Immunotherapy clinical trials have shown promising results only in some glioblastoma patients, warranting further research on glioblastoma-induced immune suppression. Cancer-driven changes in glycosylation are beginning to be appreciated as key modulators of cancer immune evasion, since antigen-presenting cells express glycan-recognizing receptors that trigger immune suppressive signalling upon interaction with their ligands.
In a new study that is released today, the Immune System CytOMICs group, led by Dr. Garcia Vallejo (Dept. Molecular Cell Biology & Immunology) has identified a glycan signature as a modulator of immune suppression in glioblastoma via the tolerogenic receptor MGL. Using an orthotopic glioblastoma in vivo model and state-of-the-art high-dimensional immunophenotyping methods, they showed that overexpression of the MGL-ligand in glioblastoma led to increased infiltration of PD-L1+ macrophages, which could also be found in patient-derived glioblastoma tissues.
An improved understanding of the glioblastoma glyco-code will lead to new prognostic and therapeutic clinical applications. This project is the result of a long-standing partnership between the Departments of Molecular Cell Biology & Immunology and NeuroSurgery and has also involved prestigious collaborators, such as Xandra Breakefield (Massachussets General Hospital, Boston) and Gabriel Rabinovich (IBYME, CONICET, Buenos Aires).
You can find the article here: Dusoswa SA et al. Proc Natl Acad Sci U S A, in press.