Welcome to the Salomon Research Group
Welcome to the Salomon Laboratory
We uncover how immune cells and their targets reshape one another.
The Salomon Laboratory combines mechanistic biochemistry with quantitative phosphoproteomics to discover hidden feedback, pathway crosstalk, and unexpected signaling consequences in T cells, CAR T cells, and cancer-relevant target cells.
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How are signals controlled?
We define feedback, phosphatase control, and pathway crosstalk that set immune-cell activation thresholds.
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What changes during cell contact?
We measure signaling in both engineered immune cells and their targets to reveal responses hidden by one-cell-at-a-time analysis.
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Which mechanisms matter?
We connect quantitative phosphorylation networks to cell behavior so that molecular detail can inform safer immune therapies.
Latest published discovery Science Signaling
CAR target cells are active participants
Most CAR studies ask what the engineered T cell does. Our recent study asks what happens inside the contacted target cell. Cell-of-origin phosphotyrosine proteomics shows that a CSF1R-directed CAR triggers CSF1R-like signaling in THP-1 target cells, whereas CD19-CAR contact does not produce the same signaling response in Raji targets.
- The target signals: CSF1R Tyr723 and downstream ERK phosphorylation increase after CSF1R-CAR contact.
- The mechanism is target-cell intrinsic: the response requires CSF1R kinase activity but not T-cell Lck activity or actin polymerization.
- Cell ratio changes the outcome: target-rich conditions promote THP-1 growth, whereas effector-rich conditions produce target-cell lysis.
Read the Science Signaling paper (opens in a new tab)
View in PubMed (opens in a new tab)
Text description of CAR target-cell diagram
Overall structure: The diagram reads from left to right as the number of CSF1R-CAR T cells per target cell increases. Rose circles represent CAR T cells, gold circles represent CSF1R-positive target cells, and an arrow along the bottom shows the increasing effector-to-target ratio.
- Target-rich contact, low effector-to-target ratio
- A CAR T cell contacts a target cell and activates CSF1R phosphotyrosine signaling. Under these target-rich conditions, the observed outcome is target-cell growth.
- The target is not passive
- Cell-of-origin phosphoproteomics separates signals from the two cell types. Target-cell signaling requires the kinase activity of CSF1R. T-cell Lck activity and actin polymerization are not required for this response.
- Effector-rich contact, high effector-to-target ratio
- Multiple CAR T cells contact a target cell. Under these effector-rich conditions, the observed outcome shifts to target-cell lysis.
CSF1R Low Ratio
A musical take on the target-cell response.
Music created with Suno.com.
