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N I Brody

Publications and source records attributed to N I Brody.

9 recordsLinked to original sources
PubMed1993

Suppression of the delayed type hypersensitivity response by tumor facilitating factor of B16 melanoma. A tumor factor suppresses immune responses.

BACKGROUND: Tumor facilitating factor is a cell surface glycoprotein produced by B16 melanoma that has been found to reduce the lethal inoculum for B16. Tumor facilitating factor induces macrophage spreading in vitro, reduces macrophage chemotaxis in vivo, and depresses lymphocyte mitogenesis in vitro. OBJECTIVE: It is assumed that the immune modifying effects are responsible for tumor facilitation. As tumors may be poor immunogens or inducers of inflammation, studies were conducted to determine whether tumor facilitating factor alters the inflammatory cascade of cells found in infiltrates of delayed type hypersensitivity. RESULTS: Freeze-thawed B16 cells, used as the source of TFF, caused a suppression of delayed type hypersensitivity measured as ear swelling in the mouse. When culture supernatant was substituted for freeze-thawed cells as a source of TFF and injected at different time points of the delayed type hypersensitivity response, the greater suppression was with tumor facilitating factor injections at 24 hours pre-elicitation only (82%), and 24 hours both presensitization and pre-elicitation (89%). Immunohistological staining demonstrated that tumor facilitating factor decreases ear thickness and cellular infiltrates, specifically Mac-1 staining cells, to a site of delayed hypersensitivity. Peritoneal cell analysis confirmed these findings. CONCLUSION: These data are consistent with the hypothesis that tumor facilitating factor alters immune functions including macrophage and lymphocyte mobility and recruitment to a target site, thereby allowing for facilitation of tumor growth.

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PubMed1983

The effects of tumor facilitating factor of B16 melanoma on the macrophage.

B16 cells produce a tumor facilitating factor (TFF) that increases B16 tumor incidence in mice injected with a small number of B16 cells. TFF was derived from serum-free culture supernatant concentrated on an Amicon PM10 membrane. One milliliter of concentrated material represented the product 10(8) B16 cells during a 6-h incubation. We report data that indicate TFF may act by altering macrophage function. In the nude mouse deficient in T cell, but not macrophage function, the injection of 0.8 ml of TFF facilitated tumor development. Subcutaneous injection of 0.7 ml of TFF induced mouse peritoneal macrophages to spread when removed and plated on glass coverslips. This effect peaked 3 days after injection of TFF and was abrogated by heating the TFF to 70 degrees C for 1 h. The injection of TFF was also able to induce macrophage spreading in nude mice. Injection of viable B16 cells induced spreading, as would be predicted if TFF is produced by B16 cells in vivo. In vitro incubation of peritoneal cells with TFF was also able to induce macrophage spreading. Finally, subcutaneous injection of TFF reduced by 80% the accumulation of peritoneal cells in response to intraperitoneal injection of phytohemagglutinin. We suggest that one mode by which TFF facilitates tumor growth is by reducing the numbers of macrophages chemotaxing to the tumor site.

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PubMed1980

Increased incidence of tumor takes to B16 melanoma in C57BL/6J mice injected with B16 products.

The injection of either viable B16 melanoma cells, killed B16 cells, or B16 cell products increased the incidence of melanomas in C57Bl/6J mice inoculated with a threshold dose of B16 cells. In all cases the effect was seen whether the facilitating injection was at a site distant from the challenge inoculum or at the same site. Facilitation was seen with B16 cells and products both from in vivo tumors and from tissue culture. However, cells detached from tissue culture flasks with trypsin no longer had facilitating activity. Facilitating activity was found in concentrated cultured supernatants centrifuged at 100,000 X g for 1.5 hr and dialyzed. No activity was detected in the less than 10,000 mol wt fraction. Facilitation was not associated with a change in the time of tumor appearance nor with enhanced growth of B16 cells in culture.

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PubMed1969

Studies on antigenic competition.

Antigenic competition was studied in a haptenic system. It was found that: (a) The extent of competition is greater when larger doses of antigen are employed. (b) Antigenic competition appears to be independent of the carrier molecule. (c) The affinity of the antibody produced in antigenic competition is approximately equal to the affinity of antibody formed by animals immunized with only one antigen. (d) Antigenic competition only occurs when both antigens are injected so as to drain into the same regional lymph nodes. The results suggest that antigenic competition occurs locally at the site of antigen stimulation and is not mediated by a circulating factor, by tolerance induction, or by suppression due to synthesis of cross-reacting antibodies.

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PubMed1967

Studies on the control of antibody synthesis. Interaction of antigenic competition and suppression of antibody formation by passive antibody on the immune response.

In the system studied, antigenic competition between two haptenic determinants was found to be of the same extent whether the haptens were on the same or on separate carrier molecules. Suppression of antibody formation to one determinant by administration of passive antibody partially eliminated the depressive effects of antigenic competition when the two haptens were located on separate carrier molecules but had no effect on antibody production to the second hapten when the two determinants were present on the same molecule. The results are discussed in terms of the mechanisms of suppression, antigenic competition, and control of antibody formation.

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