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Cells
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Novel Immunotherapies for Diffuse Large B-Cell Lymphoma
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Novel Immunotherapies for Diffuse Large B-Cell Lymphoma

A special issue of Cells (ISSN 2073-4409).

Deadline for manuscript submissions: 31 October 2026 | Viewed by 1649

Special Issue Editor

Dr. Waseem Lone

E-Mail Website
Guest Editor
Department of Pathology, Microbiology and Immunology, University of Nebraska Medical Center, Omaha, NE, USA
Interests: B-cell lymphoma; T-cell lymphoma; high-grade B-cell lymphoma (HGBCL); Burkitt lymphoma (BL); diffuse large B-cell lymphoma (DLBCL); angioimmunoblastic T-cell lymphoma (AITL); T-follicular helper-like

Special Issue Information

Dear Colleagues,

Diffuse large B-cell lymphoma (DLBCL) is the most common aggressive non-Hodgkin lymphoma, characterized by remarkable biological heterogeneity and diverse clinical outcomes. Although standard immunochemotherapy regimens such as R-CHOP have improved survival, a significant proportion of patients experience relapse or refractory disease, underscoring the urgent need for innovative therapeutic strategies. In recent years, novel immunotherapies have transformed the treatment landscape, offering new hope for patients with limited options.

Advances in CAR-T cell therapies, bispecific antibodies, immune checkpoint inhibitors, and antibody–drug conjugates have demonstrated promising efficacy in relapsed/refractory DLBCL. At the same time, insights from genomic, transcriptomic, and tumor microenvironment studies are guiding the development of more precise immune-based interventions. These approaches not only target malignant B cells but also modulate immune evasion pathways, highlighting the central role of the immune system in disease progression and treatment response.

This Special Issue, “Novel Immunotherapies for Diffuse Large B-Cell Lymphoma”, will bring together cutting-edge original research, comprehensive reviews, and translational insights that explore new immunotherapeutic avenues. We invite contributions spanning molecular mechanisms, preclinical models, biomarker discovery, and translational applications, with the goal of advancing precision medicine and improving patient outcomes in DLBCL.

Dr. Waseem Lone
Guest Editor

Manuscript Submission Information

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Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. Cells is an international peer-reviewed open access semimonthly journal published by MDPI.

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Keywords

  • diffuse large B-cell lymphoma
  • immunotherapy
  • CAR-T cells
  • bispecific antibodies
  • immune checkpoint inhibitors
  • antibody–drug conjugates
  • tumor microenvironment
  • biomarkers
  • translational research

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Published Papers (2 papers)

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Research

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18 pages, 2797 KB  
Article
CD74-Targeted Cathepsin-Inhibitor Antibody–Drug Conjugate Triggers Apoptosis in DLBCL
by Ihab Abd-Elrahman, Noha Khairi, Reut Sinai-Turyansky, Ivan Zlotber, Riki Perlman, Emmanuelle Merquiol, Galia Blum and Dina Ben Yehuda
Cells 2026, 15(3), 291; https://doi.org/10.3390/cells15030291 - 4 Feb 2026
Cited by 1 | Viewed by 997
Abstract
Transcriptomic analyses of public datasets (TCGA and GTEx) revealed that both CD74 and Cathepsin L (CTSL) are significantly overexpressed in diffuse large B-cell lymphoma (DLBCL) compared to normal tissues, and that their expression levels are highly correlated to each other (Spearman R = [...] Read more.
Transcriptomic analyses of public datasets (TCGA and GTEx) revealed that both CD74 and Cathepsin L (CTSL) are significantly overexpressed in diffuse large B-cell lymphoma (DLBCL) compared to normal tissues, and that their expression levels are highly correlated to each other (Spearman R = 0.64, p = 3 × 10−46). Kaplan–Meier analysis showed that elevated expression of both genes is associated with reduced overall survival (OS), defining a high-risk CD74+/CTSL+ DLBCL subgroup. This is the first study demonstrating coordinated overexpression of CD74 and CTSL and proposing their dual targeting via antibody–drug conjugates (ADCs) to improve outcomes in relapsed or refractory DLBCL. Cysteine cathepsins, a family of proteases, are upregulated in many cancers, facilitating tumor invasion and metastasis. Cathepsins are overexpressed and play key roles in DLBCL progression. GB111-NH2, a potent broad-spectrum cathepsin inhibitor, significantly reduced cathepsin activity in lymphoma cell lines and patient samples. GB111-NH2 treatment increased apoptosis and caspase-3 activation in DLBCL patient cells and chronic lymphocytic leukemia (CLL) mononuclear cells. Here, we developed a modified cathepsin inhibitor, M-GB, containing a maleimide linker for site-specific antibody conjugation. While M-GB alone has poor cell permeability, when conjugated to an antibody, it forms an ADC (M-GB–ADC) that selectively induces lymphoma cell death. One M-GB–ADC demonstrated high specificity for CD74-expressing lymphoma cells while exhibiting minimal toxicity to non-target cells in vitro. Our findings highlight the potential of another M-GB–ADC as a targeted therapy for overcoming rituximab resistance and treatment failure in DLBCL. This strategy enhances therapeutic efficacy and represents a preclinical proof-of-concept treatment option by directing a cathepsin-inhibitor payload specifically to malignant B cells. Full article
(This article belongs to the Special Issue Novel Immunotherapies for Diffuse Large B-Cell Lymphoma)
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Review

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20 pages, 941 KB  
Review
Molecular Mechanisms of Resistance to Bispecific Antibodies in Diffuse Large B-Cell Lymphoma
by Nawar Maher, Bashar Al Deeban, Ndeye Marie Diop, Joelle Assaf, Riccardo Moia, Samir Mouhssine and Gianluca Gaidano
Cells 2026, 15(9), 794; https://doi.org/10.3390/cells15090794 - 27 Apr 2026
Viewed by 187
Abstract
CD20 × CD3 bispecific antibodies (BsAbs) have emerged as a meaningful therapeutic option for relapsed or refractory diffuse large B-cell lymphoma (DLBCL), redirecting endogenous T cells against malignant B cells independently of major histocompatibility complex-mediated antigen presentation, and have received regulatory approval after [...] Read more.
CD20 × CD3 bispecific antibodies (BsAbs) have emerged as a meaningful therapeutic option for relapsed or refractory diffuse large B-cell lymphoma (DLBCL), redirecting endogenous T cells against malignant B cells independently of major histocompatibility complex-mediated antigen presentation, and have received regulatory approval after at least two prior lines of therapy. However, a substantial proportion of patients experience primary resistance or early relapse, underscoring the need to characterize the underlying biological mechanisms, which are the focus of this review. Several tumor-intrinsic determinants of resistance have been identified, including CD20 loss driven by MS4A1 mutations, alternative splicing, and gene deletion, as well as genomic reprogramming involving TP53, MYC, and NOTCH1 alterations. T-cell dysfunction represents another critical resistance domain, encompassing inadequate intratumoral cytotoxic CD8+ T-cell infiltration, expansion of immunosuppressive regulatory and follicular helper T cells, progressive exhaustion with upregulation of PD-1, LAG-3, TIM-3, and TIGIT, and impaired T-cell fitness from prior treatment exposure. Microenvironmental barriers, including checkpoint ligand upregulation, PD-L1-enriched extracellular vesicles, spatial exclusion of effector cells from immune-cold germinal center-like niches, hypoxia, and metabolic competition, further reinforce immune escape. Emerging strategies to overcome resistance include epigenetic priming, checkpoint inhibitor combinations, 4-1BB costimulatory approaches, and next-generation multispecific antibody designs. Full article
(This article belongs to the Special Issue Novel Immunotherapies for Diffuse Large B-Cell Lymphoma)
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