Macrophages and lymphoid tissues in mice with concomitant tumour immunity

Nelson, D. S.; Kearney, R

doi:10.1038/bjc.1976.155

Cited by 25 publications

(10 citation statements)

References 20 publications

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“…The general decline in the proportion of cells expressing T cell markers in the spleens of mice with MC-2 tumours might in part be explained by an expansion of non-T cells associated with splenomegaly. Splenomegaly occurs in mice carrying any of a number of independently derived methylcholanthrene-induced fibrosarcomas, and is coincident with haemopoiesis and plasmacytopoiesis (32). Spleen weights, and the number of splenic leucocytes recoverable from mice with large MC-2 tumours, can be more than twice those in normal littermates (23, and unpubl.…”

Section: Discussionmentioning

confidence: 99%

Differences in the phenotypes of cells mediating anti‐tumour immunity at various stages of tumour progression in mice

et al. 1989

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Summary In Winn assays, T cells from donors immunized by tumour excision, or from mice with small tumours, mediate rejection of the metastasizing murine fibrosarcoma MC‐2. As the mean size of primary tumours in spleen donors increases, the strength of anti‐tumour activity declines, until it is frequently undetectable in spleen cells from mice with very large tumour burdens. Loss of splenic anti‐tumour activity is coincident with the appearance of cells capable of suppressing an otherwise protective anti‐tumour response in Winn assays. This paper defines the phenotypes of T cells mediating immunity against MC‐2. Eleven or more days after tumour inoculation the proportions of tumour‐bearer splenic leucocytes expressing Ly 1.2 (CD5), Ly 2.2 (CD8a) or L3T4 (CD4) surface antigens were significantly less than similar preparations from normal animals. Depletion of Ly 1.2+ or L3T4+ cells from spleen cells of donors with small tumours, or from donors immunized by tumour excision, diminished protection in the Winn assay. Depletion of Ly 2.2+ cells from these donors had no effect on immunity. In contrast, spleen cells taken from donors with large tumours lost all anti‐tumour activity if pretreated with any one of anti‐Ly 1.2 or anti‐Ly 2.2 or anti‐L3T4 antibodies in the presence of complement. These results suggest that cells bearing the Ly 2.2 marker may be important to weak immunity remaining in the spleens of mice with large tumours, but are not critical to strong immunity generated early in tumour growth, nor to that following tumour excision. That is, in addition to an Ly 1.2+, Ly 2.2−, L3T4+ spleen cell subset also seen early in the growth of the MC‐2 tumour, a cell population which expresses the Ly 2.2 marker and which is important to anti‐tumour immunity emerges late in tumour growth.

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Section: Discussionmentioning

confidence: 99%

Differences in the phenotypes of cells mediating anti‐tumour immunity at various stages of tumour progression in mice

et al. 1989

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“…Circulation of sensitized lymphocytes also explains the presence of concomitant immunity. As in other murine systems [14,15,16] the concomitant immunity in the SL2-bearing DBA/2 mouse would be divided into two phases. The first phase was tumor specific and has been ascribed to tumor specific Tcells in cooperation with macrophages [15,16].…”

Section: Discussionmentioning

confidence: 99%

Immune reactivity in SL2 lymphoma-bearing mice compared with SL2-immunized mice

Weger

Wilbrink

Moberts

et al. 1987

Cancer Immunol Immunother

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We have studied the rather paradoxical phenomenon of the growth of an antigenic tumor in an immunocomponent host. This phenomenon was studied by comparing the lymphocyte reactivity and the macrophage cytotoxicity, during SL2 growth in DBA/2 mice (SL2-bearing mice) and in DBA/2 mice immunized against SL2 tumor cells (SL2-immune mice). Immune mice rejected a challenge of tumor cells. The immune T-lymphocytes rendered macrophages cytotoxic (arming) and were able to transfer tumor resistance to naive animals. Nonimmunized mice did not reject a challenge of SL2 cells. In these tumor-bearing mice various forms of immune reactivity were tested. Lymphocytes with the capacity to arm macrophages could not be found in the lymphoid organs. However, lymphocytes isolated from the tissue directly surrounding the subcutaneous SL2 tumor could arm macrophages in vitro. Shortly after subcutaneous tumor grafting cytotoxic macrophages were found in the peritoneal cavity. In the serum macrophage arming factors were detected that rendered macrophages cytotoxic in vitro. This cytotoxicity of the peritoneal macrophages and the presence of macrophage arming factors in the serum showed a similar biphasic pattern. The first phase of cytotoxicity between day 3 and 8 after tumor grafting was tumor (SL2) specific. The second phase from day 12 and onwards was not tumor specific. During the first 4 days after SL2 grafting the DBA/2 mice expressed a specific concomitant immunity to a second tumor graft. Then 7 or more days after grafting the first SL2 tumor, the concomitant immunity was nonspecific as the growth of a second SL2 tumor graft and a L5178Y (DBA/2) tumor graft were inhibited. In addition, the immune suppressive activity of serum and lymphocytes was tested. Neither serum nor lymphocytes from SL2-bearing mice suppressed the macrophage arming capacity of SL2 immune lymphocytes. Lymphocytes from tumor-bearing mice did not inhibit the capacity of SL2-immune lymphocytes to transfer resistance to naive animals. On the contrary, lymphocytes obtained from SL2-bearing mice 14 days after SL2 grafting transfered tumor resistance in a Winn-type assay. These data suggest that the growth of an antigenic tumor is due to the inability of the immune system to mount an effective antitumor effector cell population during tumor growth, rather than an immune suppression of the antitumor reactivity, as a limited immune reactivity could be detected in tumor-bearing mice, whereas immune suppression could not be detected.

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“…This dif ference might be explained by their extensive use of a Moloney sarcoma-induced tumor [32] as opposed to our methylcholanthrene-induced fibrosarcoma. Results from the work of Nelson and Kearney [33][34][35] using methylcholanthrene-induced tumors, indicated that there is a link between activated TBM Mg and enhance ment (not inhibition) of splenic T cell activity. It is also possible that the inhibition seen by Herberman's group could be due to a purely quantitative increase in the number of Mg seen by us [17] and others [36] in TBM.…”

Section: Discussionmentioning

confidence: 99%

Enhancement of T Cell MLR Reactivity by Addition of Macrophage Supernatants from Tumor-Bearing Mice

Elgert¹,

Connolly²

1980

Oncology

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One-way mixed lymphocyte reactions (MLR) were used to establish a correlation between loss of in vitro T cell reactivity and in vivo tumor growth. Though supernatants from anti-Thy 1 treated macrophages (MÐ¤) greatly enhanced MLR activity in normal T cells, such addition had little effect in reversing the inability of T cells from 2-week palpable tumor-bearing mice (TBM) to recognize in vitro foreign histocompatibility antigens. Since normal T cells, exposed to TBM M0 supernatants, exhibited no decrease in proliferative response, TBM T cell loss of MLR reactivity could not be ascribed to tumor-induced suppressor MÐ¤.

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Macrophages and lymphoid tissues in mice with concomitant tumour immunity

Cited by 25 publications

References 20 publications

Differences in the phenotypes of cells mediating anti‐tumour immunity at various stages of tumour progression in mice

Differences in the phenotypes of cells mediating anti‐tumour immunity at various stages of tumour progression in mice

Immune reactivity in SL2 lymphoma-bearing mice compared with SL2-immunized mice

Enhancement of T Cell MLR Reactivity by Addition of Macrophage Supernatants from Tumor-Bearing Mice

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