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Galectin-2, a human lectin binding to ß-galactoside, was found to trigger apoptosis of activated T cells and leaves naive or memory T cells unaltered. Cytokine secretion of activated T cells was significantly shifted to the Th2 profile. In vitro and in vivo data suggest a therapeutic use of Galectin-2 in bowel inflammatory diseases and CD8 mediated skin disorders or analogue diseases. 

in vitro data

Galectin-2 significantly down regulates in a dose dependent way the IFN-y and TNF-a production as well as increases the IL-5 and IL-10 secretion of activated T cells. Galectin-2 binds to the ß1-integrin of activated as well as of the resting T cells. However, the apoptosis is only selectively induced in activated T cells. Only marginal necrotic cell death is induced in activated T cells using high dosages of Galectin-2. In resting T cells the cytokine production is not modulated by Galectin-2, nor does it alter the five key regulatory proteins crucial for cell cycle progression.

Interestingly, Galectin-2 treated and activated CD8+ but not CD4+ T cells showed a significantly reduced proliferation upon T cell receptor stimulation with mitogenic antibodies. Additionally, galectin-2 exposed and activated CD8+ T cells demonstrated an increased expression of annexin V indicating that galectin-2 treatment induced apoptosis in CD8+ T cells. Importantly, the pro-apoptotic effects of galectin-2 on activated CD8+ T cells could be reversed by addition of the pan caspase-inhibitor zVAD.

in vivo data Colitis

Administration of Galectin-2 to mice with acute or chronic dextran sodium sulfate (DSS) induced colitis shows that Galectin-2 has a high potency for reducing intestinal inflammation. Mice with acute or chronic colitis were treated i.p. with either physiological NaCl as control or Galectin-2 in doses ranging from 0.5 - 2 mg/kg BW once daily, twice daily or three time daily for 10 days.

Treatment of mice with acute and chronic DSS colitis with Galectin-2 significantly reduced disease activity (as measured by disease activity index), in both acute and chronic DSS induced colitis in mice using different dosing intervals and doses. Strikingly, Galectin-2 shows with optimal dosage the same efficacy like Tacrolimus which is one of the most important immunosuppressant. Albeit, the Galectin-2 efficacy is based on apoptosis whereas the one of Tacrolimus on necrosis, which indicates less side-effects for Galectin-2.    

In vivo data Contact Allergy

Furthermore, the impact of Galectin-2 was investigated for skin disorders. Groups of mice were systemically treated with galectin-2 before sensitization to contact allergen DNFB to analyse the effects of galectin-2 on contact hypersensitivity responses (CHS).

Interestingly, upon epicutaneous immunization followed by a local challenge at the ear, galectin-2 treated mice demonstrated a significantly decreased CHS response compared to controls. Even after re-challenge with the same hapten after a 2-week interval galectin-2 injected mice mounted a reduced CHS response suggesting the induction of tolerance.    

International patent have been filed. Additional information is provided in the attached pdf.

The technology is provided by IPAL.

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IPAL GmbH
Dr. Petra Düx
petra.duex(at)ipal.de

About IPAL 

The ipal GmbH patent agency assesses and markets the inventions of scientists in the area of Life Sciences and Physics & Engineering from Charité-Universitätsmedizin (University Medicine), Robert Koch Institute, Deutsches Herzzentrum (German Heart Institute), Bundesanstalt für Materialprüfung (BAM - Federal Institute for Materials Research and Testing), the Zuse Institute as well as the Paul Ehrlich Institute, Langen and the Jacobs University Bremen. IPAL provides all of the services necessary - from the assessment of patentable technologies to a comprehensive patent protection all the way to the evaluation of sales returns potentials on the market and successful commercialisation through the use of licensing agreements.                

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