Biomedical subjects

C B Evans

Publications and source records attributed to C B Evans.

30 records · Page 2Linked to original sources

PubMed1980

Radioimmunoassay for detecting antibodies against murine malarial parasite antigens: monoclonal antibodies recognizing Plasmodium yoelii antigens.

A solid-phase radioimmunoassay (SPRIA) in microtiter wells was established for detecting antibodies against Plasmodium yoelii Ag. The SPRIA was found 1) to require as little as 5 micrograms of crude parasite Ag per well, 2) to be able to detect 0.5 ng of monoclonal Ab, and 3) to be 10(4) times more sensitive than the indirect fluorescent Ab staining technique. In a modification of the above assay using intact RBC as an Ag, hyperimmune serum showed significant binding to the surface of erythrocytes of mice infected with P. yoelii parasites but not to RBC of normal mice. Hybridomas were prepared by fusing infected mouse spleen cells with P3-NS1/I-Ag4-1 myeloma cells. Using the SPRIA, hybrids secreting Ab against P. yoelii 17XL Ag were detected. All the hybrids detected by SPRIA secreted Ab binding to free parasites but not to the surface membrane Ag on the infected RBC. The number of positive hybrids produced by fusing spleen cells from mice given a double infection (17XNL and 17 XL) was not greater than that produced by freezing spleen cells from mice given a single infection (17 XL).

Animals↗

PubMed1979

Resistance of mice suppressed for IgM production to Babesia microti infection.

The immunological mechanisms responsible for overcoming infections with Babesia, an intra-erythrocytic protozoan, are not fully understood. Although high titres of specific anti-babesial antibodies have been observed in several species of animals, and protection has been obtained by transfer of large volumes of recovery serum, the role of antibody in the immune response to an infection is uncertain. The present study investigates the nature of B-cell participation during Babesia microti infections by observing the course of the disease in mice in which IgM production has been suppressed from birth and which contain no B cells. The results show that, in contrast to control mice, which develop and subsequently clear circulating parasitaemias, suppressed mice show an unexpected resistance to infection as reflected by a virtual absence of parasites in the peripheral circulation.

Animals↗

PubMed1978

Immunity to Plasmodium berghei yoelii in mice. II. Specific and nonspecific cellular and humoral responses during the course of infection.

The kinetics of various specific and nonspecific immunologic responses were examined in BALB/c mice infected with 17X nonlethal Plasmodium berghei yoelii (a self-limiting infection). The sequence of events after infection was characterized by rapid sensitization of splenic T cells to malaria antigen and polyclonal B cell activation, followed by a period of depressed splenic proliferative responses in vitro to mitogens (PHA and LPS) and malaria (specific) antigen. At the same time, suppressed primary in vitro splenic PFC responses to trinitrophenyl-aminoethylcarbamylmethyl-Ficoll (TNP-F) were seen. This suppression was an active process requiring adherent cells. During this period, levels of antimalarial antibody also increased exponentially. As the infection was cleared, splenic malaria antigen-specific proliferative responses were again observed and splenic PFC and in vitro mitogen responses returned to preinfection levels after variable periods of time. Both splenic proliferative responses to malaria antigen and antimalarial antibody responses remained persistently elevated. In addition, some responses were examined in mice infected with 17X lethal P.b. yoelii (a fatal infection); in comparison to the early responses of mice infected with the nonlethal substrain, there was a decrease and delay in the development of a splenic T cell response to malaria antigen and a blunted antimalarial antibody response.

Animals↗

PubMed1976

Immunity to Plasmodium Berghei yoelii in mice. I. The course of infection in T cell and B cell deficient mice.

The course of infection with 17X nonlethal Plasmodium berghei yoelii was examined in BALB/c mice which were deficient in either T cells or B cells. Markedly increased parasitemia and mortality were observed in athymic (nude) mice which had been backcrossed on a BALB/c background (T cell deficient) compared to similar mice which had been grafted with neonatal BALB/c thymus, and were also observed in BALB/c mice suppressed from birth with goat antiserum to mouse mu-chain (B cell deficient) compared to age- and sex-matched BALB/c controls. These results establish the requirement for the presence of both T cells and B cells for effective resistance to an intercurrent infection with 17XNL P.b. yoelii in adult BALB/c mice. Mechanisms by which the requirement for both T cells and B cells could be explained were discussed. The model of mu suppression was shown to be a valuable tool for an evaluation of the cellular basis of immunity to an infectious disease.

Animals↗

PubMed1976

An in vitro assay for T cell immunity to malaria in mice.

After infection with a nonlethal strain of murine malaria (17XNL Plasmodium berghei yoelli), BALB/c mice are then resistant to a lethal strain (17XL P.b. yoelli). BALB/c mice were infected with 17XNL, anc challenged 3 weeks later, after clearing their parasitemias, with 17XL. Three weeks thereafter, spleen cells from such immune animals were used to define an early peaking T-dependent (anti-theta sensitive) antigen-specific proliferative response when incubated in vitro with 17XL infected RBC, or a saline soluble 17XL antigen preparation. T dependent responsiveness of spleen cells from uninoculated control animals to the 17XL antigen preparation was also observed, but demonstrated a much different (delayed) kinetics from that observed with immune cells.

Animals↗

PubMed1973