Equillium to Present Poster at 2024 American Association of Immunologists Annual Meeting
Equillium, Inc., a biotechnology company focused on developing therapeutics for severe autoimmune and inflammatory disorders, recently presented a poster at the IMMUNOLOGY2024 annual meeting hosted by The American Association of Immunologists. The event took place at the McCormick Place Convention Center in Chicago from May 3 to May 7.
The presentation highlighted new data on CD6, a molecule that plays a crucial role in cell adhesion and migration. CD6 facilitates these processes through its interactions with activated leukocyte cell adhesion molecule (ALCAM) and by stabilizing the cell membrane protein VLA4. The study demonstrated that itolizumab, a monoclonal antibody developed by Equillium, can disrupt these interactions and reduce the migration of effector T cells across endothelial cells.
Dr. Stephen Connelly, Equillium’s chief scientific officer, emphasized the significance of these findings. He noted that the data provided deeper insights into the molecular mechanisms by which CD6 contributes to the migration of pathogenic effector T cells into inflamed tissues. Importantly, it was shown that itolizumab could modulate not only the activity of these T cells but also their movement.
The poster, titled "Surface CD6 regulates T cell adhesion and migration through direct ligand interaction and stabilization of VLA4," was presented by Valeria Marrocco, a senior scientist at Equillium. It detailed several key findings:
- Itolizumab blocks CD6 from binding to ALCAM and induces the removal of CD6 from T cells' surfaces when antigen-presenting cells are present, leading to CD6-low T cells.
- Reducing CD6 on T cells or blocking ALCAM on human umbilical vein endothelial cells (HUVEC) prevents effector T cells from adhering to the endothelial layer.
- Itolizumab significantly decreases the trans-endothelial migration of pathogenic T cells. This reduction correlates strongly with the levels of CD6 on the cell surface.
- Treatment with itolizumab also reduces the expression of genes important for cell motility and lowers the levels of VLA4 integrin on the cell surface and in total protein content.
The data underscored a novel role for the CD6-ALCAM pathway in the adhesion and migration of effector T cells. It revealed that CD6 expression is necessary for the stabilization of VLA4 integrin, which suggests that the CD6-ALCAM pathway directly influences T cell mobility and indirectly regulates it through VLA4 downregulation.
About Itolizumab
Itolizumab is a first-in-class monoclonal antibody designed to target the CD6-ALCAM signaling pathway. This pathway is crucial in regulating the activity and movement of T cells involved in immuno-inflammatory diseases. Itolizumab selectively downregulates pathogenic T effector cells while preserving T regulatory cells, which are essential for maintaining immune balance.
About Equillium
Equillium is a clinical-stage biotechnology firm dedicated to developing innovative treatments for severe autoimmune and inflammatory conditions. Their pipeline includes various novel immunomodulatory assets:
- EQ101, a tri-specific cytokine inhibitor targeting IL-2, IL-9, and IL-15, is in Phase 2 clinical trials for alopecia areata.
- EQ302, an orally delivered bi-specific cytokine inhibitor targeting IL-15 and IL-21, is in pre-clinical development.
- A multi-cytokine platform that creates composite peptides to selectively block key cytokines at the receptor level, targeting pathogenic redundancies while preserving non-pathogenic signaling.
- Itolizumab, under evaluation in a Phase 3 study for acute graft-versus-host disease and recently completed a Phase 1b study for lupus/lupus nephritis.
Equillium acquired itolizumab rights through an exclusive partnership with Biocon Limited and a strategic partnership with Ono Pharmaceutical Co., Ltd., aiming to develop and commercialize the antibody.
These advancements highlight Equillium's commitment to addressing significant unmet medical needs in autoimmune and inflammatory disorders through innovative therapeutic strategies.
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