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Data showing that IdeS can silence memory B-cells published in Journal of Immunology

Regulatory information
Hansa Medical AB (publ) today announced that results on IdeS effect on B-cells have been published in Journal of Immunology

The scientific article entitled “The bacterial enzyme IdeS cleaves the IgG-type of B-cell receptor, abolishes BCR-mediated cell signaling and inhibits memory B-cell activation”, by Sofia Järnum, Robert Bockermann, Anna Runström, Lena Winstedt and Christian Kjellman, shows that IdeS not only inactivates plasma IgG but also cleaves IgG present on B-cells.

Activation via the B-cell receptor on memory cells is a critical step in the development of antibody producing cells. The now published data show that IdeS cleaves the IgG-type of B-cell receptor present on human memory B-cells. The IdeS-treated cells are temporarily silenced and prevented from developing into antibody producing cells. Furthermore, the data show that IdeS cleaves the B-cell receptor in vivo in humans.

“The data are conceptually very interesting and we are very pleased that our work has been accepted in this well renowned scientific journal”, commented Hansa Medical’s CSO Christian Kjellman.

The data suggest that IdeS treatment could have therapeutic benefits not only through the degradation of plasma IgG, but it might also delay or mute the activation of memory cells. IdeS is currently being developed for the removal of donor specific antibodies in highly sensitized patients on the waiting list for kidney transplantation. In transplantation, a delay in the activation of memory B-cells and production of IgG could help the organ to accommodate in its new host. Furthermore, the concept indicates therapeutic possibilities not only in transplantation but also in other situations where a memory B-cell response must be prevented or delayed.

(See full article in Journal of Immunology at

The information in this press release is disclosed pursuant to the Securities Markets Act or the Financial Instruments Trading Act. The information was released for public disclosure on November 10, 2015, at 08.00 CET.