three settings show similar transcriptional profiles, suggesting a shared differentiation trajectory rather than context-specific phenocopies (see Glaros2025 - Multilayered Identity of B Cell Memory, review, citing Holla 2021, human cross-disease transcriptomics). Supports — without proving — that the dengue CD21⁻CD11c⁺ expansion belongs to the same programme.

  • Antigen encounter and, in some cases, T cell help are required. ABC frequencies fall significantly in patients with CD40/CD40L mutations, and ABCs do not develop in mice with a fixed BCR specificity under steady-state conditions. ABCs are found within the antigen-specific pool after immunization in mice and humans, some carry SHM, and they respond to antigen restimulation (see Glaros2025 - Multilayered Identity of B Cell Memory, review). Directly strengthens the “antigen-experienced, not inflammatory bystander” reading of the origin debate below.

  • Anergic B cells are a demonstrated ABC precursor. Anergic B cells arising after chronic self-antigen engagement can be converted into ABCs, and are more prone than naive B cells to acquire the ABC phenotype under in vitro differentiation conditions (see Glaros2025 - Multilayered Identity of B Cell Memory, review, citing Imabayashi 2025, mouse + in vitro). This is the most concrete mechanism yet for the autoreactive-origin hypothesis in autoimmune settings.

  • Effector fate is plastic — PC, GCBC, or self-renewal. Adoptive transfer of ABCs between mice of the same autoimmune strain shows they can differentiate into PCs, differentiate into GCBCs, and self-renew (see Glaros2025 - Multilayered Identity of B Cell Memory, review, citing Nickerson 2023, mouse adoptive transfer). This qualifies the “probable plasma-cell precursors” transcriptomic reading above: PC priming is one available fate, not a commitment. Whether the balance is set by prior antigenic stimulation is unresolved, as is whether ABCs act principally through PC differentiation, antigen presentation to T cells, or both.

  • Homeostasis is an open question the field has not answered. The extent to which the ABC compartment is maintained by self-renewal versus replenishment from newly activated B cells remains unclear, as do the relative contributions of GC-dependent and GC-independent routes to the pool (see Glaros2025 - Multilayered Identity of B Cell Memory, review).

  • Two founding definitions, different markers — not identical populations. Hao et al. 2011 defined murine ABCs as B220⁺CD19⁺ splenic B cells lacking CD21, CD23, CD95, and CD43; Rubtsov et al. 2011 instead used CD11c⁺ expression on B220⁺CD19⁺ splenocytes as the primary criterion. The two schemes yield “largely overlapping” but non-identical populations (see Cancro2020 - Age-Associated B Cells, review — no original data; mouse).

  • Age-accumulation trajectory. ABCs are undetectable in juvenile/young-adult spleen, reach a low but distinguishable frequency at 3–6 months, form a clearly enlarging pool by 12–18 months, and comprise up to half of all splenic B cells by 24–30 months — with considerable individual variation even in age-matched, co-housed cohorts (see Cancro2020 - Age-Associated B Cells, review — no original data; mouse).

  • ★ Heterogeneity: at least three populations sit inside a single ABC gate (F4). Within the murine CD21⁻CD23⁻ splenic pool, only ~2/3 of cells are T-bet⁺, and among those, only about half are CD11c⁺ — so a CD21⁻-only gate over-calls the “ABC” population by roughly 50%. Whether these represent stable independent populations or differentiation/activation stages within one lineage is unresolved (see Cancro2020 - Age-Associated B Cells, review — no original data; mouse, splenic).

  • ★ Blood and splenic ABC pools are not in equilibrium (F5). ABCs are spleen-enriched, scarce in lymph nodes, and present but highly variable in blood and bone marrow; Cancro states this is “a cautionary interpretive note for studies that track ABCs only in peripheral blood.” Reinforced in humans: blood ABC frequencies fall in HIV patients on antiretroviral therapy, raising the possibility that circulating T-bet⁺ ABCs represent “an activated or mobilized differentiation state that wanes upon viral clearance, despite retention in the spleen or other tissues.” This cuts both ways: it invalidates blood frequency as a pool-size proxy, but makes blood frequency arguably the correct readout for questions about acute mobilisation rather than accumulation (see Cancro2020 - Age-Associated B Cells, review — no original data; mouse and human, observational).

  • BCR-refractory but viable. ABCs do not divide in response to BCR cross-linking, unlike follicular B cells, but remain viable, unlike marginal-zone and transitional B cells, which die rapidly under the same conditions. They proliferate robustly to TLR7/TLR9 ligands, and BCR cross-linking — not mitogenic alone — synergises with TLR signalling for additional rounds of division (see Cancro2020 - Age-Associated B Cells, review — no original data; mouse).

  • BAFF independence and follicular displacement. ABCs express BAFFR and TACI but are largely BAFF-independent — BAFF-blocking antibody eliminated follicular and marginal-zone pools but left ABC numbers unchanged, resembling memory B cells. ABCs nonetheless consume/sequester BAFF, occupying homeostatic space at the expense of follicular B cells: the sum of ABC + FO numbers stays roughly constant as ABCs displace FO cells with age (see Cancro2020 - Age-Associated B Cells, review — no original data; mouse).

  • Progenitor evidence: not de novo bone-marrow output. Sublethal irradiation (5 Gy) ablates peripheral B cell pools; follicular and marginal-zone compartments fully reconstitute, but the ABC pool does not return rapidly — indicating ABCs are a slowly accumulating population derived from preimmune peripheral B cells, not the output of an aged bone-marrow progenitor. Adoptive transfer confirms this directly: ABCs arise from splenic follicular B cells within 30 days, and donor-derived ABCs are found only among the most extensively divided cells; neither donor nor recipient age affected the result (see Cancro2020 - Age-Associated B Cells, review — no original data; mouse, irradiation + adoptive transfer).

  • Russell Knode repertoire result. Sequencing of sorted ABC heavy and light chains (Russell Knode et al. 2017, J Immunol) found a diverse array of germline V_H and V_κ genes, largely congruent with the follicular pool — ruling out age-associated clonal expansion of the kind described for T cells — while many ABC V regions were somatically mutated (see Cancro2020 - Age-Associated B Cells, review — no original data; mouse).

  • ★ GC origin is inference, not demonstration (F3) — Cancro’s own scepticism, and why the mutation data doesn’t settle it. Cancro states directly that “both the requisite for cognate T cell interactions and the assertion that ABCs have entered GCs are based on inference, but have not yet been directly demonstrated.” He gives three specific reasons the Russell Knode mutation data above does not resolve the question: (1) the ABC phenotype is achievable without CD40 ligation — bystander IFN-γ may suffice; (2) although T-bet⁺ B cells transiently express GC-associated markers (PNA, CD95), anatomic localisation of ABCs within GCs has never been directly shown; (3) somatic hypermutation itself can occur independent of germinal-centre formation — he cites Di Niro et al. 2015 (Immunity), where Salmonella infection drives extrafollicular affinity maturation in mice. His conclusion, in his own words: “it remains possible that ABCs arise and undergo somatic hypermutation in extrafollicular or other GC-independent niches.” This matters directly for this wiki: the same mutation evidence that Lamprinou2026 - ABCs and DN B Cells reads as supporting a GC-experienced origin, Cancro — the investigator who co-defined the subset and generated much of this repertoire data — reads as inconclusive, because mutation load is not on its own a valid GC-origin proxy. He does accept some supporting evidence for a T-help requirement: MHC-II-KO and CD40-KO follicular B cells yield no ABCs, and CD154-KO mice fail to develop natural ABCs with age (see Cancro2020 - Age-Associated B Cells, review — no original data; mouse).

  • Homeostatic-expansion alternative route, and a combination-of-routes synthesis. The Swain group reported ABC-characteristic cells emerging under limited exogenous antigen availability, with an increasing proportion of primary influenza responses recruiting ABCs as mice age. Cancro proposes a second, T-cell-analogous route in which endogenous ligands drive gradual homeostatic proliferation, yielding cells bearing hallmarks of prior activation without an antigen-specific driver. He states the two routes are “neither mutually exclusive nor mechanistically disparate,” and concludes the ABC pool most likely reflects a combination of formative routes whose relative contribution varies with age and antigenic load (see Cancro2020 - Age-Associated B Cells, review — no original data; mouse).

  • Isotype composition. Hao-defined ABCs include both IgM⁻ and IgM⁺ cells, and within the IgM⁺ fraction a range of surface IgD. Cancro’s speculative mapping: switched (IgM⁻IgD⁻) and unswitched (IgM⁺IgD⁻) memory arising from antigen-driven responses, versus homeostatically-expanded primary cells (IgM⁺IgD⁺) arising from the alternative route above. Consistent with this, ABCs include both somatically mutated and germline-configuration Ig genes (see Cancro2020 - Age-Associated B Cells, review — no original data; mouse).

  • Cytokine output and Th17-skewing APC function. On TLR7/9 activation, ABCs produce higher IFN-γ and exceptionally high IL-10 than follicular B cells (transcriptional array + ELISpot), plus IL-6. They are effective antigen-presenting cells with high MHC-II expression that skew naive CD4 T cells toward Th17 in vitro (see Cancro2020 - Age-Associated B Cells, review — no original data; mouse, in vitro + ELISpot).

  • The ABC-as-plasma-cell-depot hypothesis. The splenic ABC memory pool may be a continuously replenishing source of precursors feeding plasma cell pools, potentially explaining how the bone marrow niche sustains lifelong PC production without continuous enlargement or loss of prior specificities — consistent with Allman-group data that a significant fraction of bone marrow plasma cells turn over rapidly. Cancro flags this as explicitly untested, requiring fate-mapping tools (see Cancro2020 - Age-Associated B Cells, review — no original data; mouse).

  • Open progenitor–successor questions. Unresolved: whether unswitched/unmutated IgM⁺ ABCs are progenitors of class-switched, mutated ABCs; whether CD11c⁺ ABCs represent a differentiation state derived from CD11c⁻ ABCs; and whether there is appreciable interchange between T-bet⁺ ABC and T-bet⁻ memory B cell pools. If CD11c⁺ status is a state rather than a stable subset, a CD11c-gated ABC frequency measures activation, not compartment size (see Cancro2020 - Age-Associated B Cells, review — no original data; mouse).

  • TNF-alpha suppression of B lymphopoiesis. The Riley laboratory showed ABCs impede early B cell development through TNF-α production — directly, by inducing apoptosis in pre-B cells, and indirectly, through systemic inflammatory effects on the bone marrow microenvironment (see Cancro2020 - Age-Associated B Cells, review — no original data; mouse, in vitro + adoptive transfer).

  • Autoimmunity associations, including the IL-21→IRF5 axis and CVIDc. ABCs are elevated in nearly all murine humoral autoimmunity models tested; in NZB/W F1 and Mer⁻/⁻ SLE models they expand by 3 months and reach 15% of splenic B cells by 6 months (rarely seen in healthy mice before 12–18 months), are implicated as sources of anti-chromatin antibodies, and are TLR7-dependent. In the SWEF double-knockout model, ABC expansion is strongly IL-21-driven — IL-21-deficient SWEF DKO mice developed neither expanded ABCs nor autoantibodies — and this expansion required IRF5 (plain-text citation; no wiki page), an established human SLE risk factor. In humans, elevated blood ABCs correlate strongly with SLEDAI and are highly enriched for autoantibody specificities (Wang et al. 2018); in common variable immunodeficiency, the CVIDc subset (autoimmune cytopenia plus interstitial lung disease) — but not CVIDio (infection-only) — shows clear elevation of an atypical T-bet⁺ ABC-like population in a Th1/IFN-γ-skewed milieu (see Cancro2020 - Age-Associated B Cells, review — no original data; mouse and human, small cohorts).

  • ⚠ [2026-08-27] A cautionary example of “ABC-like” being used for a CD27-POSITIVE population. In IgG4-related disease, the authors split IgD⁻CD27⁺ switched memory into CXCR5⁺ (“classic/resting switched memory”) and CXCR5⁻ (“ABC-like”), reporting the classic fraction decreased and the ABC-like fraction expanded (both p<0.01, n=38). They state explicitly that, “given the many definitions of ABC cells,” their ABC-like gate includes both CD11c⁺ and CD11c⁻ cells, though CD11c⁺ predominated. This population is CD27⁺ and therefore has no overlap with the DN compartment at all, and it is not gated on T-bet. It is a distinct entity from every other ABC definition in this wiki and must not be pooled with them — a concrete instance of the definitional heterogeneity that Sanz2025 - Human Atypical B Cells Overview and Lamprinou2026 - ABCs and DN B Cells both warn about (see Allard-Chamard2023 - DN3 B Cells Infiltrate Inflamed Tissues, n=38).

  • ★ The fate-mapping primary for murine ABC origin: most arise without a germinal centre, but they still require Tfh help. Four orthogonal lines — absent GL-7/EphrinB1, a distinct sorted transcriptome, S1pr2-CreERT2 fate mapping showing >80% never passed through a GC (17.5% labelled vs 70.0% of GL-7⁺ early GC B cells), and a mixed bone marrow chimera showing B-cell-intrinsic Bcl6 is dispensable — with the result replicated in influenza PR8. The helper is a canonical CXCR5⁺PD-1^hi^ Tfh acting outside the GC, not Th1. As infection resolves the cells relocate to the splenic marginal zone, retained by LFA-1 and VLA-4 (see Song2022 - Tfh Outside Germinal Centers Drive T-bet CD11c B Cells, mouse, LCMV-Armstrong + influenza PR8, n=3–5 mice/group). ⚠ Species and setting boundary: entirely murine, in two acute resolving viral infections; the human ABC literature on this page is largely chronic infection and autoimmunity, and no human equivalent of the S1pr2 fate map exists — the >80% figure is not a human number.

Contradictions & Debates

  • ABC ≈ DN2 phenotypically, but ≠ DN2 transcriptomically. Even where ABCs and DN2 share the T-bet⁺CD11c⁺ phenotype, comparative transcriptomics show ABCs are distinct from other CD11c⁺ subsets including DN2, with elevated cytokine/chemokine expression not seen in the others (see Lamprinou2026 - ABCs and DN B Cells, opinion, citing Maul 2021). The wiki’s working “ABC ≈ DN2” equivalence is therefore a phenotypic approximation limited to the IgD⁻CD27⁻ ABC subset, not a transcriptomic identity.

  • Murine vs human depletion sensitivity. Murine ABCs resist anti-BLyS and anti-CD20 depletion in lupus models (Knox 2025), whereas human SLE ABCs are sensitive to the same interventions (Ramsköld 2018; Faustini 2022) — and rituximab resolves DN expansion in SLE (see Anolik2004 - Rituximab and B Cell Abnormalities in SLE). Whether this is a species difference or a context/disease-stage difference is unresolved (see Lamprinou2026 - ABCs and DN B Cells, opinion).

  • Origin unresolved: GC-experienced vs homeostatic proliferation vs extrafollicular — likely a mix that varies by context. [2026-08-16] The best direct evidence now favours GC-independent, at least in acute infection. GC-specific genetic fate mapping in mice shows that after acute viral infection the majority of antigen-specific ABCs are generated via a GC-independent pathway (see Glaros2025 - Multilayered Identity of B Cell Memory, review, citing Song 2022, mouse). This is a substantially stronger form of evidence than the repertoire/SHM inference behind the GC-experienced proposal — fate mapping assigns origin directly rather than reading it off surrogate markers. Two caveats travel with it: it is one murine acute viral model, and the review itself states that whether it generalizes to other ABC-generating contexts “remains to be elucidated.” Chronic settings (the classic ABC contexts) are untested by this method.

  • Framework provenance. Much of the ABC↔DN synthesis (and the four-subset DN taxonomy it relies on) is self-referential to the Sachinidis/Garyfallos group; cross-lab validation is incomplete — the same caveat the wiki applies to the Sanz lab’s DN classification (see Sanz2025 - Human Atypical B Cells Overview).

  • ★ Cancro’s own reading of the somatic-mutation evidence directly opposes Lamprinou2026’s — same data, two readings. Lamprinou2026 - ABCs and DN B Cells cites diverse repertoire + SHM in ABCs as support for a GC-experienced origin. Cancro2020 - Age-Associated B Cells — written by the investigator whose own group generated much of this repertoire evidence (Russell Knode et al. 2017) — reads the same category of evidence as inconclusive: SHM can occur independent of GC formation (citing Di Niro et al. 2015, extrafollicular affinity maturation in murine Salmonella infection), and neither cognate T cell interaction nor GC entry has been directly demonstrated for ABCs, only inferred (see Key Points, F3, above). This is not a new data point contradicting an old one — it is the same category of evidence read two different ways, with the more authoritative reading (the subset’s co-definer, on his own field’s dataset) landing on the sceptical side. It converges with, rather than merely adds to, the 2026-08-16 Song2022 fate-mapping entry above: the murine GC-independent-origin position is now supported from two independent angles — direct fate mapping (Glaros2025/Song2022) and an inferential critique of the GC-experienced argument’s own evidentiary basis (Cancro2020) (see Cancro2020 - Age-Associated B Cells, review — no original data; mouse).

  • ★ The ABC acronym has four incompatible expansions, and a consensus panel recommends retiring it — in a paper dedicated to Cancro’s memory. Eisenbarth2025 - A Roadmap for Defining Extrafollicular B Cell Responses lists, as separate Box 1 entries: age-associated B cells (CD11c^hi, aged mice), autoimmunity-associated B cells (CD11c^hi, mouse and human autoimmunity), atypical B cells (human blood, CD27⁻IgD⁻CD11c^hi, non-classical transcriptional profile), and activated B cells (human blood, CD71⁺, which may or may not be CD11c⁺T-bet⁺). All four are written “ABC” in the literature. The recommendation is to define the cells in each instance and avoid the acronym, and specifically that “ABC should not be used to infer an EF origin” — CD11c⁺T-bet⁺ cells arise in mouse viral infections as GC-derived memory, and in human post-influenza vaccination as CD27⁺CD21^lo cells with high SHM, i.e. recent GC emigrants. The Perspective is dedicated to the memory of Michael Cancro (1949–2025), author of Cancro2020 - Age-Associated B Cells, the paper that anchors the ABC framing on this page. Both positions are held here. Note that Cancro’s own scepticism about reading ABC origin off surrogate markers (recorded in the bullet above) is closer to the Perspective’s position than the “ABC as a defined subset” usage his terminology enabled (see Eisenbarth2025 - A Roadmap for Defining Extrafollicular B Cell Responses, consensus Perspective, 12 authors, no primary data).

Atypical B Cell, DN2 B Cell, Double-Negative B Cell, DN3 B Cell, T-bet, ZEB2, CD11c, CD27, IgD, TLR7, IL-21, CD20, Germinal Center, Extrafollicular Response, Somatic Hypermutation, Tissue-Resident Memory B Cell, GC-Independent Response

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