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L W Schierman

Publications and source records attributed to L W Schierman.

At least 19 recordsLinked to original sources
PubMed1990

Transplantable Marek's disease lymphomas. IV. Differences in lethality of lymphoma cell lines determined by route of inoculation.

Mortality caused by inoculation of cells from four Marek's disease herpes virus-induced transplantable lymphomas was studied in two related inbred lines of chickens. While i.m. inoculation of 10(4) cells from each lymphoma generally caused death of all syngeneic recipients by 18 days post-inoculation, one of the lymphomas (UG2) was unique in that the same number of cells, when inoculated i.v., caused less than 20% mortality by that time. Lethality induced by cells from the other three lymphomas, when inoculated i.v., was as high or higher than when inoculated i.m. Mortality after intra-abdominal or s.c. inoculation of cells from all four lymphomas was similar to that after i.m. inoculations. Chickens inoculated with syngeneic UG2 cells by the i.v. route were significantly protected against a subsequent i.m. challenge with the same or other syngeneic lymphoma cells. However, UG2 lymphoma cells were highly lethal when inoculated i.v. into birds previously treated with the antimacrophage agent carageenan or immunosuppressed by neonatal treatment with cyclophosphamide. Thus, UG2 cells are distinctive in that, when inoculated i.v., they do not cause death of syngeneic hosts but instead induce resistance to a lethal challenge.

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PubMed1989

Transplantable Marek's disease lymphomas. III. Induction of MHC-restricted tumor immunity by lymphoblastoid cells in F1 hosts.

F1 chickens, which were a cross between birds of the related inbred lines G-B1 and G-B2, were immunized with in vitro cultured virus-non-producer lymphoblastoid cells that were either syngeneic or allogeneic with the challenge tumor cells. The lymphoblastoid cells were derived from Marek's disease herpesvirus (MDV)-induced transplantable tumors. Previous findings showed that such immunization of G-B1 and G-B2 chickens prevented early mortality caused by the tumors. Lymphoblastoid cells syngeneic with the tumors were more effective than allogeneic cells, suggesting that an MHC-restricted immune response was induced, or, alternatively, that immune elimination of allogeneic cells prevented them from initiating strong immunity to MDV-associated tumor antigens. Immune elimination of the immunizing cells should not occur in F1 birds heterozygous for the 2 different parental MHC haplotypes (B6 and B13). Early mortality among F1 chickens immunized with lymphoblastoid cells that were syngeneic with the challenge tumor cells was significantly lower than for non-immunized control chickens or for birds immunized with lymphoblastoid cells that were allogeneic with the challenge tumor cells. Our results suggest that MDV-induced tumor antigens may be recognized by the host as altered-self MHC antigens.

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PubMed1989

Marek's disease virus-induced transient paralysis in chickens: demonstration of vasogenic brain oedema by an immunohistochemical method.

The presence of vasogenic brain oedema and its distribution in Marek's disease virus (MDV)-induced transient paralysis (TP) were determined in genetically resistant and susceptible inbred White Leghorn chickens. MDV-inoculated TP-susceptible chickens with nervous signs (9 days post-inoculation) had severe vacuolation of cerebellar white matter and associated diffuse leakage of albumin and IgG. The serum protein leakage was associated morphologically with a vasculitis and intramural pseudocyst formation in the walls of blood vessels cuffed by mononuclear cells. This transient vasculitis and resulting vasogenic oedema coincided with the temporary neurological signs seen in TP-susceptible chickens. The vasculitis and vasogenic oedema were not present in brain tissue from recovered MDV-inoculated TP-susceptible chickens, MDV-inoculated TP-resistant chickens, or uninoculated control chickens from either line.

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PubMed1988

Marek's disease virus-induced transient paralysis in chickens: alterations in brain density.

The presence of brain edema and its distribution in Marek's disease virus (MDV)-induced transient paralysis (TP) was determined in genetically resistant and susceptible inbred White Leghorn chickens. Density measurements on samples from the cerebellum, cerebral cortex, optic chiasm, and optic lobe were determined on continuous density Percoll gradients. At 9 days post inoculation of MDV, the cerebellums from the susceptible line of chickens were significantly less dense than cerebellums from the resistant line or the controls of either line. The cerebellar edema, as measured by tissue density, coincided with the transient neurological symptoms and was not present in brain tissue from clinically recovered TP birds.

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PubMed1987

Influence of the major histocompatibility complex on tumor regression and immunity in chickens.

A number of studies show that major histocompatibility complex (MHC) genes control host immune responses to viral-induced chicken tumors. The MHC gene-controlled responses to malignant neoplasms caused by Rous sarcoma virus, lymphoid leukosis virus and Marek's disease virus are reviewed. Genes that determine regression of Rous sarcomas and resistance to development of lethal Marek's disease lymphomas appear to map within the B-F region of the MHC. In some cases, genetic complementation of both MHC genes and non-MHC genes may be responsible for regression of tumors. Metastasis of Rous sarcoma cells is also influenced by the host's MHC genotype. Background genes can modify the specific MHC gene effect on resistance to progressive growth of Rous sarcomas and Marek's disease lymphomas. Studies showing that MHC-restricted immunity may be important in cytotoxic T cell reactions to virus-infected and/or transformed chicken cells are discussed. The MHC-restricted cytotoxicity, whereby the T cells and target cells must share one MHC haplotype for in vitro killing to occur, suggests that the T cells have receptors that recognize virus-altered self MHC antigens. This may be an important immune surveillance mechanism for limiting the proliferative growth of virus-induced tumors in chickens.

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PubMed1987

Evidence for MHC gene control of lesion severity in experimental allergic encephalomyelitis of chickens.

Susceptibility to experimental allergic encephalomyelitis (EAE) was studied in two related inbred lines of chickens (lines G-B1 and G-B2) as well as their F2 generation offspring. MHC (B system) genotypes of G-B1 and G-B2 birds are B13/B13 and B6/B6, respectively. Sensitization with central nervous system (CNS) tissue failed to induce clinical symptoms in any of the birds. However, brain lesions typical for EAE were found to be significantly greater in line G-B1 birds than in line G-B2 birds. Evidence for MHC gene control of EAE brain lesion severity was found with F2 offspring. Mean lesion scores were lowest for B6/B6 birds, intermediate for B6/B13 birds, and highest for B13/B13 birds.

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PubMed1986

MHC-restricted cytotoxic response of chicken T cells: expression, augmentation, and clonal characterization.

Major histocompatibility complex (MHC)-restricted cytotoxicity of chicken lymphocytes was studied by using three reticuloendotheliosis virus (REV)-transformed cell lines as targets in 51Cr-release assays. The cell lines, designated RECC-UG5, RECC-UG6, and RECC-UG8, were developed from bone marrow cells of REV-infected line G-B1, line G-B2, and (G-B1 X G-B2)F1 chickens respectively. Effector cells were obtained from spleens of G-B1, G-B2, F1, and F2 chickens 7 days after inoculation of REV. The inbred G-B1 (MHC genotype B13/B13) and G-B2 (MHC genotype B6/B6) lines originate from a common partially inbred line. Initial studies with effector cells from G-B1 and G-B2 chickens showed that significant cytotoxicity occurred only with syngeneic target cells. The degree of cytotoxicity was markedly enhanced by neonatally treating effector cell donors with cyclophosphamide (CY) and delaying virus challenge until the birds were 4 wk old. Augmentation of cytotoxicity was presumed to be due to elimination of bursal-dependent suppressor T cells by CY. The results with spleen cells from REV-inoculated F2 birds clearly showed that cytotoxicity was MHC restricted; i.e., significant lysis only occurred if effector cells and target cells had a common B system antigen. Lysis of RECC-UG5 targets was three to four times higher than lysis of RECC-UG6 targets when effector cells were from heterozygous (B6/B13)F1 and F2 birds. Because these two target cell lines generally showed a similar degree of lysis by effector cells from syngeneic B homozygous birds, the differences obtained with effector cells from B heterozygous birds was most likely due to differences in the number of effector cells with specificity for each target line. Evidence for an additive cytotoxic effect, considered to be due to the lytic activity of two separate T cell clones, was obtained when F1 effector cells were tested with the F1-derived RECC-UG8 targets. The results of other experiments indicated that the effector cells were of T cell lineage and that their activity was probably directed against virus-induced antigens on the transformed target cells.

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PubMed1985

The structure of Marek disease virus DNA: the presence of unique expansion in nonpathogenic viral DNA.

DNA of Marek disease virus (MDV) consists of two unique regions UL and US flanked by long inverted repeat regions TRL and IRL, and short inverted repeat regions TRS and IRS, respectively, similar to herpes simplex virus DNA. Comparison of restriction patterns between pathogenic and nonpathogenic MDV DNA was made to identify a region of viral DNA different between these two types of MDV, as it may be responsible for the tumorigenicity of MDV in chickens. The results indicated that BamHI-D and -H, located at the long inverted repeat regions TRL and IRL, were specifically expanded in nonpathogenic viral DNA. The location of the expanded region has been determined within 1.5 kilobase pairs of the Bgl I/Pst I fragment of BamHI-D and -H, close to the junction between the inverted repeat and the unique region. The possibility that a gene responsible for tumor induction may be disrupted by such expansion has been discussed.

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PubMed1985

Variation in histology and growth characteristics of transplantable Marek's disease lymphomas.

A comparative study was made of the histology and growth characteristics of three different Marek's disease virus-induced transplantable lymphomas. These lymphomas were developed previously in related inbred chicken lines G-B1 and G-B2. The UG1 lymphoma was developed by serial i.m. passage in G-B1 chickens, and the UG2 and UG4 lymphomas were developed similarly in G-B2 chickens. While all three lymphomas grow progressively and cause rapid death in syngeneic hosts, differences in pathogenicity exist. For equivalent passage levels, the mean time to death of syngeneic chickens inoculated with 10(5) lymphoma cells was 10.8, 12.8, and 16.3 days postinoculation for UG1, UG2, and UG4, respectively. Histological features examined at the light microscopic level included tumor necrosis, muscle invasion, mitotic activity, and presence of heterophils (comparable to mammalian neutrophils). The UG2 lymphoma was characterized by a high degree of necrosis during all stages of growth. This feature was least pronounced in UG4 lymphomas, which generally grow to a much larger size than UG1 or UG2 lymphomas. Vascular invasion was a feature of UG2 lymphoma cells in skeletal muscle and may account for the necrosis. The UG2 cells, which are somewhat larger than UG4 cells, occasionally contained cytoplasmic vacuoles. While the number of heterophils was highest in early stages of UG2 tumors, the role of these cells is unclear. The findings provide the basis for utilizing the transplantable lymphomas as a model to study mechanisms underlying variable pathogenicity of malignant tumors.

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PubMed1984

Transplantable Marek's disease lymphomas. II. Variable tumor immunity induced by different lymphoblastoid cells.

The effectiveness of cells from 6 different Marek's disease (MD) lymphoblastoid cell lines to induce immunity to syngeneic transplantable MD lymphomas was investigated in 2 related inbred lines of White Leghorn chickens (lines G-B1 and G-B2) that have different major histocompatibility complex (MHC) genotypes. Cells from 2 line G-B1 lymphomas (MDCT-NYM1 and MDCT-UG1) and 1 line G-B2 lymphoma (MDCT-UG2) were used for challenge. Three of the lymphoblastoid cell lines tested were developed from these lymphomas. Growth of palpable lymphomas was lowest among G-B2 chickens immunized with syngeneic lymphoblastoid cells. Protection against the early lethal effects of the highly virulent transplantable lymphomas was greatest in both lines of chickens when the lymphoblastoid cells were syngeneic with the hosts. Lymphoblastoid cells of unknown MHC type either failed to induce immunity to the lymphomas in both lines or protected some line G-B2 chickens challenged with syngeneic MDCT-UG2 lymphoma cells.

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PubMed1983

Marek's disease virus-induced transient paralysis: a comparison of lesions in susceptible and resistant lines of chickens.

A study was conducted to determine the causative lesion of Marek's disease virus-induced transient paralysis. Brain histologic lesions were quantitated and compared in genetically resistant and susceptible inbred chickens. Comparisons were made 11 days post inoculation (PI) of virus when clinical signs were evident in susceptible birds and on day 17 PI when these signs had remitted. Clinically-affected birds from the susceptible line on day 11 PI had consistent evidence of neuropil vacuolation compatible with brain edema; two of these birds also had vasculitis. These lesions were absent in both clinically-recovered birds from this line evaluated on day 17 PI and genetically resistant birds studied on day 11 PI. Our findings suggest that the causative lesion of transient paralysis is vasogenic brain edema.

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PubMed1983

Suppression of humoral immunity in chickens prevents transient paralysis caused by a herpesvirus.

Marek's disease virus (MDV)3 is a highly oncogenic herpesvirus that usually causes visceral lymphomas and lymphoid infiltration of the peripheral nerves in chickens. A relatively rare encephalitic condition, first found in farm flocks and referred to as transient paralysis (TP), is also caused by MDV(1). TP symptoms occur 9 to 11 days after MDV inoculation and range from mild ataxia to profound coma. Most birds recover by 24 to 72 hr after onset of symptoms, although severely affected birds may die within the same time period. Previous studies in this laboratory (2) showed that susceptibility to TP is a recessive trait controlled by major histocompatibility complex (MHC) genes (i.e., B complex genes of chickens). Inbred line G-B1 chickens (B13/B13) are resistant to TP, whereas chickens from related inbred lines G-B2 (B6/B6) and G-B3 (B15/B15) are highly susceptible. In this study chickens were immunosuppressed by neonatal cyclophosphamide (CY) treatment or surgical bursectomy (BX) to determine the possible role of antibodies in the pathogenesis of TP.

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PubMed1983

Motor nerve conduction velocity in normal chickens.

Muscle potentials evoked by proximal and distal tibial nerve stimulation were evaluated and used to calculate motor nerve conduction velocity in 65 chickens. Two potentials analogous to the M and F waves recorded in persons consistently were evoked. The mean tibial motor nerve conduction velocity +/- SD of the birds was 32.3 +/- 4.0 m/s. This value varied significantly (P less than 0.05) with both age and cloacal temperature.

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PubMed1983

Marek's disease virus-induced transient paralysis: clinical and electrophysiologic findings in susceptible and resistant lines of chickens.

Results of neurologic examination, EEG, and motor nerve conduction velocity quantitation were analyzed in a line of chickens susceptible to Marek's disease virus-induced transient paralysis and compared with findings in a resistant line. Both lines were evaluated on the day before virus inoculation (day 1; base line) and on days 12 and 19. The susceptible birds frequently became depressed and paretic on day 11 or 12 and then recovered, and the resistant line rarely was affected clinically. The EEG of clinically affected birds from the susceptible line correlated well with the clinical course of the disease. Electroencephalographic abnormalities were absent in these birds at base line, evident at 12 days, and had remitted when they were reevaluated on day 19. The pattern in these clinically affected birds was predominantly low voltage-fast activity with frequent spikes. In contrast, the EEG recorded in resistant birds remained essentially the same throughout the study. Mean motor nerve conduction velocity values for the 2 lines of birds did not differ significantly when compared either between or within groups. These findings indicate that Marek's disease virus-induced transient paralysis may be an inflammatory encephalopathy.

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PubMed1981

MHC gene control of growth of avian sarcoma virus-induced tumours in chickens: a study on the role of virus strains.

A comparison was made of growth patterns (progression/regression) of tumours induced by different strains of avian sarcoma virus in two partially congenic inbred lines of chickens homozygous for different MHC haplotypes. In each instance studied, the ability to regress tumours was shown to be a dominant trait controlled by MHC-linked genes. The results also demonstrate a difference in growth pattern between tumours induced by different strains of virus in an inbred line as well as different growth patterns of tumours induced by the same strain of virus in the two inbred lines. We conclude that the MNC-linked resistance gene is part of a polymorphic genetic region and, in addition, that there is immunogenic heterogeneity of the viral gene product expressed on tumour cells induced by closely related viral strains which is relevant to tumour regression. We suggest that the product of the src gene, p60src, is a plausible candidate for the immunogenic target of the MHC-linked rejection response.

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PubMed1980

Independence of chicken major histocompatibility antigens and tumor-associated antigen on the surface of herpesvirus-induced lymphoma cells.

Capping of chicken major histocompatibility (MHC) antigens on normal thymus, spleen, and peripheral blood leukocytes was demonstrated, although MHC antigens appeared to be present on only 15 to 18% of normal thymus cells. MHC antigen capping also occurred on cells from a Marek's disease herpesvirus-induced transplantable lymphoma (MDCT-NYM1). Capping of a Marek's disease tumor-associated surface antigen (MATSA) could be induced on MDCT-NYM1 lymphoma cells as well as on cells of two Marek's disease in vitro lymphoblastoid cell lines (MDCC-MSB1 and MDCC-LS1). Cocapping of MHC antigens and MATSA did not occur on MDCT-NYM1 lymphoma cells. The results suggest that MHC antigens and MATSA are not structurally associated on the cell membrane.

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