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Biomedical subjects

E M Lord

Publications and source records attributed to E M Lord.

97 records · Page 6Linked to original sources
PubMed1980

Comparison of in situ and peripheral host immunity to syngeneic tumours employing the multicellular spheroid model.

The multicellular tumour spheroid was used as a model system to assess the in situ host immune response to the EMT6/Ro mammary tumour in syngeneic BALB/cKa mice. In sensitized mice the spheroids were rapidly infiltrated by host cells including macrophages, lymphocytes and granulocytes. Tumour cell killing was evident within 1 day and resulted in the eventual complete destruction of the spheroids. Host cells within the spheroids had a greater cytolytic capacity than the surrounding peritoneal cells and virtually no cytolytic activity was detectable in cells from the spleen. A similar discrepancy between in situ and peripheral immunity was found in mice bearing solid EMT6/Ro tumours.

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PubMed1979

Morphological and functional characteristics of cells infiltrating and destroying tumor multicellular spheroids in vivo.

EMT6 mammary sarcoma cells were grown in vitro as multicellular spheroids to model for the heterogeneity of microenvironments and structural changes which develop in many tumors, including micrometastases. Spheroids of 700-900 micron diameter were implanted into and recovered at different times from the peritoneal cavities of sensitized or nonsensitized allogeneic and syngeneic mice. The colony forming efficiency of spheroid tumor cells recovered at 24 and 48 h from sensitized allogeneic mice was markedly decreased as compared with those from nonsensitized allogeneic or syngeneic animals. These recovered spheroids were extensively infiltrated by both lymphocytes and macrophages, which ultrastructurally had very close membrane associations with tumor cells. Host cells recovered from spheroids exhibited cytotoxic activity in an in vitro 51Cr release assay. Thus, multicellular spheroids in vivo provide a unique experimental model to study the functional capacity of host cells within a spheroical tumor. Although lacking the stroma and the vasculature of in vivo solid tumors, this model does have many similarities to in vivo tumors and is thus suitable for studying the tumor cell-host cell interactions within the tumor microenvironment. In addition, the system offers the potential for quantitative study of the effects of treatment modalities on tumor cell-host cell interactions.

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PubMed1977

Immunosuppressive activity of human seminal plasma. I. Inhibition of in vitro lymphocyte activation.

A high molecular weight fraction prepared from human seminal plasma by gel filtration chromatography suppresses human lymphocyte transformation and DNA synthesis induced by mitogens (PHA, Con A, PWM), antigens (Candida albicans, tetanus toxoid), and allogenic cells. This same fraction also suppresses the stimulated response of mouse lymphocytes to allogenic cells and to various mitogens, including T cell-dependent and T cell-independent mitogens. The induction, but not the expression, of cell-mediated cytotoxicity is also suppressed. Similar high molecular weight fractions suppress the in vitro humoral response of mouse spleen cells to both a T cell-dependent (SRBC) and a T cell-independent (DNP-F) antigen. The high m.w. fraction exhibited in vitro suppressive activity at concentrations of 0.1 to 1.0 mg/ml which corresponds to a 1/50 or greater dilution of human seminal plasma. These observations support the concept that a local immune response against sperm in the female reproductive tract is actively suppressed by a component in seminal plasma.

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PubMed1975

Antigen suppression of the in vitro development of plaque-forming cells to autologous erythrocyte antigens.

Peritoneal cell cultures from NZB and C57BL/6 mice develop large numbers of PFC directed against antigens present on bromelain-treated isologous erythrocytes. The development of these autoimmune PFC can be suppressed by the addition of small numbers of BrMRBC at the start of the culture period. The possibility that the development of the plaque is prevented by the presence of antigen in vivo is discussed.

Animals↗
PubMed1975

The properties of plaque-forming cells from autoimmune and normal strains of mice with specificity for autologous erythrocyte antigens.

Treatment of mouse erythrocytes with the proteolytic enzymes, bromelain, reveals antigenic determinants not normally exposed on the erythrocyte surface. It was found that not only NZB mice, a known autoimmune strain, but also several normal strains of mice contain cells in small numbers in their spleens and in larger numbers in their peritoneal cavities which will form plaques against bromelain-treated MRBC. During in vitro culture the number of anti-BR-MRBC PFC increases slightly in the spleen cell populations whereas the number of these PFC in peritoneal cells increases dramatically to as many as 100,000 PFC/10(6) cells. The plaques detected in this assay contain a central lymphoid cell and their development, which requires the presence of complement and protein synthesis, is inhibited by anti-mouse immunoglobulin.

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PubMedDate not supplied

Murine Pam 212 cutaneous squamous cell carcinoma is nonimmunogenic in normal syngeneic hosts and resistant to immune effector mechanisms.

We established a mouse model of cutaneous squamous cell carcinoma (SCC) using the Pam 212 cell line to study antitumor immunity in normal syngeneic hosts. In vitro, Pam 212 cells expressed very low levels of class I major histocompatibility complex (MHC) antigen; interferon-gamma (IFN-gamma) significantly increased the expression of this antigen. In vivo, Pam 212 tumors grew progressively in normal BALB/c hosts and resembled poorly differentiated human cutaneous SCC. Immunization of normal syngeneic hosts with irradiated, class I-negative or -positive Pam 212 cells failed to prevent tumor growth or induce specific cytotoxic T lymphocytes (CTL). However, Pam 212 tumor cells were rejected by C3H allogeneic mice, indicating adequate and functional class I antigen expression in vivo. Rejection of Pam 212 tumors by C3H hosts was in part dependent on CD8+ CTL lysis, as alloreactive anti-H-2d CTL lysed class I-positive Pam 212 cells, demonstrating that Pam 212 cells express functional class I MHC antigens. Both class I-positive and -negative Pam 212 cells were resistant to natural killer cell lysis. We hypothesize that ineffective syngeneic immune responses against Pam 212 cells may involve multiple mechanisms: inability of Pam 212 cells to elicit a primary immune response, as well as resistance to cell-mediated lysis.

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