CIITA (Class II Major Histocompatibility Complex Transactivator)

Our study identifies an IFN-γ/STAT1/CIITA axis as the central regulator of MHC-II expression in fibroblasts and reveals IL-1β as a potent suppressor of this pathway. These findings highlight a novel cytokine-mediated regulatory mechanism underlying CAF-driven immunosuppression within the tumor microenvironment.

Further experiments confirmed that CIITA knockdown decreased BMDM surface MHC-II expression, whereas CIITA overexpression rescued MHC-II expression in SerpinB9-knockout BMDMs and restored their capacity to induce Th1 cell differentiation. In conclusion, this study demonstrates that under WGP induction, SerpinB9 regulates macrophage MHC-II expression and Th1 differentiation-inducing ability by maintaining CIITA expression, providing new insights into macrophage immune regulation mechanisms.

T-cell exhaustion and menin-KMT2A binding to genes encoding for negative regulators of T-cell activation were reduced by menin-inhibition. These findings indicate that menin-inhibition enhances the GVL-effect via the HERV/MHC-II axis in AML cells and promotes cytotoxicity of donor T-cells, which provides a rationale for a clinical trial using menin-inhibition as maintenance after allo-HCT.

Overexpressed CIITA promoted ferroptosis and inhibited gastric cancer growth by upregulating ACSL4. CIITA may be a potential therapeutic target for gastric cancer and may have certain predictive value in future clinical applications.

Cell-free DNA analysis in follicular lymphoma may become a complementary approach, overcoming the limitations of assessing disease status from single biopsy sites. Further studies will examine the usefulness of cell-free DNA in predicting disease progression in follicular lymphoma.

A prognostic nomogram incorporating CIITA expression shows robust predictive value for overall survival, offering potential clinical utility. These findings highlight CIITA as a promising prognostic biomarker and immunomodulatory target in breast cancer, shedding light on its role in shaping the tumor immune microenvironment.

On-treatment CCL5 plasma levels were increased only in patients with long progression-free survival, and pre-treatment secretomics identified cytokines related to myeloid cells significantly associated with poor prognosis. In summary, combining Dasa with immunotherapy represents a strategy to treat SCLC, with CCL5 as a cytokine that could serve to monitor response.

By concurrently targeting MYC and multiple PRMTs, 3-alkenylindol-2-one overcomes the limitations of single-target therapies, offering a novel strategy to suppress proliferation and promote antitumor immunity in AML. These findings establish PRMTs as critical downstream mediators of MYC-driven leukemogenesis and position 3-alkenylindol-2-one as a promising clinical candidate for AML treatment, providing a mechanism-based approach to target MYC-driven leukemia through its downstream epigenetic regulators.

RCOR2 loss potentiated anti-PD-1 therapy in mouse models of cancer and correlated with better response to anti-PD-1 therapy in human patients. Collectively, these findings uncover a "two birds with one stone" effect for RCOR2, highlighting its potential as a valuable target for improved cancer therapy.

A retrospective, single-center study included 254 newly diagnosed PMBCL patients treated with rituximab, dose-adjusted etoposide, prednisone, vincristine, cyclophosphamide, doxorubicin (R-DA-EPOCH), rituximab, modified protocol NHL-BFM-90 (RmNHL-BFM-90), or R-DA-EPOCH combined with nivolumab. Incorporating nivolumab into the R-DA-EPOCH regimen as a first-line therapy has shown potential in reducing adverse prognostic factors. These findings suggest that high-risk patients may benefit significantly from the early incorporation of ICIs into their treatment plans.

Astragalus antagonized the therapeutic effect of anti-PD-1 in melanoma. These effects were partially through inhibiting JAK/STAT signaling and down-regulating MHC-II expression.

In tumor cells, silencing MAP1LC3C inhibits CIITA expression and suppresses HLA class II production. These findings suggest that cancer cells are selected for low MAP1LC3C expression to evade efficient immune responses.