Alien histocompatibility antigens on tumor cells

Allostimulation of patients' lymphocytes generates both T and NK-like cells cytotoxic for autologous melanoma

“…Lysis of tumour cells by allostimulated Pt-PBL is not due to cross-reactivity between allogeneic N-PBL and melanoma cells The above findings prompted us to investigate whether autologous tumour lysis by allostimulated Pt-PBL occurred through a cross-reactivity between normal alloantigens and TAA as has been found for some experimental neoplasms ( (Parmiani et al, 1979;Greenberg et al, 1981;Kedar et al, 1982a;Sensi et al, 1983). To test this hypothesis, PBL from 13 metastatic melanoma patients were stimulated with allogeneic N-PBL from single donors and then tested for cytotoxicity on auto-Me and on the N-PBL used as stimulators.…”

“…To explain these findings it has been suggested by experiments on some animal and human tumours that the lysis of tumour cells by T lymphocytes occurs through a cross-reaction between TAA and normal histocompatibility antigens of allogenic lymphocytes (Parmiani et al, 1979;Zarling & Bach, 1978a;Paciucci et al, 1980;Greenberg et al, 1981;Kedar et al, 1982b;Taylor & Bradley, 1983 Hurrell & Zarling, 1983). The analysis of auto-Me cytotoxicity with MLCor MLTC-derived clones also tends to rule out the possibility that the lysis of autologous tumour targets by alloactivated Pt-PBL is due to crossreactivity between TAA and allogeneic MHC determinants (Vose & White, 1983;De Vries & Spits, 1984).…”

“…The pathway of the allostimulation-induced killing of autologous tumour cells is still unclear since different types of effectors can be generated and expanded in mixed lymphocyte culture (MLC), including non-specific effectors such as NK-like cells or lymphokine-activated killer cells (LAK) (Grimm et al, 1982;Lopez-Bonet et al, 1982;MacPhail et al, 1984). The cytotoxicity of alloactivated patients' PBL (Pt-PBL) might be specific and due either to a cross-reactivity between alloantigens and tumour cells (Zarling et al, 1978a;Parmiani et al, 1979), or to the presence of T cells previously sensitized in vivo to tumour-associated antigens (TAA), and which are then activated and expanded during the MLC through the release of lymphokines, mainly interleukin 2 (IL-2) (Vose & White, 1983). On the other hand, tumour cell lysis could be due to activation by IL-2 of NK-like cells which can lyse autologous and allogeneic tumour cells, or of LAK cells which can kill also NKresistant fresh tumours (Grimm et al, 1982;Lotze et al, 1981).…”

Alloantigen-Activated Lysis of Syngenic Tumor Augmented by Allogenic Lymphocytes as Cold Targets

“…This suggested that not all lytic determinants on tumor cells were alloantigenic. In other words, the determinant(s) on tumor cell caus ing lysis was not an alien histocompatibility antigen [14]. These observations may suggest that one popula tion of effector cells was active against alloantigens and another was active against an additional deter minants) on tumor cell surfaces.…”

Expression of alien histocompatibility antigens on SJL/J tumors detected by cell-mediated and serological analyses

“…In the past few years, several groups have reported the observation of 'inappropriate H-2' antigens on tumor cells, i.e., tumor expression of H-2 antigens that had been presumed to be unique to haplotypes other than that of the tumor host [2,5,7,10], recently reviewed by Parmiani et al [14]. We present here similar biological evidence for the expression of apparently inappropriate H-2 antigens on both primary and in vivo-and in vitro-passaged SJL/J RCS tumors.…”