CD74 (CD74 Molecule)

This study identifies S100A4+ CAFs-particularly the antigen-presenting S100A4+apCAF subset-as key components of the ROC microenvironment linked to favorable immune contexture and surgical outcomes. These findings highlight S100A4+apCAFs as potential prognostic biomarkers and immunomodulatory targets, offering new perspectives for personalized therapeutic strategies in ROC.

These findings define a UBTF/HSP90A/MIF axis linking proteostasis and cytokine signaling to immune-metabolic dysfunction and lenvatinib resistance in HCC. MIF emerges as both a mechanistic driver and a predictive biomarker, supporting prospective evaluation of therapeutic strategies combining lenvatinib-PD-1 with MIF- or HSP90A-targeted interventions to personalize TKI-ICI therapy.

Notably, heterozygosity of Nf1 within the tumor microenvironment does not cause marked changes in the immune tumor microenvironment, gene expression, or differentiation states of neoplastic cells. These data indicate that allografted HGG lines from NPcis mice are an effective model of NF1-HGG, mimicking the complexity observed in human HGG, that can be used for larger scale in vivo drug screening and evaluation.

This integrative multi-omics and experimental study identified CCL5 and CD74 as key immune-oncogenic drivers of breast cancer progression. Their modulation of the MIF-CD74 signaling axis highlights potential therapeutic targets for immunomodulatory interventions and combination therapy in breast cancer.

The deep learning framework scTenifoldXct verified the App-Cd74 axis as a significant ligand-receptor interaction. Our research provides a new perspective for in-depth understanding of the immune pathological mechanism of ICI-myocarditis and lays the foundation for the development of targeted therapeutic strategies.

Single‑cell transcriptomic analysis further supported the functional relevance of the CD74‑Pax5 axis in septic B cells. In summary, this study identifies CD74 as a critical regulator of sepsis-associated B-cell immunosuppression and highlights its therapeutic potential for immune reconstitution in sepsis.

Overexpression of CD74, CLEC7A, and IFI30 in macrophages further enhanced M2 polarization, which was associated with increased tumor-promoting functions, including enhanced invasion and reduced apoptosis in GBM cells. Together, these findings highlight the role of M2 macrophage polarization in promoting GBM progression and suggest that targeting macrophage polarization pathways may offer therapeutic potential.

In conclusion, this study suggests LY6E as a potential target for the selective imaging and therapy of TNBC, identified by transcriptomics analysis and cell line experiments. It lays the groundwork to augment clinical impact of future preclinical studies for the development of diagnostic and treatment approaches for TNBC.

Strikingly, its combination with the immune checkpoint inhibitor Nivolumab synergistically boosted antitumor immunity and reshaped the immunosuppressive TME. These findings uncover the APP-CD74 axis as a novel immunoregulatory pathway in GC and provide a nanotherapeutic strategy leveraging macrophage plasticity to overcome immune resistance and enhance immunotherapeutic efficacy.

In vivo studies confirmed that the candidate drugs targeting CD74, doxorubicin and milatuzumab, have a tendency to inhibit EMT. IGHG1+ MEC collaborate with myCAF to shape a pro-metastatic microenvironment, with the MIF-CD74/APP-CD74 interaction network serving as a driver of NSCLC brain metastasis. CD74-targeting therapies show promising clinical potential.

The brain-penetrant drug ibudilast, which prevents the binding of MIF to CD74, decreased brain metastasis in experimental models in vivo and in patient-derived organotypic cultures ex vivo in a primary tumor-agnostic manner. These findings suggest that MIF/CD74-induced reprogramming of myeloid cells in brain disorders is a vulnerability that could be exploited therapeutically against brain metastases, and possibly other brain disorders.

Functional organoid assays validate that these epithelial states exhibit differential sensitivity to tamoxifen and demonstrate that inflammatory signals can induce immune-modulatory epithelial programs. Together, our findings identify hormone signaling and immune programs as key determinants of endocrine responsiveness in breast tissue and provide a biological basis for interpreting radiologic markers relevant to cancer prevention.