Evidence map›Paper›PMID 42776800›Full record

ReviewAntibodies (Basel, Switzerland)2026

B Cells and Tumor Immunometabolism: Emerging Insights into Immune Regulation and Therapeutic Resistance.

Swati Gupta, Sandip Rath, Surathi Maiti, Tapas Das, Farhat Afrin

Abstract readReview
In one paragraph

Review in Antibodies (Basel, Switzerland), 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

0 citing papers in PubMed.

No citing paper in PubMed yet.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

5 authors.

Swati GuptaCentre for Interdisciplinary Sciences, JIS Institute of Advanced Studies and Research, JIS School of Medical Science & Research Campus, JIS University, Santragachi, Howrah 711112, West Bengal, India.
Sandip RathCentre for Interdisciplinary Sciences, JIS Institute of Advanced Studies and Research, JIS School of Medical Science & Research Campus, JIS University, Santragachi, Howrah 711112, West Bengal, India.
Surathi MaitiCentre for Interdisciplinary Sciences, JIS Institute of Advanced Studies and Research, JIS School of Medical Science & Research Campus, JIS University, Santragachi, Howrah 711112, West Bengal, India.
Tapas DasCentre for Interdisciplinary Sciences, JIS Institute of Advanced Studies and Research, JIS School of Medical Science & Research Campus, JIS University, Santragachi, Howrah 711112, West Bengal, India.
Farhat AfrinCentre for Interdisciplinary Sciences, JIS Institute of Advanced Studies and Research, JIS School of Medical Science & Research Campus, JIS University, Santragachi, Howrah 711112, West Bengal, India.ORCID 0000-0003-4443-4284

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Cancer progression and therapeutic resistance are shaped by reciprocal dynamic interactions between malignant cells and the metabolically altered tumor microenvironment (TME). Tumor-associated hypoxia, glucose and amino acid competition, extracellular acidity, lactate accumulation, adenosine, prostaglandin E2 (PGE2) and other metabolic signals can remodel immune cell function and determine whether inflammation is tumoricidal or tumor-supportive. Although B lymphocytes have traditionally been viewed as antibody-producing cells, tumor-infiltrating B (TIL-B) cells comprise functionally heterogeneous populations that can act as antigen-presenting cells, cytokine and chemokine producers, antibody-secreting cells, cytotoxic effectors, regulatory B cells (Bregs) and organizers of tertiary lymphoid structures (TLSs). Their functional state is strongly influenced by the metabolic and spatial context in which they reside. This review focuses on the intersection of B cell biology and tumor immunometabolism, emphasizing how hypoxia, lactate, nutrient limitation, adenosine, PGE2, kynurenine and B cell-derived γ-aminobutyric acid (GABA) may shape B cell states and their interactions with myeloid and lymphoid cells. We discuss how metabolically conditioned Bregs and immunoglobulin (Ig)A-skewed humoral responses can contribute to immune suppression, whereas metabolically competent antigen-presenting, IgG-biased and TLS-associated B cell responses may support effective anti-tumor immunity. Importantly, the effects are tumor type- and context-dependent: B cell/TLS signatures are associated with favorable outcomes in several breast, lung and other solid tumors, whereas B cell-centered immune landscapes can be suppressed or neutral in pancreatic cancer and IgA-dominated responses may be unfavorable in selected malignancies. We further examine how these states may influence sensitivity or resistance to immune checkpoint blockade, chemotherapy, radiotherapy and cellular therapies. Finally, we highlight B cell metabolic pathways as potential therapeutic entry points and identify priorities for spatial metabolomics and prospective interventional studies.

Indexed as

adenosineGABAhypoxiaimmune checkpoint blockadelactatemetabolic reprogrammingPGE2regulatory B cellstertiary lymphoid structurestherapeutic resistancetumor immunometabolismtumor-infiltrating B cellstumor microenvironment

Identifiers

PMID42776800
PMCPMC13600041

What OpenQuestion holds

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Registered trials

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.