# Vijay Kumar Kuchroo Samuel L. Wasserstrom Professor of Neurology ![kuchroo_vijay_0.jpg](/sites/g/files/omnuum5411/files/styles/hwp_4_5__320x400/public/2024-08/kuchroo_vijay_0.jpg?itok=HKHexvWa) location\_on The Gene Lay Institute of Immunology and Inflammation BTM 10016E 60 Fenwood Road Boston, MA 02115 smartphone [617-525-5350](tel:617-525-5350) email laptop\_windows [Lab Website](https://kuchroolab.bwh.harvard.edu/) laptop\_windows [Publications](https://www.ncbi.nlm.nih.gov/myncbi/vijay.kuchroo.1/bibliography/public/) laptop\_windows [Gene Lay Institute](https://genelayinstitute.org/) In the Kuchroo laboratory, our overarching goal is elucidating the mechanisms that regulate immune functions in health, aging and different disease contexts. We focus on the functions of different CD4+ T helper subsets, and the role of costimulatory pathways in the activation and differentiation of T cells. Aside from Th1/Th2 cells, it is now appreciated that other T cell subsets – including IL-17-secreting Th17 cells, IL-9/IL-10-secreting Th9 cells, and IL-10-secreting Tr1 cells – have a major influence on tissue inflammation and autoimmunity (Schnell et al., *Cell* 2021). Our laboratory was among the first to characterize and identify factors required to induce the differentiation Th17 cells, Th9 cells and Tr1 cells from naïve T cells. Specifically, we demonstrated that a combination of pro- and anti-inflammatory cytokines, IL-6 and TGF-b, induce Th17 cell differentiation (Bettelli et al., *Nature* 2006), and that Th17 cells produce IL-21, which further amplifies the generation of Th17 cells. We also identified IL-27 as a major inducer of Tr1 cells and showed that IL-27-induced Tr1 cells suppress autoimmune inflammation. In ongoing work, we are investigating the molecular mechanisms that drive the development of Th17 and Tr1 cells by expression profiling and CRISPR-Cas9 screening of T cell differentiation (Hou et al., *Nature* 2024) in the context of infection, autoimmunity and cancer, studies which have revealed key steps in the differentiation of T cell subsets. We have a long-standing interest in immune checkpoint pathways. The identification of a negative regulator of T cell function, Tim (T cell Immunoglobulin and Mucin)-3 (Monney et al., *Nature* 2002), in our lab led to the subsequent discovery of the TIM family of molecules, including Tim-1, Tim-2, Tim-3 and Tim-4. Such immune checkpoint receptors ensure contraction of antigen-specific lymphocytes during an immune response. Defects in these immune regulators have been implicated in the pathogenesis of multiple autoimmune diseases. Conversely, we demonstrated that Tim-3 is expressed on exhausted T cells in chronic viral infections and constrains the function of tumor infiltrating lymphocytes that exhibit an exhausted phenotype. We discovered that Tim-3 expression is not limited to T cells and are currently studying how Tim-3 expressed on dendritic cells regulate the generation of stem-like T cells and T cell exhaustion in cancer and chronic viral infections. Motivated by recent human genomic studies that link Tim-3 with Alzheimer’s disease, we are exploring the role of Tim-3 and other immune checkpoint molecules in microglial cells, the immune cells of the brain (Kimura et al., *Nature* 2025). Our research also revealed that another member of the TIM family, Tim-1, acts as a checkpoint molecule in B cells, where it regulates anti-tumor immunity (Bod et al., *Nature* 2023). More recently, our research has expanded to neuroimmune interactions that regulate immune responses. We were the first to describe the immuno-modulatory role of neuropeptides, by demonstrating that Neuromeudin U (NMU) (Wallrapp et al., *Nature* 2017) promotes type II inflammation. We revealed that immune cell-derived type II cytokines, like IL-4 and IL-13, reciprocally induces the production of neuropeptides like NMU during type II inflammation at barrier sites (Barilla et al., *Science* 2025). - ## Experimental Approach [Cellular Immunology](/experimental-approach/cellular-immunology) [Genomics](/experimental-approach/genomics) [Lymphocyte Biology](/experimental-approach/lymphocyte-biology) [Molecular Immunology](/experimental-approach/molecular-immunology) [Transgenic/Knockout Animals](/experimental-approach/transgenicknockout-animals) - ## Field of Study [Autoimmunity](/field-study/autoimmunity) [Cytokines](/field-study/cytokines) [Immune Regulation](/field-study/immune-regulation) [Neuro-Immunology](/field-study/neuro-immunology) [T Cells](/field-study/t-cells) [Tolerance](/field-study/tolerance) - ## Location [The Gene Lay Institute of Immunology and Inflammation](/location/gene-lay-institute-immunology-and-inflammation) - ## Organism [Mouse](/organism/mouse) - ## People [Executive Committee of Immunology](/people/executive-committee-immunology) [Faculty](/people/faculty) [Graduate Committee of Immunology](/people/graduate-committee-immunology)