Targeting of Cdc42 GTPase in regulatory T cells unleashes antitumor T-cell immunity.

Background: Cancer immunotherapy has taken center stage in cancer treatment. However, the current immunotherapies only benefit a small proportion of patients with cancer, necessitating better understanding of the mechanisms of tumor immune evasion and improved cancer immunotherapy strategies. Regulatory T (Treg) cells play an important role in maintaining immune tolerance through inhibiting effector T-cell function.

Graded RhoA GTPase Expression in Treg Cells Distinguishes Tumor Immunity From Autoimmunity.

RhoA of the Rho GTPase family is prenylated at its C-terminus. Prenylation of RhoA has been shown to control T helper 17 (Th17) cell-mediated colitis. By characterizing T cell-specific RhoA conditional knockout mice, we have recently shown that RhoA is required for Th2 and Th17 cell differentiation and Th2/Th17 cell-mediated allergic airway inflammation.

Emergence of livestock-associated MRSA ST398 from bulk tank milk, China.

Objectives: To detect livestock-associated MRSA (LA-MRSA) ST398 from bulk tank milk in China and to determine the phenotypic and genomic characteristics of the strains.

Methods: LA-MRSA ST398 strains were isolated from bulk tank milk samples in Shanghai and their susceptibilities to antimicrobials were determined using the broth dilution method. Genomic characterization of MRSA ST398 strains was performed by WGS and their evolutionary relationships were assessed by phylogenetic analysis.

Rational Targeting of Cdc42 Overcomes Drug Resistance of Multiple Myeloma.

Multiple myeloma (MM) drug resistance highlights a need for alternative therapeutic strategies. In this study, we show that CASIN, a selective inhibitor of cell division cycle 42 (Cdc42) GTPase, inhibited proliferation and survival of melphalan/bortezomib-resistant MM cells more profoundly than that of the sensitive cells. Furthermore, CASIN was more potent than melphalan/bortezomib in inhibiting melphalan/bortezomib-resistant cells.

Ablation of RhoA impairs Th17 cell differentiation and alleviates house dust mite-triggered allergic airway inflammation.

Asthma is a heterogeneous chronic airway inflammation in which Th2 and Th17 cells are key players in its pathogenesis. We have reported that RhoA of Rho GTPases orchestrated glycolysis for Th2 cell differentiation and allergic airway inflammation by the use of a conditional RhoA-deficient mouse line. However, the role of RhoA in Th17 cells remains to be elucidated.