Treating autoimmune and inflammatory diseases with enhanced regulatory T-cells [electronic resource] / David Klatzmann.

By: Material type: FilmFilmPublisher number: 11002 | Henry Stewart TalksSeries: Henry Stewart talks. Biomedical & life sciences collection.Publication details: London : Henry Stewart Talks, 2022.Description: 1 online resource (1 streaming video file (54 min.) : color, sound)Subject(s): Online resources: Summary: Interleukin-2 (IL-2) is the main cytokine supporting regulatory T-cells (Tregs) development, survival and suppressive activity. However, Tregs cannot produce IL-2 and fully depend on exogenous IL-2. Treg cell therapy products are grown for weeks in culture medium containing IL-2 concentration that are 10 000-fold higher than the IL-2 serum concentration in humans. This generates "IL-2 addicted" Tregs that might not survive well and/or function optimally when reinjected in patients. We reasoned that Tregs that could produce their own IL-2 would have markedly improved therapeutic potential. ... Altogether, we believe that Treg cell products should be supported by IL-2 after injection to patients. This could be done by injecting low-dose IL-2 or advantageously by an autocrine production of IL-2 that dramatically improves the therapeutic potential of Tregs. This approach could be introduced in any form of Treg cell therapy, from polyclonal Tregs to antigen specific or targeted Tregs.
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Interleukin-2 (IL-2) is the main cytokine supporting regulatory T-cells (Tregs) development, survival and suppressive activity. However, Tregs cannot produce IL-2 and fully depend on exogenous IL-2. Treg cell therapy products are grown for weeks in culture medium containing IL-2 concentration that are 10 000-fold higher than the IL-2 serum concentration in humans. This generates "IL-2 addicted" Tregs that might not survive well and/or function optimally when reinjected in patients. We reasoned that Tregs that could produce their own IL-2 would have markedly improved therapeutic potential. ... Altogether, we believe that Treg cell products should be supported by IL-2 after injection to patients. This could be done by injecting low-dose IL-2 or advantageously by an autocrine production of IL-2 that dramatically improves the therapeutic potential of Tregs. This approach could be introduced in any form of Treg cell therapy, from polyclonal Tregs to antigen specific or targeted Tregs.

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