PubMed Health⌕ Search

Biomedical subjects

L L Perry

Publications and source records attributed to L L Perry.

51 records · Page 3Linked to original sources
PubMed1981

T cell subset interactions in the regulation of syngeneic tumor immunity.

Suppressor T cell (Ts) regulation of immunity to chemically induced syngeneic tumors has been investigated with regard to the mechanism of Ts stimulation and cell-to-cell communication. It has been determined that suppressor cells generated by the presence of tumor antigen participate in a suppressive circuit involving both cells and cell-derived factor(s) in the expression of suppressive effects. Evidence is provided that these interactions occur via idiotype--antiidiotype recognition in a manner similar to those in hapten-specific immune response. Conditions for induction of Ts activity in vivo have been artificially created by a variety of means, including the intravenous administration of soluble antigen and the inhibition of antigen-presenting function by anti-I-A antibodies or by in vivo treatment with ultraviolet irradiation. Suppression appears to be directed against the Ly-1+ cell, which mediates tumor immunity in this system. The summary of evidence suggest that responses to tumor antigen are in many aspects analogous to those occurring in response to more conventional antigens, but are subject to the dampening effects of suppressor cells generated continually during the period of primary tumor growth.

Antibodies, Anti-Idiotypic↗
PubMed1981

The role of T cell sets in the rejection of a methylcholanthrene-induced sarcoma (S1509a) in syngeneic mice.

The ability of different T cell sets to confer protection in mice against a methylcholanthrene-induced sarcoma, S1509a, was examined. Intravenous infusion of lymph node and spleen cells from A/J donors immunized with S1509a into normal A/J recipients retarded subcutaneous growth of S1509a but did not lead to complete eradication of the tumor during a 9-day period of observation. This protective effect was lost if the transferred cells were treated with anti-Thy 1.2 and complement. The ability of different populations of lymphoid cells to retard tumor growth after inoculation with tumor cells subcutaneously was examined (Winn assay). Nylon-wool-passed cells from lymph nodes and spleens of tumor immunized animals were treated either with anti-Ly 1.2 or with anti-Ly 2.2 antiserums and complement and inoculated with tumor cells in normal A/J mice. The tumor was measured daily for 10 or more days. Ly l cells and unfractionated T cells efficiently suppressed tumor growth; Ly 23 cells had little or no effect. When small numbers of Ly 1 cells were injected along with twice as many Ly 23 cells, the growth of the tumor was also inhibited. Histologic examination of inoculated sites at 24-72 hours after local transfer showed a more intense mononuclear infiltrate in animals inoculated with tumor cells and T cells from immunized animals than in animals given injection with tumor cells alone, or with tumor cells and T cells from nonimmunized animals. The findings indicate that Ly 1 cells are capable of retarding the growth of the sarcoma, presumably by eliciting a delayed hypersensitivity reaction. By contrast, Ly 23 cells, which can mediate cytotoxicity, had little or no effect on tumor growth.

Animals↗
PubMed1979

Regulation of immune response to tumor antigen: interference with syngeneic tumor immunity by anti-IA alloantisera.

We present evidence for a role of I-A subregion-encoded determinants in syngeneic tumor immunity. In animals rendered immune to the S1509a fibrosarcoma, daily treatment with microliter quantities of antisera directed against Kk and I-Ak determinants expressed on lymphoid cells of host origin decreased the capacity for immune tumor rejection. Absorption studies revealed that anti-I-Ak antibody activity alone was sufficient for the manifestation of this effect. Furthermore, experiments utilizing F1 hybrids showed that an antiserum that was genetically unable to interact with H-2 determinants expressed on the tumor was equally effective in inhibiting tumor immunity. Suggestive evidence that the activity of this antiserum is related to interference with the generation of effector T cell function was provided by the observation that hyperimmune animals pretreated with an anti-Kk,I-Ak antiserum were no longer capable of adoptively transferring tumor immunity to naive recipients. Thus, it is possible to regulate the secondary immune response to tumor antigens by using antisera with specificity for I-A determinants expressed on cells or possibly on factors of the host lymphoid system.

Animals↗
PubMed1979

Regulation of the immune response to tumor antigen.

Reduction of syngeneic tumor growth in primary tumor-bearing murine hosts has been accomplished using a variety of treatments designed to decrease endogenous suppressor cell activity or augment host effector responses. Selective interference with suppressor cell function can be achieved by in vivo administration of anti-thymocyte serums at critical times during the early stages of tumor development or by continuous treatment with antiserums directed to interact with I-J determinants on suppressor cells or suppressor factors. This later mode of therapy also results in a delay in tumor appearance when suboptimal doses of tumor are given. Preferential diminution of suppressor cell precursor activity has also been observed by pretreatment of tumor recipients with low doses of cyclophosphamide. Normal animals so treated are capable of adoptively transferring primarily helper-type activity to tumor-bearing recipients. Decreased tumor growth and prolonged host survival have also been achieved using BCG as a means of augmenting host effector potential. Thus, it is possible to inhibit tumor development in a murine model by modes of immunotherapy which may be relevant to the early treatment of certain human neoplasms.

Animals↗
PubMed1978

Differentiation of progressive versus regressive Rous virus-induced avian sarcomas according to tumor and infiltrating lymphocyte fine structure.

Electron microscope examination of progressing and regressing Rous virus-induced sarcomas in an inbred line of White Leghorns revealed that regressing tumors contained moderate to marked lymphocyte infiltration, frequent contact between lymphocytes and tumor cells, and extensive areas of necrosis. Lymphocytes infiltrating regressing tumors exhibited a polar accumulation of organelles at the point of contact between lymphocyte and target cell. On the other hand, progressing tumors contained low to moderate numbers of lymphocytes, infrequent lymphocyte-tumor cell interaction and less evidence of tumor cell degeneration. Lymphocytes from progressing tumors lacked the polar organization of organelles. This experimental system is offered as a means of studying the role of lymphocytes in tumor regression.

Animals↗
PubMed1978

Enhanced syngeneic tumor destruction by in vivo inhibition of suppressor T cells using anti-I-J alloantiserum.

The cellular response to a methylcholanthrene-induced sarcoma S1509a has been investigated. Histologic analysis of the in vivo response to S1509a included a study of tumor development in nonimmune, tumor immune, or hyerimmune syngeneic mice, as well as in nonimmune animals treated with antiserum produced to interact solely with determinants encoded by the I-J subregion of the H-2 major histocompatibility complex. Tumors from immune or hyperimmune mice showed marked infiltration by mononuclear and, to a lesser extent, polymorphonuclear cells, with marked tumor cell necrosis. Anti-I-J treated mice displayed similar but quantitatively reduced leukocytic infiltrates and less evidence of tumor cell degeneration. Untreated nonimmune mice, on the other hand, revealed only mild leukocytic infiltration with little or no necrosis of the tumor. Thus, the administration of anti-I-J antiserum, which has been shown to diminish suppressor cell activity, is associated with increased leukocytic infiltration and enhanced syngeneic tumor destruction in vivo in the nonimmune host.

Animals↗
PubMed1978

Regulation of the immune response to tumor antigen. IV. Tumor antigen-specific suppressor factor(s) bear I-J determinants and induce suppressor T cells in vivo.

The nature and function of suppressor factor(s) elaborated by suppressor T cells in response to certain chemically induced tumors have been further defined. Thus, suppressor factor(s) specific for the S1509a methylchol-anthrene-induced fibrosarcoma have been shown to bear determinants encoded by the I-J subregion of the murine MHC since suppressive activity is removed by passage of the factor through an immunoadsorbent composed of anti-I-Jk coupled to Sepharose. No loss of activity was observed after passage of factor through control columns composed of normal mouse globulin. Furthermore, activity could be recovered from the relevant immunoadsorbent by elution with high salt. The administration of crude suppressor factor(s) to normal animals for 4 days resulted in the development of a population of suppressor cells that act in a manner analogous to the suppressor cell population used for production of factor. These factor-induced suppressor cells are T cells and exhibit an antigen specificity similar to that displayed by the tumor-induced suppressor cells. Thus, tumor-specific suppressor factor(s) bear I-J determinants and are capable of inducing the appearance of suppressor T cells in the nontumor-bearing host, which may then act in a specific manner to limit host responsiveness to tumor antigen.

Animals↗
PubMed1978

Regulation of the immune response to tumor antigen. VI. Differential specificities of suppressor T cells or their products and effector T cells.

Suppressor T cells arising during the development of certain murine methylcholanthrene-induced fibrosarcomas have previously been shown capable of limiting only those effector responses generated against the homologous tumor. Thus, S1509a-induced suppressor T cells inhibit immune reactivity only to the S1509a tumor in S1509a immune mice and have no effect on the rejection of SAI tumors in SAI-immune animals. In contrast to this is the cross-reactivity of effector cells in this system, whereby animals rendered immune to either the S1509a or SAI sarcoma are equally capable of rejecting a challenge of the opposite tumor. The specificity of suppression has been further defined in the present study, which demonstrates that S1509a-induced suppressor cells can inhibit responsiveness only to the S1509a sarcoma, even in the simultaneous presence of both the S1509a and SAI tumors. Furthermore, the suppressor factor that is obtainable from suppressor T cells demonstrates a similar precise specificity in its ability to limit selectively reactivity only against the inducing tumor, regardless of the simultaneous expression of antigens on other tumors recognized by cross-reactive effector cells. These results suggest that the antigenic determinants recognized by effector and suppressor T cells are different, and may provide a model for further dissection of suppressor cell function in vivo.

Animals↗