Exploring the Biological Activity of a Humanized Anti-CD99 ScFv and Antibody for Targeting T Cell Malignancies.

CD99, a type I transmembrane protein, emerges as a promising therapeutic target due to its heightened expression in T cell acute lymphoblastic leukemia (T-ALL). This characteristic renders it a potential marker for minimal residual disease detection and an appealing target for antibody-based treatments. Previous studies have revealed that a mouse monoclonal antibody, mAb MT99/3, selectively binds to CD99, triggering apoptosis in T-ALL/T-LBL cells while preserving the integrity of healthy cells.

Transcriptome Analysis Reveals the Induction of Apoptosis-Related Genes by a Monoclonal Antibody against a New Epitope of CD99 on T-Acute Lymphoblastic Leukemia.

CD99 was demonstrated to be a potential target for antibody therapy on T-acute lymphoblastic leukemia (T-ALL). The ligation of CD99 by certain monoclonal antibodies (mAbs) induced T-ALL apoptosis. However, the molecular basis contributing to the apoptosis of T-ALL upon anti-CD99 mAb engagement remains elusive.

Very low concentration of lipopolysaccharide can induce the production of various cytokines and chemokines in human primary monocytes.

Objective: Lipopolysaccharide (LPS), a component of gram-negative bacteria, is a potent innate immune stimulus. The interaction of LPS with innate immune cells induces the production of proinflammatory cytokines and chemokines, thereby leading to the control of infection. In the present study, we investigated the effect of a wide range of LPS concentrations on the regulation of various proinflammatory cytokines and chemokines in human primary monocytes and T lymphocytes.