Showing papers by "Lewis L. Lanier published in 1979"

Early detection of the CH1 murine lymphoma by tumor-associated idiotype in the serum.

Abstract: In this report, we describe a sensitive C-dependent251Cr release inhibition assay using anti-idiotype antiserum which allows early detection of the CH1 murine B-cell lymphoma by the presence of 19S tumor-associated immunoglobulin in the serum The assay is based on the finding that sera from mice bearing the CH1 lymphoma specifically inhibit C-dependent 51Cr release from labelled CH1 cells in the presence of A-Id serum Groups of mice were injected ip with 102, 103, or 104 CH1 cells and serum samples were collected every other day until host death Tumor-specific idiotype was detectable as early as 8 days after a 104 CH1 tumor cell challenge and by 12–14 days in mice inoculated with 103 or 102 CH1 cells The amount of idiotype increased in parallel with tumor burden and reached a peak titer just before host death In all cases, tumor-associated idiotype was present in the serum time significantly prior to observation of a visible tumor mass (ca day 20–28) In subsequent experiments, mice were inoculated with 104 CH1 cells and treated 16 days later with a single dose of melphalan (10 mg/kg), vincristine sulfate (075 mg/kg), or cyclophosphamide (100 mg/kg) Serum samples were taken from these animals and the level of serum idiotype was monitored After M or VS drug therapy, the level of idiotype decreased in all mice, however host survival was not significantly prolonged By contrast, mice treated with Cy survived significantly longer than untreated controls, and the serum idiotype titer in these mice decreased to undetectable levels from day 20–28 By day 37, idiotype was detectable again in the serum and all mice died of ascites tumor by day 44 The results of these experiments suggest that the presence of idiotype in the serum of a lymphoma-bearing host may provide a marker which will allow early detection of tumor growth during periods of tumor remission induced by conventional chemotherapy

Tolerance to non-H-2 histocompatibility antigens. Transplantation tolerance to the H-4 and H-7 histocompatibility antigens.

Abstract: There have been several reports of observations which suggest that transplantation tolerance may be a result of positive immunoregulation rather than simply unresponsiveness attributable to a lack of competent effector cells. In particular, several investigators have reported that tolerance of the H-Y and H-1 histocompatibility antigens is mediated by a population of thymus-derived lymphocytes. In a companion report, we have presented evidence that supports the existence of a suppressor cell to the H-Y antigen. Furthermore, we have observed that female mice rendered tolerant of the H-Y antigens by neonatal exposure to male lymphoid cells or by multiparity accept male skin grafts indefinitely, but inactivate male peritoneal exudate cells (PEC) in a second-set fashion. This observation has led us to investigate whether tolerance of other non-H-2 antigens is controlled by a similar mechanism. Using mice congenic with C57BL/10 at the H-4 and H-7 loci, we have shown that mice rendered tolerant of the H-7a and H-4b antigens by neonatal exposure to histoincompatibe lymphoid cells are incapable of rejecting either skin or peritoneal cell allografts, suggesting that identical histocompatibility antigens are present on skin and peritoneal cells. Tolerance induced in neonatal mice to the H-4b and H-7a antigens could not be adoptively transferred to syngeneic recipients. These results suggest that tolerance involving the H-4 and H-7 antigens is most likely because of a clonal inactivation of alloantigen-reactive cells as a consequence of neonatal exposure to antigen.