Transfection of genes for human cell surface antigens identified by monoclonal antibodies.

Six murine L cell lines expressing five different human cell surface antigens have been prepared by DNA-mediated gene transfer. Ltk- cells were transfected with calcium phosphate co-precipitates of human genomic DNA and a plasmid containing the Herpes simplex thymidine kinase gene. After HAT selection, transfectants expressing specific cell surface antigens were identified by in situ immune rosetting using monoclonal antibodies. In this way, transfected cell lines expressing the CD9 antigen, the CD31 antigen (two lines), a unique platelet antigen, an X-linked antigen (R1), and a previously unreported monocyte antigen 11D1 were prepared. These cell lines have proved useful in the definitive assignment of monoclonal antibodies to specific CD groups. In addition, they provide a source of mRNA for use in expression cloning of the genes for these antigens.

Requirements for the stimulation of allogeneic T lymphocytes by acute non-lymphoblastic leukaemia cells.

Blast cell populations from 32 patients with acute non-lymphoblastic leukaemia of various morphological types have been examined for their ability to stimulate allogeneic T lymphocytes from normal donors in one-way mixed leucocyte culture (MLC). At the same time, these leukaemic cell populations were examined for the amounts of major histocompatibility complex Class I and Class II antigens they expressed, and their ability to release interleukin 1 (IL1) in culture both with and without stimulation by lipopolysaccharide. The abilities of the leukaemic cell populations to stimulate in MLC, and to produce IL1, were found to be associated with the expression of morphological characteristics of monocytic differentiation, and correlated significantly. In contrast, no correlation was observed between the extent of Class I or Class II expression and MLC stimulatory ability. Many myeloblast populations of immature phenotype were unable to stimulate allogeneic T cells despite their strong expression of these antigens. This lack of stimulatory ability was not overcome by the addition of exogenous IL1. We therefore conclude that the correlation between the production of IL1 and MLC stimulatory ability does not necessarily imply a cause/effect relationship, and that the interaction between allo-antigen and the T cell receptor together with a supply of lymphokine 'co-stimulator' is not sufficient to activate resting T lymphocytes. The failure of some Class I and II antigen positive leukaemic blasts to stimulate in MLC even in the presence of exogenous IL1 may be due to the lack of other differentiation-associated cell surface molecules necessary for stable cell-cell interaction.

Tumour enhancement associated with induction of abscesses in mice bearing a transplantable solid tumour.

A model of intraabdominal sepsis in the tumour-bearing host was established in order to study the interactions between host, tumour and infecting organisms. BALB/c mice bearing a transplanted tumour were given an intraperitoneal inoculum containing Bacteroides fragilis, Escherichia coli and bran as an abscess-potentiating agent. Tumour-bearing mice formed abscesses which were not significantly smaller than in controls except late in tumour growth. The bacterial contents of the abscesses were not significantly different to controls. In contrast, mice given an abscess-inducing mixture at or near the time of tumour cell inoculation had tumours which were significantly larger than in controls. The mechanism of tumour enhancement is not known.