K. M. Khanna

Tumor-intrinsic LKB1-LIF signaling axis establishes a myeloid niche to promote immune evasion and tumor growth

This study identifies a LKB1-LIF signaling axis in tumors that promotes immune evasion by reprogramming myeloid cells, and shows that inhibiting LIF signaling reduces tumor growth.

Glutamine antagonist DRP-104 suppresses tumor growth and enhances response to checkpoint blockade in KEAP1 mutant lung cancer

This study shows that DRP-104, a glutamine antagonist, suppresses KEAP1 mutant lung tumor growth and enhances response to checkpoint blockade by inhibiting glutamine metabolism and improving T cell function.

Single-cell analysis of CX3CR1+ cells reveal a pathogenic role for BIRC5+ myeloid proliferating cells driven by Staphylococcus aureus leukotoxins

The paper identifies BIRC5+ myeloid cells as pathogenic during S. aureus infection using scRNA-seq and genetic fate mapping.

A neonatal mouse model characterizes transmissibility of SARS-CoV-2 variants and reveals a role for ORF8

This study establishes a neonatal mouse model to study SARS-CoV-2 transmissibility, showing variant differences in infectious shedding and identifying ORF8's role in transmission.

MAVS signaling is required for clearance of chikungunya heart infection and prevention of chronic inflammation in vascular tissue

This study investigates CHIKV-induced heart disease using mouse models and human cells, showing MAVS signaling is critical for viral clearance and preventing chronic vascular inflammation.

KEAP1 mutation in lung adenocarcinoma promotes immune evasion and immunotherapy resistance

This study shows KEAP1 mutations in lung adenocarcinoma lead to immune evasion by reducing dendritic cell and T cell responses, contributing to immunotherapy resistance.

Ketogenesis restrains aging-induced exacerbation of COVID in a mouse model

This study shows that a ketogenic diet reduces inflammation and improves outcomes in aged mice infected with a coronavirus, suggesting potential therapeutic benefits for elderly COVID-19 patients.

Serum Amyloid A Proteins Induce Pathogenic TH17 Cells and Promote Inflammatory Disease

This study shows serum amyloid A proteins drive pathogenic TH17 cell differentiation and promote inflammatory disease through STAT3-activating cytokines.