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Biomedical subjects

J Cerny

Publications and source records attributed to J Cerny.

At least 91 records · Page 5Linked to original sources
PubMed1981

Target cell heterogeneity in murine leukemia virus infection. II. Demonstration of Friend leukemia-virus-permissive and non-permissive subsets of splenic T cells.

The permissiveness of normal splenic lymphocytes to Friend murine leukemia virus was determined by enumeration of cells producing infectious MuLV following infection with Friend virus in vitro. The infection was enhanced greatly in the presence of mitogens in the culture medium. The number of infected cells in cultures stimulated with bacterial lipopolysaccharide increased progressively between days 1 and 7 whereas in cultures with concavalin A, the number of infected cells reached a maximum on days 3-4 post infection and then declined to the level observed in unstimulated cultures. The con-A-enhanced infection was absent in cultures of splenocytes from nude mice but was present in cultures from nude mice implanted with thymus glands 6 weeks or more before use as donors of spleen cells. The cells permissive to MuLV upon con-A stimulation segregated in the nylon-wool-adherent fraction (together with B cells involved in the LPS-dependent infection) whereas the nylon-non-adherent fraction, containing approximately 90% T cells, was refractory to in vitro infection. The con-A-dependent infectious centers were inhibited by cytotoxic treatment with anti-Thy 1.2 antibody plus complement. These results indicate the existence of two subpopulations of splenic T cells, a major nylon-non-adherent and a minor, nylon-adherent subpopulation, which are, respectively, non-permissive and permissive to MuLV-Friend.

Animals↗
PubMed1981

Sertoli cell testicular tumors.

The testicular Sertoli cell tumor is generally considered a benign tumor that can be treated by orchiectomy and close follow-up. It accounts for less than 1.5 per cent of testis tumors and may be malignant in 10 per cent of cases. Approximately 30 per cent have endocrine activity. We present 5 additional cases to the 75 previously reported in the world literature.

Adult↗
PubMed1980

Thymic requirement for cyclical idiotypic and reciprocal anti-idiotypic immune responses to a T-independent antigen.

The role of the thymus in the cyclical appearance of the dominant idiotype of the myeloma protein secreted by the TEPC-15 plasmacytoma (T-15)-bearing plaque-forming cells (PFC) and anti-idiotypic cells (i.e., cells with receptors for T-15) in the spleen during a primary response to the phosphorylcholine determinant of Streptococcus pneumoniae, strain R36a (Pn) was studied using normal mice, thymus-deficient nude mice, and thymus gland-grafted nude mice (TG-nude). The nude mice and their phenotypically normal littermates (LM) were backcrossed on the BALB/c genetic background. The kinetics of the anti-Pn PFC response of BALB/c inbred mice, littermates of nude mice, and TG-nude mice were essentially the same. There was an initial peak on day 5-6 followed by a decline to near background, and then a second peak on day 12. In nude mice, the first peak of anti-Pn PFC (day 5) was comparable in magnitude to that of mice with an intact thymus; however, there was no second peak. In contrast to the cellular response measured at the level of PFC, the serum antibody response to Pn (assayed by passive hemagglutination of sheep erythrocytes coated with Pn polysaccharide) was comparable in all groups of mice and did not show a measurable oscillation. The anti-idiotypic cellular activity was determined by the ability of spleen cells to bind radiolabeled (125I) TEPC-15 myeloma protein (IgA, kappa) which carries an idiotypic determinant indistinguishable from that of most anti-phosphorylcholine antibodies in BALB/c mice. Binding of radiolabeled McPC-603 (IgA, kappa) and MOPC-315 (IgA, lambda 2) myeloma proteins (which lack the T-15 idiotypic determinant) served as controls. The changes in T-15 binding by splenic lymphocytes following the Pn immunization differed between normal and athymic mice. BALB/c, LM, and TG-nude mice showed a biphasic pattern with peaks at days 3--4 and 10--11 that was nearly reciprocal to the PFC curve. On the other hand, T-15 binding in nude mice either declined and remained depressed or was not affected by the ongoing anti-Pn response. These observations demonstrate that mature T cells are required for cyclical idiotypic and anti-idiotypic responses to immunization with a T-independent antigen and suggest that the cyclical immune response may result from an interaction between idiotypic and anti-idiotypic cell clones.

Animals↗
PubMed1980

Regulation of the T 15 idiotype-positive, T-independent immune response to Streptococcus pneumoniae R 36 a (Pn). I. Specific suppressor T cells induced by Pn in vitro are antigen-specific and idiotype-positive.

Normal BALB/c spleen cells incubated for 2 days with Streptococcus pneumoniae R 36 a (Pn) vaccine in vitro acquired the specific ability to inhibit the T-independent anti-Pn response of fresh lymphocytes. The activated suppressor cells were susceptible to cytotoxic treatment with mouse anti-theta serum plus complement, and they inhibited the anti-Pn response of B lymphocytes deprived of T cells. The suppressive effect was eliminated by adsorbtion of cells on dishes coated with the C polysaccharide from Pn, and treatment of the suppressor cells with a rabbit antibody specific for TEPC-15 myeloma protein, in the presence of complement, abolished the suppressive effect. The results indicate that stimulation of lymphocytes with a T-independent antigen in vitro activates suppressor T cells bearing a specific antigen receptor that may express the idiotype(s) characteristic of anti-Pn antibody, and that these cells inhibit the Pn-reactive B cells directly.

Animals↗
PubMed1979

Inhibition of in vitro Friend murine leukemia virus infection of lipopolysaccharide-activated B-cells with concanavalin A.

Stimulation with bacterial lipopolysaccharide (LPS) of splenic B-lymphocytes infected in vitro with Friend virus complex increased the number of cells with replicating murine leukemia virus (MuLV) [i.e., infectious centers (IC)] up to 100-fold. Concanavalin A (Con A) did not have such an effect. However, the addition of Con A to the LPS-stimulated cultures decreased the number of IC. The inhibitory concentration of Con A (2.5 microgram/ml) was eightfold less than that capable of neutralizing the in vitro infectivity of MuLV (20 microgram/ml). The effect of Con A was not mediated by T-cells; the inhibition of infection was comparable with use of whole spleen cell suspensions from normal BALB/c mice, with T-cell-depleted cell suspensions, or with spleen cells with congenitally athymic nude mice. However, specific removal of Con A from the surface of B-cells with alpha-methyl-D-mannopyranoside prior to the infection reversed the inhibitory effect entirely. It is suggested that the lectin interferes with MuLV on the membrane of B-cells.

Animals↗
PubMed1978

Regulation of the immune response. I. Regulatory cell equilibrium in the "virgin" state.

Spleen cells from pairs of inbred mice (age- and sex-matched) were challenged in vitro with a T-independent antigen. The specific plaque-forming cell (PFC) response in cultures containing cells from both donors was not intermediate to the responses of independently cultured donor spleen cells. Instead, a pattern of significant suppression (67% of pairs tested) or enhancement (22% of pairs tested) was observed. The suppression or enhancement was antigen-specific and did not represent a general phenomenon within the mixed cultures. A suppressive outcome in mixed cell cultures seems to be associated with cells from the donor with the higher individual PFC response. The converse is true for enhancement. The nonadditive nature of the PFC response in mixed cultures and the frequency of suppression to enhancement (3:1) imply that (a) specific, ongoing immunoregulation occurs even in the naive individual, and (b) this regulation is characterized by regular cycles of specific suppression and enhancement.

Animals↗
PubMed1977

Immunosuppression by spleen cells from Moloney leukemia. III. Evidence for a suppressor cell that is not the leukemic, virus-producing cell.

Spleens of mice bearing MuLV (Moloney)-induced leukemia contain cells that inhibit the antibody response of normal syngeneic lymphocytes to sheep RBC in Marbrook cultures. In order to determine whether these immunosuppressive cells are virus-infected tumor cells or normal cells we pretreated leukemic spleen cell suspensions with syngeneic mouse antiserum to Moloney leukemia antigen(s) (plus complement) and with rat anti-Moloney serum (plus complement). The cytotoxic treatment killed approximately 20% to 30% and 60% to 70% of the cells, respectively. The remaining viable cell population was tested for MuLV production (in an infectious center assay on S+L-fibroblasts), for lethal effect on newborn mice, and for immunosuppressive activity. After the treatment with anti-Moloney sera the number of MuLV-releasing cells decreased 10-fold and the leukemogenic potential in vivo decreased 100-fold as compared to leukemic spleen cells pretreated with nonimmune mouse and rat sera (plus complement). In contrast, the ability of the antisera-treated cells to inhibit anti-SRBC response remained undiminished. This indicates that, in part, the immunosuppressive cells in the leukemic spleen are normal, noninfected cells, involved, perhaps, in immune regulation.

Animals↗
PubMed1976

Interactions of murine leukemia virus (MuLV) with isolated lymphocytes. I. Virus replication in lymphocytes infected with Friend virus and cultures in diffusion chambers in vivo.

A new technique for infection of mature lymphocytes with murine leukemia virus (Friend) MuLV-F) is described. Spleen cells for normal, non-infected donors were placed into diffusion chambers (constructed with 0.22 mum por size Millipore filters) which were then implanted into the peritoneal cavities of normal syngeneic recipient mice. The cells were infected with an injection of MuLV-F into the peritoneal cavity and, in some instances, also by placing virus into the chambers. Cells were recovered by treating the chamber content with elastase and collagenase. The infection was determined in two ways: (1) cells with replicating MuLV were enumerated as infection centers (IC) on S+L- indicator cells; and (2) virus-related cell membrane antigen (MA) was detected by immunofluorescence. Cells recovered from chambers after 2-3 weeks of culture represented about 10% of the original inoculum; viability was approximately 90%. The number of IC in MuLV-F-infected chambers was about 10 times higher than obtained by infection and cultivation of spleen cells in vitro. The kinetics of IC and MA in chamber-cultured. MuLV-F-infected spleen cells was similar to that in the spleen of infected mice during the first 10 days after infection. Later on, the process of infection within the chambers slowed down, reaching about 50% MA-positive and about 10% IC-positive cells, whereas the number of both IC- and MA-positive cells in the spleen reached 80% or more. The infection of splenic lymphocytes in diffusion chambers occurred equally well when chambers were implanted into: (1) syngeneic, virus susceptible hosts; (2) syngeneic, lethally irradiated hosts; and (3) allogeneic, virus-resistant hosts, suggesting that the process within the chamber is independent of MuLV replication in the tissues of the chamber-bearing mouse. The diffusion chamber technique seems to provide an environment in which various types of isolated lymphocytes of different mouse strains can interact with MuLV almost as efficiently as in vivo.

Animals↗
PubMed1976

Interactions of murine leukemia virus (MuLV) with isolated lymphocytes. II. Infections of B and T cells with Friend virus complex indiffusion chambers and in vitro: effect of polyclonal mitogens.

The infection of isolated B and T cells by a murine leukemia virus (Friend) MuLV-F) was studied both in vitro and in vivo with an implanted diffusion chamber system. Lymphocytes were obtained from pools of normal spleen cells by filtration of the cell suspension through a nylon-wool column. The purity for both Ig positive and theta-positive cells varied between 85% and 90% in the B-cell and T-cell fractions; both lymphocyte fractions responded very well to stimulation with their respective specific polyclonal mitogens, bacterial lipopolysaccharide (LPS) and concanavalin A (Con A). Lymphocytes were infected by incubating pelleted cells in 2-6 x 10(4) FFU MuLV for 1 h at 4 degrees C and were then cultured for 5-10 days. Cells releasing infectious MuLV were enumerated as infectious centers (IC). IC were really detectable in the cultures of infected B-cells but none were found in the T-cell cultures. Addition of LPS to the culture medium increased the number of IC in B-cell fractions up to 1,000-fold. Furthermore, in T-cell cultures with LPS, IC also appeared in number which approximately correlated with the contaminating Ig+ cells of the T-cell fraction. In contrast, Con A had no consistent effect on the infection of either B or T cells. In the absence of MuLV-F, mitogenic stimulation alone did not elicit any endogenous IC. In subsequent experiments, purified lymphocytes were infected in diffusion chambers in vivo. The number of IC in infected B cells increased 1,000-fold as compared to infection in tissue culture. The peak of infection at 10 days was followed by a slight decline. Infected cells were also found in diffusion chambers containing T-cell fractions; these IC had very similar kinetics to those in B-cell-containing chambers, but their number was 10 times lower, suggesting that the infected cells were B cells, which comprised about 10% of the T-cell fraction. The virus-related antigens were detectable by immunofluorescence on the membrane of cells recovered from B-cell-bearing chambers but not on cells from T-cell-bearing chambers.

Animals↗