gms | German Medical Science

60. Jahrestagung der Deutschen Gesellschaft für Neurochirurgie (DGNC)
Joint Meeting mit den Benelux-Ländern und Bulgarien

Deutsche Gesellschaft für Neurochirurgie (DGNC) e. V.

24. - 27.05.2009, Münster

Hematopoiesis and microglia. Immunotherapeutic options in gliomas and CNS-trauma?

Meeting Abstract

Suche in Medline nach

  • Y. Yasin - Klinik und Poliklinik für Neurochirurgie, Universitätsklinikum Münster
  • H. Wassmann - Klinik und Poliklinik für Neurochirurgie, Universitätsklinikum Münster

Deutsche Gesellschaft für Neurochirurgie. 60. Jahrestagung der Deutschen Gesellschaft für Neurochirurgie (DGNC), Joint Meeting mit den Benelux-Ländern und Bulgarien. Münster, 24.-27.05.2009. Düsseldorf: German Medical Science GMS Publishing House; 2009. DocMO.13-01

DOI: 10.3205/09dgnc089, URN: urn:nbn:de:0183-09dgnc0895

Veröffentlicht: 20. Mai 2009

© 2009 Yasin et al.
Dieser Artikel ist ein Open Access-Artikel und steht unter den Creative Commons Lizenzbedingungen (http://creativecommons.org/licenses/by-nc-nd/3.0/deed.de). Er darf vervielfältigt, verbreitet und öffentlich zugänglich gemacht werden, vorausgesetzt dass Autor und Quelle genannt werden.


Gliederung

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Objective: Hematopoiesis can be inhibited by various agents. In 1998, Wagner et al found out, that Kell (K1-) Antibodies are able to inhibit in vitro erythropoiesis, whereas RhD-antibodies are not. Later Kell antigens were found expressed on other hematopoietic cells and even on microglial cells. In cerebral gliomas of higher grade, the microglial immunological activity was found to be increased. This correlates with a faster progress and worse prognosis. In gemistocytic astrocytomas WHO grade II, which progress faster than other astrocytomas of the same grade, the microglial activity was found to be increased. This was shown by the increased expression of MHCII. Furthermore, immunomodulation with minocyclin improved the outcome of spinal and cerebral trauma in mice. An immunological inhibition of microglia with kell antibodies could open a new therapeutic option in cerebral gliomas and CNS-trauma.

Methods: Hematopoietic stem cells, isolated from patients by apheresis of peripheral venous blood after GM-CSF treatment, were cultured in semisolid methyl cellulose medium on 24-well-plates. After 6 days, the cultures were treated with K11-antibodies, normal IgG and methotrexate. The growth rate was compared by counting the BFU-E's after 14 days of culturing.

Results: The compariion between native culture, IgG-, methotrexate- and anti-K11-treated cultures revealed a significant reduction of hematopoiesis in anti-K11- treated cultures. In highly concentrated K11 antibodies, this inhibitory effect is nearly the same as the effect of methotrexate. The BFU-E counts in anti-K11 plasma treated cultures ranged between 120 and 200 per well, whereas this count was 200 to 300 in the native or normal plasma treated cultures. The BFU-E count in the methotrexate treated culture averaged 150 per well.

Conclusions: Anti-K11 antibody seems to inhibit in vitro hematopoiesis. Since microglial cells also express Kell antigens, this antibody might also inhibit microglial activity. This could provide immunotherapeutic options, downgrading gliomas and improve the outcome of their treatment. Furthermore, the treatment of neurotraumatic injuries with anti-K11 antibodies could help to inhibit inflammatory reactions and therefore improve the outcome of their treatment. One problem might be that increased apoptosis or destruction of microglial cells which might occur due to treatment with anti-Kell antibodies could increase the incidence of neurodegenerative diseases such as M. Alzheimer or Creutzfeldt-Jacob's disease.