Heavenly Bodies RSVP

The purpose of the Heavenly Bodies RSVP project was to design and fabricate planet props, as well as a mechanism by which they could be raised and lowered in California Polytechnic State University’s Pavilion theater. The project team was comprised of four fourth year mechanical engineering students: Allison Turnbaugh, Braden Lockwood, Jack Boulware, and Justin Spitzer. We conducted extensive research to determine the ideal solution for the design problem brought to us by our sponsor. In our analysis, we discovered that the most important aspects of our design were the absolute reliability of the system, fire retardant material selection, and the overall aesthetics of the planets. These criteria along with our past product research allowed us to design a product that aligned with the vision of our sponsor. The system of planets was planned for use by the Music Department for the 25th installment of their annual diverse transmedia series entitled RSVP XXV: Call and Response. Sponsored by Dr. Antonio Barata, the show’s artistic director and producer, and professor in Cal Poly’s Music Department, the project featured design considerations unique to the location and nature of the production. For instance, the project had a hard completion deadline set for May 17, 2020, as stage construction would have been completed in preparation for rehearsals the following week. We determined that approximately 20 planets would be manufactured by the end of the project as well as a system to deploy them. Our objective was to make these planets safe, quiet, aesthetically pleasing, lightweight, and suitably reliable for use in the play. Though our design was unique to the needs of our sponsor, research of patented mechanisms provided inspiration for a system to raise and lower the planets. This information was utilized during ideation, which resulted in the creation of a few viable solutions, discussed later in this document. Working with our sponsor and advisor, the team finalized and tested a design, then created a structural prototype. However, due to the outbreak of COVID-19, the team was forced to forgo construction of a final product, as the production was cancelled. In response, the team devoted its remaining time to creating a set of online instructions to assist others in building and implementing the developed system

Allogeneic IgG combined with dendritic cell stimuli induce antitumour T-cell immunity.

Whereas cancers grow within host tissues and evade host immunity through immune-editing and immunosuppression, tumours are rarely transmissible between individuals. Much like transplanted allogeneic organs, allogeneic tumours are reliably rejected by host T cells, even when the tumour and host share the same major histocompatibility complex alleles, the most potent determinants of transplant rejection. How such tumour-eradicating immunity is initiated remains unknown, although elucidating this process could provide the basis for inducing similar responses against naturally arising tumours. Here we find that allogeneic tumour rejection is initiated in mice by naturally occurring tumour-binding IgG antibodies, which enable dendritic cells (DCs) to internalize tumour antigens and subsequently activate tumour-reactive T cells. We exploited this mechanism to treat autologous and autochthonous tumours successfully. Either systemic administration of DCs loaded with allogeneic-IgG-coated tumour cells or intratumoral injection of allogeneic IgG in combination with DC stimuli induced potent T-cell-mediated antitumour immune responses, resulting in tumour eradication in mouse models of melanoma, pancreas, lung and breast cancer. Moreover, this strategy led to eradication of distant tumours and metastases, as well as the injected primary tumours. To assess the clinical relevance of these findings, we studied antibodies and cells from patients with lung cancer. T cells from these patients responded vigorously to autologous tumour antigens after culture with allogeneic-IgG-loaded DCs, recapitulating our findings in mice. These results reveal that tumour-binding allogeneic IgG can induce powerful antitumour immunity that can be exploited for cancer immunotherapy

Allogeneic IgG combined with dendritic cell stimuli induce antitumour T-cell immunity.

Whereas cancers grow within host tissues and evade host immunity through immune-editing and immunosuppression, tumours are rarely transmissible between individuals. Much like transplanted allogeneic organs, allogeneic tumours are reliably rejected by host T cells, even when the tumour and host share the same major histocompatibility complex alleles, the most potent determinants of transplant rejection. How such tumour-eradicating immunity is initiated remains unknown, although elucidating this process could provide the basis for inducing similar responses against naturally arising tumours. Here we find that allogeneic tumour rejection is initiated in mice by naturally occurring tumour-binding IgG antibodies, which enable dendritic cells (DCs) to internalize tumour antigens and subsequently activate tumour-reactive T cells. We exploited this mechanism to treat autologous and autochthonous tumours successfully. Either systemic administration of DCs loaded with allogeneic-IgG-coated tumour cells or intratumoral injection of allogeneic IgG in combination with DC stimuli induced potent T-cell-mediated antitumour immune responses, resulting in tumour eradication in mouse models of melanoma, pancreas, lung and breast cancer. Moreover, this strategy led to eradication of distant tumours and metastases, as well as the injected primary tumours. To assess the clinical relevance of these findings, we studied antibodies and cells from patients with lung cancer. T cells from these patients responded vigorously to autologous tumour antigens after culture with allogeneic-IgG-loaded DCs, recapitulating our findings in mice. These results reveal that tumour-binding allogeneic IgG can induce powerful antitumour immunity that can be exploited for cancer immunotherapy

Allogeneic IgG combined with dendritic cell stimuli induce antitumour T-cell immunity

Whereas cancers grow within host tissues and evade host immunity through immune-editing and immunosuppression, tumours are rarely transmissible between individuals. Much like transplanted allogeneic organs, allogeneic tumours are reliably rejected by host T cells, even when the tumour and host share the same major histocompatibility complex alleles, the most potent determinants of transplant rejection. How such tumour-eradicating immunity is initiated remains unknown, although elucidating this process could provide the basis for inducing similar responses against naturally arising tumours. Here we find that allogeneic tumour rejection is initiated in mice by naturally occurring tumour-binding IgG antibodies, which enable dendritic cells (DCs) to internalize tumour antigens and subsequently activate tumour-reactive T cells. We exploited this mechanism to treat autologous and autochthonous tumours successfully. Either systemic administration of DCs loaded with allogeneic-IgG-coated tumour cells or intratumoral injection of allogeneic IgG in combination with DC stimuli induced potent T-cell-mediated antitumour immune responses, resulting in tumour eradication in mouse models of melanoma, pancreas, lung and breast cancer. Moreover, this strategy led to eradication of distant tumours and metastases, as well as the injected primary tumours. To assess the clinical relevance of these findings, we studied antibodies and cells from patients with lung cancer. T cells from these patients responded vigorously to autologous tumour antigens after culture with allogeneic-IgG-loaded DCs, recapitulating our findings in mice. These results reveal that tumour-binding allogeneic IgG can induce powerful antitumour immunity that can be exploited for cancer immunotherapy