Excited to share our study @CellCellPress introducing a novel class of macrophage-targeted immunocytokines (MiTEs) that engage myeloid, T and NK cells to boost anti-tumor immunity in solid tumors. Led by @MVLocquenghien, @PascaleZwicky & @CuriousKX (1/16) https://t.co/2z69HAdAEs

A festive start to the holiday season @WeizmannScience #Science_Park_Campus @IdoAmitLab @Elinav_Lab @ErezNeta Happy and peaceful holidays everyone!

Beautiful work from @AleksDeLab showing the crucial relationship between the immune and nervous systems and its effects on cognition and development #Neuroimmunology

New ‘al-MiTE-y’ TAM reprogramming strategy https://t.co/4cmy6wVnE2 @MVLocquenghien @PascaleZwicky @CuriousKX @idoamitlab @WeizmannScience @immunaitech

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.@MVLocquenghien, from the @idoamitlab, and collaborators developed myeloid-targeted immunocytokines and natural killer/T cell enhancers harnessing myeloid and lymphoid synergy for #immunotherapy. 📍@CellCellPress | https://t.co/SzTcVIcNf8

Save the date: #ReThinkNeuroimmunology is back in Weizmann - October 26-28 2026 🏄 Registration opening soon! Co organized with: @jonykipnis @QuintanaLabHMS @stevens1lab @RejaneRua

Now online! Macrophage-targeted immunocytokine leverages myeloid, T, and NK cell synergy for cancer immunotherapy

Myeloid-targeted TREM2 antagonism & protease-activated IL-2 prodrug rewires tumor microenvironment, enhancing CD8+ T and NK cell killing & synergy with anti-PD1 @CellCellPress @MVLocquenghien @idoamitlab @PascaleZwicky @CuriousKX @WeizmannScience https://t.co/k336mjhKRh 🇮🇱

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In a new study, published in @CellCellPress, scientists from @IdoAmitLab have developed a new, dual-action strategy for cancer immunotherapy >> https://t.co/oU8ImeKXIi

This work was a true team effort. We are deeply grateful for all contributors and collaborators, including @idoamitlab, @WeizmannScience, @Immunaitech, the editorial team @CellCellPress (16/16)

MiTEs represent next-generation, multi-axis immunotherapies, integrating TREM2 antagonism with T and NK cell activation- safely and effectively. This approach could transform treatment of ICI-resistant tumors by overcoming barriers like MHC-I loss. (15/16)

In human patient-derived tumor fragments (PDTFs) originating from renal cell carcinoma, MiTEs induced a highly conserved response and strong immune reprogramming across all cellular compartments (± αPD-1) ex vivo. (14/16)

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But what about the effector cells? Within the lymphoid compartment, we noted ↑ cytotoxic responses, ↑ T & NK proliferation, ↑ T cell stemness, ↑ NK maturation, and ↓ exhaustion. Combination with αPD-1 or αCTLA-4 further amplified these effects. (13/16)

Single-cell RNA-seq revealed profound TME remodeling after MiTE-144 treatment. In the myeloid compartment, we observed ↑ inflammatory monocytic signatures, ↑ cDC1 cross-presentation, and ↓ TREM2-linked suppressive programs. (12/16)

In transgenic hTREM2 mice, MiTE-144 preferentially accumulated in the tumor, achieved strong tumor regression, and synergized with immune checkpoint blockade. (11/16)

Our lead candidate, MiTE-144, remained completely inert to the peripheral immune system, showing no systemic cytokine activity, hepatotoxicity, or weight loss in vivo. But the key question remained: does safety come at the cost of efficacy? (10/16)

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In vitro, intact MiTEs showed no IL-2 activity, but MMP14 digestion restored their function, evidenced by a ~100× increase in STAT5 phosphorylation and robust T cell proliferation. (9/16)

We designed diverse MiTE variants, trans-acting immunocytokine prodrugs incorporating one or two IL-2 molecules masked by IL-2Rβ-derived blocking domains and linked via a protease-cleavable sequence, selected for high MMP14 specificity and cleavage efficiency. (8/16)

To achieve spatially-restricted cytokine activity, we screened proteases across 14.1M single cells (tumor, adjacent, healthy tissues & blood). MMP14 emerged as a TAM-specific, TREM2-co-expressed protease, an ideal tumor-confined molecular switch for IL-2 activation. (7/16)

…but we examined a lethal cytokine storm in vivo (IFNγ↑ IL-2↑ IL-6↑ ALT/AST↑), highlighting the challenge of safely coupling TAM modulators with cytokines due to systemic activation. (6/16)

Using an αTREM2×IL-2 molecule, we reprogrammed TAMs and potently induced IL-2 signaling in vitro… (5/16)

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