ICAM1 overexpression

Consistently, CD4 T cells from moderate-to-severe SLE patients with high ICAM-1 expression mediated less IgG production after T-B coculture. Therefore, ICAM-1-mediated human CD4 T-B cell adhesion provides dual roles on B cell differentiation and IgG production partially depending on expression levels of PD-1 on B cells, supporting cell adhesion and subsequent PD-1 induction as an alternative intrinsic checkpoint for B cell differentiation.

LINC02193, a novel lncRNA identified in AAV could function as competing endogenous RNAs (ceRNA) for miR-485-5p to promote ICAM1 expression and neutrophils activation, suggesting its potential as a therapeutic target of AAV.

Conclusions T cell-depleted allo-HSCT can be a viable treatment platform for treating relapsed NBL when combined with adoptive transfer of ex-vivo-stimulated NK cells and TIM 3 checkpoint blockade. These studies demonstrate that multi-modal approaches incorporating combination immunotherapy are needed for NBL and that immunotherapies that enhance NK cell function should be prioritized.

Immunohistochemistry results on clinical specimens showed that higher fibrinogen levels, higher ICAM1 expression, higher blood vessel density, and higher macrophage levels were present simultaneously. Collectively, this study indicates fibrinogen promotes metastasis and extravasation by inducing ICAM1 expression to enhance tumor cell migration, cell adhesion, transendothelial migration and promote angiogenesis and increase vascular endothelial permeability.

This work highlights the importance of CAR T cell binding avidity and adhesion for optimal cytotoxicity. Better understanding of CAR T cell function will inform future construct design for successful therapies against solid tumors.

The CAR T cells are engineered to co-express somatostatin receptor 2 (SSTR2), which allows for the tracking of CAR T cells in vivo via PET/CT scan using FDA-approved DOTATATE. AIC100 was generated by affinity tuning the I-domain of LFA-1, the physiological ligand to ICAM-1... We have developed affinity tuned CAR T cells designed to selectively target ICAM-1 overexpressing tumor cells and to spatiotemporally image CAR T cells. Near-synchronous FDG and DOTATATE scans will enhance patient safety by early detection of off-tumor CAR T activity and validation of tumor response. We anticipate that our “tune and track” technology will be widely applicable to developing potent yet safe CAR T cells against hard-to-treat solid cancers.

AIC1010 CAR T cells demonstrate superior cancer elimination compared to AIC100 CAR T cells in subcutaneous and IP tumor models in mice. We anticipate that cytokine delivery, paired with our “Tune & Track” technology will be widely adaptable to develop potent and safe affinity-tuned CAR T cells against hard-to-treat solid cancers.

Exosomal ICAM1 is the key molecule regulated by RelB, which increased the aggressiveness of DU145. The study suggests that cell-cell communication via exosomal ICAM1 is a novel mechanism by which RelB promotes PC progression.

In lung tissues, the activation of NF-κB pathway and the expression of its downstream genes (ICAM-1, VCAM-1, and E-selectin) were decreased by dauricine, consistent with what was found in vitro. In summary, we concluded that dauricine could alleviate endothelial inflammation by suppressing NF-κB pathway, which might serve as an effective candidate for diseases related with endothelial inflammation.

Trial Registration NCT04420754 IRB number 19-12021154IACUC (animal welfare): All animal experiments were performed in accordance with the National Institute of Health’s Guide for the Care and Use of Laboratory Animals. Animal handling protocols were approved by the Institutional Laboratory Animal Use and Care Committee of Weill Cornell Medicine (Permit Number: 2012–0063).