Rakesh Rudraboina
Current Organizations / Institutes
The organizations/institutes from the scholar's latest article
Previous Organizations / Institutes
The organizations / institutes from the scholar's other articles in the past ten years
Research Subjects
Rakesh Rudraboina has a total of 10 co-authors. Here are the top co-authors by number of shared publications:
- Alyssa Rocha
Department of Experimental Medicine, Dana-Farber Cancer Institute, Boston, Massachusetts, USA
1 shared publication - Ayse Ece Gulen
Department of Child Health, University of Missouri, Columbia, USA
1 shared publication - Esma S. Yolcu
Department of Pediatrics Department of Molecular Microbiology and Immunology NextGen Precision Health Institute University of Missouri Columbia USA
1 shared publication - Eva Guinan
DF/CH Hematopoietic Stem Cell Transplant Program, Dana-Farber Cancer Institute, USA
1 shared publication - Haval Shirwan
Department of Molecular Microbiology and Immunology, Department of Pediatri, NextGen Precision Health Institute, Ellis Fischel Cancer Center, University of Missouri, Columbia, United States of America
1 shared publication - Laura Contreras-Ruiz
Department of Experimental Medicine, Dana-Farber Cancer Institute, Boston, Massachusetts, USA
1 shared publication
Latest Publications
- Open Access
- 9 July 2024
- Published by Elsevier in American Journal of Transplantation
- Vol. 24 (11) , 1968-1978
Allostimulation leads to emergence of a human B cell population with increased expression of HLA class I antigen presentation–associated molecules and the immunoglobulin receptor FcRL5
- 9 July 2024
- Published by Elsevier in American Journal of Transplantation
- Vol. 24 (11) , 1968-1978
Open AccessAllostimulation leads to emergence of a human B cell population with increased expression of HLA class I antigen presentation–associated molecules and the immunoglobulin receptor FcRL5
- 22 August 2023
- Published by Springer Nature in Cancer Immunology, Immunotherapy
- Vol. 72 (11) , 3567-3579
A novel agonist of 4-1BB costimulatory receptor shows therapeutic efficacy against a tobacco carcinogen-induced lung cancer
Immunotherapy utilizing checkpoint inhibitors has shown remarkable success in the treatment of cancers. In addition to immune checkpoint inhibitors, immune co-stimulation has the potential to enhance immune activation and destabilize the immunosuppressive tumor microenvironment. CD137, also known as 4-1BB, is one of the potent immune costimulatory receptors that could be targeted for effective immune co-stimulation. The interaction of the 4-1BB receptor with its natural ligand (4-1BBL) generates a strong costimulatory signal for T cell proliferation and survival. 4-1BBL lacks costimulatory activity in soluble form. To obtain co-stimulatory activity in soluble form, a recombinant 4-1BBL protein was generated by fusing the extracellular domains of murine 4-1BBL to a modified version of streptavidin (SA-4-1BBL). Treatment with SA-4-1BBL inhibited the development of lung tumors in A/J mice induced by weekly injections of the tobacco carcinogen NNK for eight weeks. The inhibition was dependent on the presence of T cells and NK cells; depletion of these cells diminished the SA-4-1BBL antitumor protective effect. The number of lung tumor nodules was significantly reduced by the administration of SA-4-1BBL to mice during ongoing exposure to NNK. The data presented in this paper suggest that utilizing an immune checkpoint stimulator as a single agent generate a protective immune response against lung cancer in the presence of a carcinogen. More broadly, this study suggests that immune checkpoint stimulation can be extended to a number of other cancer types, including breast and prostate cancers, for which improved diagnostics can detect disease at the preneoplastic stage.
- 22 August 2023
- Published by Springer Nature in Cancer Immunology, Immunotherapy
- Vol. 72 (11) , 3567-3579
A novel agonist of 4-1BB costimulatory receptor shows therapeutic efficacy against a tobacco carcinogen-induced lung cancer
Immunotherapy utilizing checkpoint inhibitors has shown remarkable success in the treatment of cancers. In addition to immune checkpoint inhibitors, immune co-stimulation has the potential to enhance immune activation and destabilize the immunosuppressive tumor microenvironment. CD137, also known as 4-1BB, is one of the potent immune costimulatory receptors that could be targeted for effective immune co-stimulation. The interaction of the 4-1BB receptor with its natural ligand (4-1BBL) generates a strong costimulatory signal for T cell proliferation and survival. 4-1BBL lacks costimulatory activity in soluble form. To obtain co-stimulatory activity in soluble form, a recombinant 4-1BBL protein was generated by fusing the extracellular domains of murine 4-1BBL to a modified version of streptavidin (SA-4-1BBL). Treatment with SA-4-1BBL inhibited the development of lung tumors in A/J mice induced by weekly injections of the tobacco carcinogen NNK for eight weeks. The inhibition was dependent on the presence of T cells and NK cells; depletion of these cells diminished the SA-4-1BBL antitumor protective effect. The number of lung tumor nodules was significantly reduced by the administration of SA-4-1BBL to mice during ongoing exposure to NNK. The data presented in this paper suggest that utilizing an immune checkpoint stimulator as a single agent generate a protective immune response against lung cancer in the presence of a carcinogen. More broadly, this study suggests that immune checkpoint stimulation can be extended to a number of other cancer types, including breast and prostate cancers, for which improved diagnostics can detect disease at the preneoplastic stage.