Tania Baccega

Scopus Publications

Chemical and synthetic biology tools to interrogate and control cell-cell interactions in vivo
Tania Baccega, Enrico Dotta, Giulia Pasqual
Current Opinion in Chemical Biology, 2026
Cell-cell interactions are fundamental to multicellular organisms, governing development, maintaining tissue homeostasis, and enabling responses to perturbations. Accordingly, the development of effective tools to investigate cell-cell communication in its native context is essential for addressing fundamental biological questions. In recent years, substantial progress has been made toward studying these processes directly in vivo, where cellular dynamics, tissue architecture, and environmental cues are preserved. This review discusses these in vivo advances, focusing on how chemical and synthetic biology tools enable the interrogation and control of cell- and protein-mediated communication in living organisms. We discuss the evolution of these technologies and illustrate how they are being applied to uncover general principles of cellular interaction within complex biological systems.
Dendritic cells steering antigen and leukocyte traffic in lymph nodes
Enrico Dotta, Agnieszka Katarzyna Maciola, Tania Baccega, Giulia Pasqual
FEBS Letters, 2025
Dendritic cells (DCs) play a central role in initiating and shaping the adaptive immune response, thanks to their ability to uptake antigens and present them to T cells. Once in the lymph node (LN), DCs can spread the antigen to other DCs, expanding the pool of cells capable of activating specific T‐cell clones. Additionally, DCs can modulate the dynamics of other immune cells, by increasing naïve T‐cell dwell time, thereby facilitating the scanning for cognate antigens, and by selectively recruiting other leukocytes. Here we discuss the role of DCs in orchestrating antigen and leukocyte trafficking within the LN, together with the implications of this trafficking on T‐cell activation and commitment to effector function.
Engineering of immune checkpoints B7-H3 and CD155 enhances immune compatibility of MHC-I−/− iPSCs for β cell replacement
Raniero Chimienti, Tania Baccega, Silvia Torchio, Fabio Manenti, Silvia Pellegrini, Alessandro Cospito, Angelo Amabile, Marta Tiffany Lombardo, Paolo Monti, Valeria Sordi, Angelo Lombardo, Mauro Malnati, Lorenzo Piemonti
Cell Reports, 2022
iPSC pancreatic derivatives.
Galectin-3 in Prostate Cancer Stem-Like Cells Is Immunosuppressive and Drives Early Metastasis
Sara Caputo, Matteo Grioni, Chiara S. Brambillasca, Antonella Monno, Arianna Brevi, Massimo Freschi, Ignazio S. Piras, Angela R. Elia, Valentina Pieri, Tania Baccega, Angelo Lombardo, Rossella Galli, Alberto Briganti, Claudio Doglioni, Elena Jachetti, Matteo Bellone
Frontiers in Immunology, 2020
Galectin-3 (Gal-3) is an extracellular matrix glycan-binding protein with several immunosuppressive and pro-tumor functions. The role of Galectin-3 in cancer stem-like cells (CSCs) is poorly investigated. Here, we show that prostate CSCs also colonizing prostate-draining lymph nodes of transgenic adenocarcinoma of the mouse prostate (TRAMP) mice overexpress Gal-3. Gal-3 contributes to prostate CSC-mediated immune suppression because either Gal-3 silencing in CSCs, or co-culture of CSCs and T cells in the presence of the Gal-3 inhibitor N-Acetyl-D-lactosamine rescued T cell proliferation. N-Acetyl-D-lactosamine also rescued the proliferation of T cells in prostate-draining lymph nodes of TRAMP mice affected by prostate intraepithelial neoplasia. Additionally, Gal-3 impacted prostate CSC tumorigenic and metastatic potential in vivo, as Gal-3 silencing in prostate CSCs reduced both primary tumor growth and secondary invasion. Gal-3 was also found expressed in more differentiated prostate cancer cells, but with different intracellular distribution as compared to CSCs, which suggests different functions of Gal-3 in the two cell populations. In fact, the prevalent nuclear and cytoplasmic distribution of Gal-3 in prostate CSCs made them less susceptible to apoptosis, when compared to more differentiated prostate cancer cells, in which Gal-3 was predominantly intra-cytoplasmic. Finally, we found Gal-3 expressed in human and mouse prostate intraepithelial neoplasia lesions and in metastatic lymph nodes. All together, these findings identify Gal-3 as a key molecule and a potential therapeutic target already in the early phases of prostate cancer progression and metastasis.
In vivo CRISPR editing with no detectable genome-wide off-target mutations
Pinar Akcakaya, Maggie L. Bobbin, Jimmy A. Guo, Jose Malagon-Lopez, Kendell Clement, Sara P. Garcia, Mick D. Fellows, Michelle J. Porritt, Mike A. Firth, Alba Carreras, Tania Baccega, Frank Seeliger, Mikael Bjursell, Shengdar Q. Tsai, Nhu T. Nguyen, Roberto Nitsch, Lorenz M. Mayr, Luca Pinello, Mohammad Bohlooly-Y, Martin J. Aryee, Marcello Maresca, J. Keith Joung
Nature, 2018
Nicotinic acid timed to feeding reverses tissue lipid accumulation and improves glucose control in obese Zucker rats
Tobias Kroon, Tania Baccega, Arne Olsén, Johan Gabrielsson, Nicholas D. Oakes
Journal of Lipid Research, 2017
Nicotinic acid (NiAc) is a potent inhibitor of lipolysis, acutely reducing plasma free fatty acid (FFA) concentrations. However, a major FFA rebound is seen during rapid NiAc washout, and sustained exposure is associated with tolerance development, with FFAs returning to pretreatment levels. Our aim was to find a rational NiAc dosing regimen that preserves FFA lowering, sufficient to reverse nonadipose tissue lipid accumulation and improve metabolic control, in obese Zucker rats. We compared feeding-period versus fasting-period NiAc dosing for 5 days: 12 h subcutaneous infusion (programmable, implantable mini-pumps) terminated by gradual withdrawal. It was found that NiAc timed to feeding decreased triglycerides in liver (−47%; P < 0.01) and heart (−38%; P < 0.05) and reduced plasma fructosamine versus vehicle. During oral glucose tolerance test, plasma FFA levels were reduced with amelioration of hyperglycemia and hypertriglyceridemia. Furthermore, timing NiAc to feeding resulted in a general downregulation of de novo lipogenesis (DNL) genes in liver. By contrast, NiAc timed to fasting did not reduce tissue lipids, ameliorate glucose intolerance or dyslipidemia, or alter hepatic DNL genes. In conclusion, NiAc dosing regimen has a major impact on metabolic control in obese Zucker rats. Specifically, a well-defined NiAc exposure, timed to feeding periods, profoundly improves the metabolic phenotype of this animal model.
Differential induction of Ly6G and Ly6C positive myeloid derived suppressor cells in chronic kidney and liver inflammation and fibrosis
Bastian Höchst, Julita Mikulec, Tania Baccega, Christina Metzger, Meike Welz, Julia Peusquens, Frank Tacke, Percy Knolle, Christian Kurts, Linda Diehl, Isis Ludwig-Portugall
Plos One, 2015
CD11b+Gr1+ myeloid derived suppressor cells (MDSC) are known to be very potent suppressors of T cell immunity and can be further stratified into granulocytic MDSC and monocytic MDSC in mice based on expression of Ly6G or Ly6C, respectively. Here, using these markers and functional assays, we aimed to identify whether MDSC are induced during chronic inflammation leading to fibrosis in both kidney and liver and whether additional markers could more specifically identify these MDSC subsets. In an adenine-induced model of kidney inflammation/fibrosis suppressive Ly6Gpos MDSC were induced. The suppressive function within the Ly6G+ MDSC population was exclusively present in IFNγRβ expressing cells. In contrast, in chronic inflammation in the liver induced by bile duct ligation, suppressive capacity was exclusively present in the Ly6Cpos MDSC subset. Gene expression analyses confirmed the differential origins and regulation of those MDSC subsets. Additionally, depletion of MDSC in either kidney or liver fibrosis enhanced fibrosis markers, indicating a protective role for MDSC in organ fibrosis. Thus, our data demonstrate that during liver inflammation and kidney fibrosis MDSC with similar function arise bearing a distinct marker profile and arising from different cell populations.