Brianna Naizir
Research Subjects
Brianna Naizir has a total of 7 co-authors. Here are the top co-authors by number of shared publications:
- Andrea Schietinger
Immunology Program, Memorial Sloan Kettering Cancer Center, New York, NY, USA; Immunology and Microbial Pathogenesis Program, Weill Cornell Graduate School of Medical Sciences, New York, NY, USA
1 shared publication Andrew C. Scott
Immunology Program, Memorial Sloan Kettering Cancer Center, New York, USA
1 shared publication- Doron Betel
Applied Bioinformatics Core, Weill Cornell Medicine, New York, USA
1 shared publication - Joe N. Frost
Immunology Program, Memorial Sloan Kettering Cancer Center, New York, USA
1 shared publication - Joseph C. Sun
Immunology Program, Memorial Sloan Kettering Cancer Center, New York, NY, USA
1 shared publication Paul Zumbo
Department of Systems and Computational Biomedicine, Weill Cornell Medicine, New York, USA
1 shared publication
Latest Publications
- 27 February 2026
- Published by Springer Nature in Nature Immunology
- p. 1-13
TOX drives CD4+ TH1 effector function, antitumor immunity and autoimmune pathology
TOX is a nuclear factor critical for thymic development of CD4+ thymocytes, natural killer and innate lymphoid cells. In post-thymic antigen-specific CD8+ T cells, TOX is highly expressed in settings of chronic antigen encounter such as cancer and chronic infection and required for the persistence of exhausted CD8+ T cells. The role of TOX in CD4+ T cells is less clear. Here, we show that TOX is critical for CD4+ type 1 helper T (TH1) cell differentiation. Gain-of-function and loss-of-function studies show that TOX induces TH1 cell-associated molecular programs that drive TH1 cell-like phenotypes and interferon-γ production. TOX expression in CD4+ T cells from individuals with cancer was associated with increased cytotoxicity, antitumor immunity and improved responses to immunotherapy, as well as pathogenic responses in autoimmune and inflammatory diseases in mice and humans. Thus, TOX has opposing functions in CD4+ versus CD8+ T cells: while TOX is associated with CD8+ T cell exhaustion and generally with poor responsiveness to immunotherapy, in CD4+ T cells TOX drives TH1 cell fate commitment and is associated with antitumor immunity and pathogenic autoimmune responses.
- 27 February 2026
- Published by Springer Nature in Nature Immunology
- p. 1-13
TOX drives CD4+ TH1 effector function, antitumor immunity and autoimmune pathology
TOX is a nuclear factor critical for thymic development of CD4+ thymocytes, natural killer and innate lymphoid cells. In post-thymic antigen-specific CD8+ T cells, TOX is highly expressed in settings of chronic antigen encounter such as cancer and chronic infection and required for the persistence of exhausted CD8+ T cells. The role of TOX in CD4+ T cells is less clear. Here, we show that TOX is critical for CD4+ type 1 helper T (TH1) cell differentiation. Gain-of-function and loss-of-function studies show that TOX induces TH1 cell-associated molecular programs that drive TH1 cell-like phenotypes and interferon-γ production. TOX expression in CD4+ T cells from individuals with cancer was associated with increased cytotoxicity, antitumor immunity and improved responses to immunotherapy, as well as pathogenic responses in autoimmune and inflammatory diseases in mice and humans. Thus, TOX has opposing functions in CD4+ versus CD8+ T cells: while TOX is associated with CD8+ T cell exhaustion and generally with poor responsiveness to immunotherapy, in CD4+ T cells TOX drives TH1 cell fate commitment and is associated with antitumor immunity and pathogenic autoimmune responses.