Products of the Major Histocompatibility Complex on Tumor Cells

Callahan, Gerald N.

doi:10.1007/978-1-4612-5176-7_5

Cited by 2 publications

(1 citation statement)

References 68 publications

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“…Similar variability in the expression of class I antigens was demonstrated by immunohistologital techniques on solid human tumors [2,8,21,38,40,43,48,59,60]. The results showed that in 28/40 (70%) squamous cell sarcomas of the lung, in 24/35 (69%) adenocar¢inomas of the lung, in 12/22 (55%) ovarian carcinomas, in 1/3 breast car¢inomas and in 3/3 hypernephromas > 50% of cells were reactive with W6/32 mAb.…”

Section: Discussionsupporting

confidence: 71%

Expression of the adhesion molecule ICAM-1 and major histocompatibility complex class I antigens on human tumor cells is required for their interaction with autologous lymphocytes in vitro

Vánky

Wang

Patarroyo

et al. 1990

Cancer Immunol Immunother

128

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In a group of 30 human tumors, comprising 12 lung, 14 ovarian, 2 breast carcinomas, 1 hypernephroma and 1 mid-gut carcinoid, the expression of major histocompatibility complex (MHC) class I molecules and the intercellular adhesion molecule 1 (CAM-1, CD54) was found to vary independently. Some tumors expressed both or neither of these molecules. Among 9/13 ICAM-1+ tumors, in which greater than 50% cells reacted with the anti-ICAM-1 monoclonal antibody (mAb) (LB-2), the class I antigen was also detected on greater than 50% of the cells. Only 2 ICAM-1+ tumors were class-I-. In 5/17 cases the tumors were MHC-class-I+ and ICAM-1-. Lymphocytes collected from the blood or from the tumor site were assayed for recognition on the tumor cells in the auto-tumor cytotoxicity test and in mixed lymphocyte tumor cell culture (MLTC). Positive results were obtained only with the MHC-class-I+/ICAM-1+ tumors. In vitro treatment of the tumor cell suspensions with interferon gamma and tumor necrosis factor alpha (TNF alpha) induced or enhanced the ICAM-1 and/or class I antigen expression in 8/12 cases. Of the tumor samples treatged, 8/9 acquired stimulatory capacity and 3/10 became susceptible to lysis by the lymphocytes. In 6/6 MLTC performed with the cytokine-treated tumor cells, cytotoxicity against the autologous tumor was generated. Three of these MLTC lymphocytes also lysed the untreated targets. mAb directed to class I antigens or to ICAM-1 inhibited both the stimulation by and the lysis of tumor cells when confronted with fresh lymphocytes. The cytotoxicity generated in the MLTC was also inhibited. If, however, the cytotoxic function was induced in MTLC containing interleukin-2 (5 U/ml), inhibition was obtained only by pretreatment of the targets with mAb against ICAM-1. The results show thus (a) that the lymphocytes react in vitro with tumor cells only if these express both MHC class I molecules and ICAM-1; (b) that expression of these molecules can be induced by interferon alpha and TNF alpha; (c) that cytotoxic effectors generated in the MLTC with cytokine-treated tumors can also act on the untreated tumor cells. The requirement of the two surface moieties for the interaction with lymphocytes was also substantiated by blockade with relevant mAb.

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Section: Discussionsupporting

confidence: 71%

Expression of the adhesion molecule ICAM-1 and major histocompatibility complex class I antigens on human tumor cells is required for their interaction with autologous lymphocytes in vitro

Vánky

Wang

Patarroyo

et al. 1990

Cancer Immunol Immunother

128

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Aberrant expression of Ia‐like antigens on tumor cells of regressing but not of progressing Rous sarcomas

1987

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Unlike many other tumors, experimentally induced Rous sarcomas in chickens have a definite tendency to regress spontaneously. Regression is under genetic control, but it is immunologically mediated although the target antigens that stimulate an immune response are unknown. Tumor cells in regressing sarcomas were found to express class II major histocompatibility complex (Ia-like) antigens while tumor cells from progressing sarcomas were negative. This suggests that the induction of Ia-like antigen expression has a role in the initiation or perpetuation of regression, similar to that postulated for class II antigen expression in a variety of autoimmune diseases.

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Products of the Major Histocompatibility Complex on Tumor Cells

Cited by 2 publications

References 68 publications

Expression of the adhesion molecule ICAM-1 and major histocompatibility complex class I antigens on human tumor cells is required for their interaction with autologous lymphocytes in vitro

Expression of the adhesion molecule ICAM-1 and major histocompatibility complex class I antigens on human tumor cells is required for their interaction with autologous lymphocytes in vitro

Aberrant expression of Ia‐like antigens on tumor cells of regressing but not of progressing Rous sarcomas

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