       Document 0535
 DOCN  M9650535
 TI    Apparent bypass of negative selection in CD8+ tumours in CD2-myc
       transgenic mice.
 DT    9605
 AU    Cameron ER; Campbell M; Blyth K; Argyle SA; Keanie L; Neil JC; Onions
       DE; Department of Veterinary Pathology, University of Glasgow;
       Veterinary School, UK.
 SO    Br J Cancer. 1996 Jan;73(1):13-7. Unique Identifier : AIDSLINE
       MED/96146594
 AB    A role for antigen stimulation in lymphoid neoplasia has been postulated
       and is supported by indirect evidence that suggests that the interaction
       of antigen with both T cells and B cells may constitute an epigenetic
       event that can contribute to tumour induction or tumour progression.
       Using myc-bearing transgenic mice that develop mainly clonal T-cell
       lymphomas we have investigated the possibility that endogenous
       antigen-mediated clonal deletion might be overridden in tumorigenesis.
       CD2-myc transgenic mice were backcrossed on to a CBA/Ca background to
       ensure Mtv-mediated deletion of V beta 11-expressing T cells in the
       resultant offspring. Lymphomas arising from these mice were subsequently
       screened for V beta 11 expression. There was a clear correlation between
       the age at which mice developed neoplasia and the tumour phenotype. Mice
       with CD4- CD8+ tumours succumbed to thymic lymphoma at a significantly
       younger age than mice developing CD4+ CD8+ tumours. A small number of
       tumours consisted of the 'forbidden' V beta 11 phenotype, showing that
       cells vulnerable to transformation could escape negative selection. The
       majority of the V beta 11-positive tumours were CD4- CD8+ and were only
       observed in mice showing clinical evidence of tumour development at a
       relatively young age. The phenotype of these cells and the age at which
       tumours arose suggests that T cells escaping tolerance may be
       susceptible to transformation.
 DE    Animal  Antigens, CD2/*GENETICS  Cell Transformation,
       Neoplastic/*IMMUNOLOGY  CD4-CD8 Ratio  CD4-Positive
       T-Lymphocytes/IMMUNOLOGY  CD8-Positive
       T-Lymphocytes/*IMMUNOLOGY/PATHOLOGY  *Genes, myc  Lymphoma,
       T-Cell/GENETICS/*IMMUNOLOGY/PATHOLOGY  Mice  Mice, Inbred CBA  Mice,
       Inbred C57BL  Mice, Transgenic  Phenotype  Receptors, Antigen, T-Cell,
       alpha-beta/GENETICS/IMMUNOLOGY  Superantigens/IMMUNOLOGY  Support,
       Non-U.S. Gov't  JOURNAL ARTICLE

       SOURCE: National Library of Medicine.  NOTICE: This material may be
       protected by Copyright Law (Title 17, U.S.Code).

