SIRPA (Signal Regulatory Protein Alpha)

These findings suggest that 1B2-10 demonstrates a favorable efficacy and safety profile, indicating great therapeutic potential for cancer. Based on these studies, 1B2-10 has been renamed as DS003 and is currently advancing through Phase I clinical trials in China to further evaluate its safety profile and preliminary efficacy in human subjects.

Our study presents the discovery of an anti-CD47/CD24 bispecific antibody that offers a promising therapeutic strategy to address the challenges associated with both the efficacy and safety of CD47-targeting agents, offers insight into macrophage-driven cancer immunotherapy, and could potentially provide a therapeutic option for patients non-responsive to immunotherapy.

The GEMs also improved the efficacy of ICIs in the ICI-resistant gene engineering tumor models and demonstrated significant anti-tumor efficacy in the metastasis models. Our study showed the potential clinical application of GEMs in the treatment of tumors.

The cytotoxic T cells in pRMS bear markers of exhaustion (LAG3, HAVCR2, EOMES), and the macrophages express myeloid checkpoint-related genes (SIGLEC1, SIRPA, CSF1R, HAVCR2). This transcriptomic data suggests that targeting MIF and APP signaling in pRMS may have therapeutic potential; however, studies on multiple-patient cohorts, protein verification, and in vitro and in vivo validation are still needed for clinical actionability.

In this Review, we examine the evidence supporting phagocytic checkpoints as targets for cancer therapy, while highlighting current challenges associated with this therapeutic strategy. We also offer recommendations for enhancing the efficacy and safety of this approach in future work.

Our synthesis provides an appraisal of reproducible communication architectures in glioma and outlines pragmatic reporting standards and trial-ready pharmacodynamic endpoints for myeloid-informed precision immuno-oncology. We hope these insights will assist researchers and clinicians as they design multi-omics pipelines and interventions to convert suppressive ecosystems into responsive ones.

SIRPα is robustly expressed in monocyte/macrophage lineages within human sarcoidosis tissues, and inhibition of SIRPs (ELA026) suppresses sarcoidosis granuloma formation by preventing macrophage adhesion/aggregation.

Although NDV-mediated CD47 blockade resulted in increased numbers of PD-1+ CD8 T cells, synergy between NDV, CD47, and PD-L1 blockade was limited. Together these data highlight the importance of considering tumor-intrinsic factors when combining cancer immunotherapies for improved outcomes.

Our results establish a proof-of-concept for this dual-function nanovesicle approach, highlighting its potential to engage both adaptive and innate immunity synergistically. The BITE platform offers a versatile and targeted strategy to overcome immune resistance in cancer, representing a promising therapeutic avenue in biomedical engineering and nanomedicine.

In 4T1 murine breast cancer models, Ir1-PDT achieves potent tumor suppression and transforms immunologically "cold" tumors into "hot" lesions through the synergistic interplay of ICD and CD47 pathway disruption. Collectively, this work establishes a photodynamic CD47-signaling platform for precise immune modulation, offering a clinically translatable alternative to conventional CD47-targeting therapies.

Our model predicts an optimal RT dose (6 to 8 Gy) for maximizing ICD, a dose-dependent abscopal effect, and a hierarchy of treatment efficacy, with SIRP[Formula: see text]-knockout macrophages exhibiting the strongest tumoricidal activity. These findings provide a quantitative framework for designing more effective combination therapies, leveraging ICD to enhance immune checkpoint inhibition and radiotherapy synergy.

These novel combination strategies aim to overcome resistance to single-agent checkpoint inhibitors, while research explores monoclonal antibodies, bispecific antibodies, and antibody-drug conjugates (ADCs) within biomarker-driven personalized treatment frameworks. The ultimate goal is to improve survival and quality of life for TNBC patients through tailored immunotherapies.