These tools will no longer be maintained as of December 31, 2024. Archived website can be found here. PubMed4Hh GitHub repository can be found here. Contact NLM Customer Service if you have questions.


Pubmed for Handhelds

PUBMED FOR HANDHELDS

Search MEDLINE/PubMed

  • Title: [Autogenic anti-idiotypic suppression of autoimmune reactions--a new approach to immunotherapy of experimental leukemia].
    Author: Ter-Grigorov VS, Krupnik VE, Etkin AF, Pivnik AV, Moskovkina OIa.
    Journal: Ter Arkh; 1985; 57(7):108-12. PubMed ID: 3863256.
    Abstract:
    Experimental Rauscher's virus erythroleukemia (RVE) was employed to study the immunologic mechanisms by which leukemia develops. Experiments were performed on inbred mice, genetically opposite to the disease induction, namely on highly sensitive BALB/c, resistant C57BL/6 and moderately sensitive BDFI animals. It is shown that RVE resistance is an immunologic phenomenon that results from the functioning of the antileukemic immune defence (ALID) aimed against the tumor-specific antigenic complex. Suppression of the ALID stems from autosuppression of the H-2 complex of the histocompatibility antigen system of T suppressors, which leads to the development of the onco-specific complex of autoimmune responses (OSCAR) and to the obligate development of RVE. The recovery of the ALID with OSCAR suppression and RVE regression is a consequence of the development of strictly specific antiidiotypic immune responses (antibodies AIT-anti-OSCAR). It is demonstrated that both passive administration of AIT-anti-OSCAR and induction of their active synthesis brings about a remission of RVE.
    [Abstract] [Full Text] [Related] [New Search]