Publications by authors named "M Catucci"
T cell therapy has become a new therapeutic opportunity against solid cancers. Predicting T cell behaviour and efficacy would help therapy optimization and clinical implementation. In this work, we model responsiveness of mouse prostate adenocarcinoma to T cell-based therapies.
View Article and Find Full Text PDFAdoptive T cell therapy of solid tumors: time to team up with immunogenic chemo/radiotherapy.
Curr Opin Immunol
February 2022
Adoptive T cell therapy (ACT) with tumor-reactive lymphocytes can overcome the immune desert of poorly immunogenic tumors and instruct tumor eradication. Several hurdles limit the efficacy of this strategy against solid tumor including, but not limited to, sub optimal T cell engraftment, tumor infiltration, poor tumor antigenicity/immunogenicity, and immunosuppressive or resistance mechanisms. Recent advances indicate that concomitant treatments can be set in place to offset such barriers.
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- The thymus is vital for T cell maturation, and issues with its development can lead to severe immune problems.
- Researchers have discovered hybrid cells that can grow in the lab and recreate a functional thymus when combined with specific cells and a natural matrix from the thymus.
- This reconstructed thymus supports the development of mature T cells when transplanted into mice, highlighting potential for new treatments for immune diseases.
Article Synopsis
- Defective thymic epithelial cells (TECs) lead to issues with T-cell development, causing immunodeficiency or autoimmunity, and current treatments like HSCT and thymus transplantation are not fully effective.
- A new method for thymic regeneration is introduced, using gene-modified postnatal murine TECs to create thymic organoids in 3D collagen scaffolds that resemble the thymus structure.
- Although the organoids showed potential by growing and becoming vascularized in mice, they did not effectively support T-cell development due to limited persistence, highlighting a need for further research on this approach.
Wiskott-Aldrich Syndrome protein (WASp) regulates the cytoskeleton in hematopoietic cells and mutations in its gene cause the Wiskott-Aldrich Syndrome (WAS), a primary immunodeficiency with microthrombocytopenia, eczema and a higher susceptibility to develop tumors. Autoimmune manifestations, frequently observed in WAS patients, are associated with an increased risk of mortality and still represent an unsolved aspect of the disease. B cells play a crucial role both in immune competence and self-tolerance and defects in their development and function result in immunodeficiency and/or autoimmunity.
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