ArticleBlood neoplasia2026
Myeloid cell-mediated killing of B-ALL by CD38 and CD20 IgA antibody variants is enhanced by CD47/SIRPα interference.
Article in Blood neoplasia, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
What it found
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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.
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.
Who cites it
1 citing paper in PubMed.
- Immunomodulatory functions of glutaminyl cyclases QPCTL and QPCT.Frontiers in immunology · 2026Review
Corrections and comments
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Authors and funding
30 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Enhancing myeloid effector cell recruitment may improve immunotherapy by monoclonal antibodies, including those against acute lymphoblastic leukemia (ALL). To assess the expression of target antigens in B-cell ALL (B-ALL), we compared mRNA profiling of 559 patient leukemia samples across 18 molecular subtypes with that of representative cell lines. The latter served as target cells to compare human immunoglobulin G1 (IgG1) or IgA2 variants against CD19, CD20, or CD38 in antibody-dependent cellular phagocytosis (ADCP) by macrophages and antibody-dependent cell-mediated cytotoxicity (ADCC) by polymorphonuclear leukocytes (PMN). Interestingly, antibodies against broadly expressed CD19 were negligibly effective in mediating ADCP or ADCC. Antibodies against CD20 or CD38, the former variably expressed across subtypes, triggered ADCP by macrophages both as IgG1 and IgA2. However, PMN-mediated ADCC against CD20 or CD38 was only observed with IgA2 variants but not with respective IgG1 antibodies. Blocking the myeloid checkpoint CD47/signal regulatory protein α (SIRPα) enhanced ADCP and ADCC by IgA2 antibodies against CD20 and CD38 but not CD19. Both CD47 and its enzymatic modifier glutaminyl-peptide cyclotransferase-like protein (QPCTL), which can be inhibited by small molecules, were broadly expressed across B-ALL subtypes. QPCTL catalyzes the formation of an N-terminal pyroglutamic acid on CD47, which is directly involved in CD47/SIRPα interactions as shown by novel engineered CD47 variants. Importantly, the combination of anti-CD38 IgA2 and CD47 blockade was effective against xenografted B-ALL in human FcαRI (CD89) transgenic NXG mice. Together, these studies support combining anti-CD38 IgA2 with CD47 interference to improve myeloid effector cell recruitment for B-ALL immunotherapy.
Identifiers
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Registered trials
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.