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Biomedical subjects

J M Sharma

Publications and source records attributed to J M Sharma.

At least 55 records · Page 3Linked to original sources
PubMed1987

Mechanism of T cell immunosuppression by infectious bursal disease virus of chickens.

Spleen cells of chickens infected with IBDV responded poorly to in vitro stimulation with Con A. The mitogenic hyporesponsiveness was due to the presence of suppressor cells that could be removed by pretreatment of IS cells with carbonyl iron or cytodex-3 microcarrier beads. Addition of suppressor cells to normal spleen cells prevented the normal cells from responding to mitogen. Cell-to-cell contact between responder and suppressor cells was not necessary for suppression to occur; the effect was mediated by soluble product(s) released by the suppressor cells. IS cells were also deficient in producing mitogen-induced IL-2 and addition of exogenous IL-2 did not restore mitogenic response of IS.

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PubMed1987

Purification of avian T cell growth factor and immune interferon using gel filtration high resolution chromatography.

A protocol was outlined to separate and purify chicken T cell growth factor or IL-2 and gamma interferon from conditioned medium of Con A activated spleen cells. IL-2 was associated primarily with a protein of 30 kDa in SDS-PAGE and in high resolution gel filtration chromatography. Chicken IL-2 was of low hydrophobicity. A second species of molecular weight 14 kDa was also identified by high resolution gel filtration chromatography. Purified IL-2 gave only 50% of the maximum growth response obtained with IL-2 in crude conditioned medium. Gamma interferon activity was associated primarily with protein of 17 kDa and a second peak of activity was detected with protein of 36 kDa. I-IFN was not cross reactive with human cells and was pH sensitive.

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PubMed1986

Chicken embryonal vaccination with avian infectious bronchitis virus.

A commercial infectious bronchitis virus (IBV) vaccine of the Massachusetts 41 strain was injected in embryonating chicken eggs on embryonation day (ED) 18. The IBV vaccine was pathogenic for embryos, and it was passaged in chicken kidney tissue culture to reduce the pathogenicity. At the 40th tissue culture passage (P40-IBV), the virus became apathogenic for the embryos. Maternal antibody-positive or -negative chicks hatching from eggs injected with P40-IBV developed antibody to IBV and were protected against challenge exposure at 4 weeks of age with virulent Massachusetts 41 IBV. Although P40-IBV protected chicks when administered on ED 18, this virus did not protect chicks well if given at hatch. When combined with the turkey herpesvirus (HVT), P40-IBV given on ED 18 did not interfere with the protection against challenge exposure with virulent Marek's disease virus, nor did the presence of HVT interfere with protection by P40-IBV. Thus, under laboratory conditions, IBV vaccine could be combined with HVT to form a bivalent embryonal vaccine.

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PubMed1985

Field trials to test the efficacy of polyvalent Marek's disease vaccines in layer and broiler breeder chickens.

As a follow-up to earlier trials to evaluate the efficacy of polyvalent Marek's disease (MD) vaccines in broilers, four trials were conducted with layer or broiler breeder flocks. Chickens caccinated with trivalent (Md11/75C plus SB-1 plus HVT) and bivalent (SB-1 plus HVT) vaccines were compared with those vaccinated with turkey herpesvirus (HVT) alone. Data from three of the four trials indicated polyvalent vaccines were more efficacious than HVT. However, critical interpretations were confounded by low MD lesion frequencies, unequal exposure in different houses on a farm, and difficulty in the differential diagnosis of mortality due to neoplasms. The data confirmed our earlier observation that trivalent and bivalent vaccines were equally effective. Broiler progeny of breeders vaccinated or contact-infected with Serotype 2 MD virus were well protected by either bivalent or HVT vaccines against challenge with very virulent MD virus strains in the laboratory. A high incidence of lymphoid leukosis was observed in two trials and may have been due to post-hatch exposure to an unidentified environmental source of avian leukosis virus.

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PubMed1984

Comparative viral, immunologic, and pathologic responses of chickens inoculated with herpesvirus of turkeys as embryos or at hatch.

Chickens were vaccinated with the herpesvirus of turkeys (HVT) at embryonation day 17 or 18 or at hatch and various responses of the 2 vaccinated groups were compared. In embryo-vaccinated chickens, HVT titers were high in the lungs before HVT could be isolated from other tissues. Seemingly, embryos acquired infection via the respiratory tract. In hatch-vaccinated chickens, HVT was first isolated from spleen and then from other tissues. Titers of recoverable HVT in tissues of embryo-vaccinated chickens were higher than in those of hatch-vaccinated chickens, particularly during the 1st week of age. Anti-HVT antibodies and natural killer cell reactivity in spleen effector cells were comparably increased in both vaccinated groups. Embryo vaccination with HVT did not cause progressive lesions, reduction in body weight gain, or impairment of humoral and cellular immune functions. Seemingly, HVT can be used safely as an embryonal vaccine in chickens.

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PubMed1983

Presence of adherent cytotoxic cells and non-adherent natural killer cells in progressive and regressive Marek's disease tumors.

Marek's disease virus-induced progressive tumors and Marek's disease transplantable local regressive tumors were dispersed by treatment with collagenase and cells were examined in vitro for cytotoxic effector functions against target cells of tumor lines. Both types of tumors had adherent and non-adherent cytotoxic cells. The cytotoxicity of adherent cells was detected in an 18-hour but not in a 4-hour 51Cr-release assay. The adherent effector cells from progressive tumors were inactivated by pretreatment with carbonyl iron and carrageenan whereas the adherent effector cells from the regressive tumors were refractory to these treatments. In the progressive tumors, the 18-hour cytotoxic activity of cells of tumors and of spleens of tumor-bearing chickens was compared; the activity was higher in the tumor than in spleen. The nonadherent cell cytotoxicity detectable in a 4-hour 51Cr-release assay was associated with anti thymocyte serum-resistant natural killer cells. The incidence and levels of natural killer cell reactivity were greater in the regressive tumors than in the progressive tumors. In the regressive tumors, the natural cytotoxicity levels were higher in the tumor than in the spleen of tumor-bearing chickens. The differences in characteristics of adherent cytotoxic cells in virus-induced progressive tumors and transplantable regressive tumors and elevated levels of NK cells in regressive but not in progressive tumors may indicate a role for intratumoral immunity in tumor regression.

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PubMed1983

Effect of infectious bursal disease on natural killer cell activity and mitogenic response of chicken lymphoid cells: role of adherent cells in cellular immune suppression.

A pathogenic isolate of infectious bursal disease virus (IBDV) caused persistent and extensive lesions in the bursa but mild and transient lesions in the thymuses of chickens of lines 63 and P. The effect of IBDV on two cellular immune functions, namely, natural killer cell cytotoxicity and mitogenic response, was studied. The natural killer cell activity was not consistently influenced, but the virus, during the first 2 weeks of infection, caused transient depression of the blastogenic response of spleen cells to phytohemagglutinin. Studies on mitogenic hyporesponsiveness revealed that the functional impairment was mediated by a suppressor cell that shared several characteristics with macrophages; i.e., the suppressor cell was adherent to plastic, was phagocytic, and resisted treatment with antithymocyte and antibursa cell sera. Removal of suppressor cells from the spleens of virus-infected chickens resulted in restoration of the mitogenic response of cells. Further, in mixing experiments, the suppressor cell isolated from the spleens of virus-infected chickens also inhibited the mitogenic response of normal spleen cells. We concluded that reduced mitogenic response of lymphocytes in IBDV-infected chickens was not due to a lack of functional T-cells, as suggested previously by others, but was due to macrophage-like suppressor cells. The suppressor cells, although present in certain normal chickens, became activated during early stages of IBDV infection.

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PubMed1983

Establishment of lymphoblastoid cell lines from Marek's disease primary tumors.

Seven lymphoblastoid cell lines were developed from 15 Marek's disease primary lymphomas treated to remove adherent cells (46.7% success rate) and 1 cell line was developed from 15 untreated lymphomas (6.7% success rate). These cell lines are designated as MDCC-RP22 through MDCC-RP29. Tumor materials were from 151(5) x 7(1) chickens infected with either JM-111S clone or the GA-22 clone of Marek's disease virus. Factors contributing to the establishment of cell lines include, in addition to the removal of adherent cells at the initial stage of culture, the periodic adjustment and the concentration of viable cells, including the removal of dead cells. The cell lines bear T-cell surface markers and Marek's disease tumor associated surface antigen (MATSA). MDCC-RP22 and MDCC-RP23 are high virus producers.

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PubMed1983

A monoclonal antibody reactive with Marek's disease tumor-associated surface antigen.

An antibody-secreting hybridoma, RPH-6, to Marek's disease tumor-associated surface antigen (MATSA) was produced by somatic-cell hybridization between the mouse myeloma SP2/O-Ag/14 and spleen cells from MSB1 immunized mice. The antibody reacted with 95 to 100% of the cells from eight of 10 chicken MD cell lines and one of two turkey MD cell lines. It did not react with chicken MD cell lines RP1 and SK3, turkey MD cell line RP19, lymphoid leukosis (LL) cell lines, RP9 and RP12, and reticuloendotheliosis virus (REV) cell line RP14. A weak reaction was observed with REV cell line RP13 (10 to 20%), and a very slight reaction with normal chicken spleen cells (1 to 5%). RPH-6 produces immunoglobulin of the IgM class. Cell culture and mouse ascitic fluids have titers of 10(2) and 10(6), respectively, by fluorescent antibody (FA) test against MD tumor cell lines. The antibody did not react with Marek's disease virus (MDV) internal antigen or membrane antigen as detected by indirect FA test on chicken embryo fibroblast cultures grown on coverslips. The 51Cr release assay showed RPH-6 is highly cytotoxic (60% release) only against MD lymphoblastoid cell lines, with antibody prepared from mouse ascites having a cytotoxic titer approaching 10(6). Results from using RPH-6 for differential diagnosis of chicken lymphoid tumors of unknown origin were in complete agreement with those obtained with rabbit anti-MATSA reference serum and pathologic diagnosis.

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PubMed1982

Establishment of B-lymphoblastoid cell lines from Marek's disease virus-induced tumors in turkeys.

Four lymphoblastoid cell lines were established from tumours of turkeys inoculated with high doses of the GA strain of Marek's disease virus (MDV). Unlike other MD lymphoblastoid cell lines of chicken origin, these MDV transformed turkey line appear to be B lymphocytes and produce immunoglobulin. Growth characteristics of these cell lines are slightly different; however, they all produce low levels of MDV-specific antigen and carry the complete genome of the virus as determined by virus rescue in the chicken or in duck embryo fibroblast cultures. These cell lines are pathogenic for chickens and produce virus-induced MD lesions. All four lines are free of the herpesvirus of turkeys, reticuloendotheliosis virus, and three lines are also free of avian leukosis virus. They all have typical normal turkey chromosomes and are positive for Marek's disease tumor-associated surface antigen.

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PubMed1982

Marek's disease in turkeys: lack of protection by vaccination.

Herpesvirus of turkeys, a highly effective vaccine against Marek's disease (MD) in chickens, was ineffective in protecting turkeys against MD. Another tissue-culture attenuated vaccine virus also protected chickens, but not turkeys, from MD. Intact and immunosuppressed turkey poults inoculated with herpesvirus of turkey developed a persistent viremia, but did not have detectable gross or microscopic lesions.

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PubMed1981

Natural killer cell activity in chickens: target cell analysis and effect of antithymocyte serum on effector cells.

A battery of lymphoid and nonlymphoid cells was examined for susceptibility to lysis by natural killer cells of chickens. Several susceptible targets were recognized, and most susceptible among these were cells of line LSCC-RP9, derived from a lymphoid tumor induced by Rous-associated virus 2. The natural killer reactivity against LSCC-RP9 target cells did not appear to be directed against an antigen(s) induced by Rous-associated virus 2 because other lymphoid and nonlymphoid cells infected with this were resistant to lysis in vitro by natural killer cells. The effector cells of natural killer reactivity in chickens were refractory to treatment with potent anti-T-cell and anti-B-cell sera. Inoculation of Marek's disease virus in line 15 X 7 chickens resulted in enhanced natural killer cell activity, and the effector cells of this enhanced activity, and the effector cells of this enhanced activity were also resistant to anti-T-cell serum.

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PubMed1981

Fractionation of Marek's disease virus-induced lymphoma by velocity sedimentation and association of infectivity with cellular fractions with and without tumor antigen expression.

Cell suspensions of lymphomas induced by Marek's disease (MD) virus were fractionated by sedimentation at unit gravity on a continuous gradient of bovine fetal serum. Cells in various fractions were examined for MD tumor-associated surface antigen (MATSA) by indirect immunofluorescence, using specific antibody, and for viral infectivity by cocultivating fractionated cells with permissive monolayer cells of duck embryo fibroblasts. Most MATSA-bearing cells in the lymphomas sedimented at a sedimentation velocity of greater than 3.0 mm/hour, whereas smaller, slow-sedimentating cells were generally devoid of MATSA expression. Viral infectivity was associated with MATSA-bearing and MATSA-lacking fractions. Within the limits of the experimental procedures used, this observation provided evidence that presence of MD virus genome in lymphocytes doses not result in concurrent expression of detectable MATSA and that MATSA likely represents another stage of interaction between MD virus and certain lymphocytes.

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PubMed1981

Suppression of immunologic function and degeneration of lymphoid organs in cyclophosphamide-treated turkeys.

Neonatal administration of 8 to 20 mg of cyclophosphamide (CY) in turkey poults resulted in a marked alteration in the morphologic features of all major lymphoid organs. Cyclophosphamide induced severe deficiency in antibody response to multiple injections of Brucella abortus and sheep RBC and in vitro proliferative response of peripheral blood leukocytes to concanavalin A. The morphologic regeneration of thymus and of thymus-dependent areas was marked in all major lymphoid organs by posttreatment day 15. This regeneration preceded functional recovery of the mitogenic response of peripheral blood leukocytes. The regeneration of the bursa and bursa-dependent areas in other lymphoid organs was minimal through posttreatment day 27. Thus, CY may be used effectively in turkeys as an immunosuppressive reagent.

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PubMed1980

In vitro suppression of T-cell mitogenic response and tumor cell proliferation by spleen macrophages from normal chickens.

Adherent cells isolated from spleen of normal specific pathogen-free chickens inhibited mitogen-induced blastogenesis of autochthonous, syngeneic, or allogeneic lymphocytes. The adherent cells were also inhibitory to in vitro proliferation of cells of a rapidly dividing tumor line, MDCC-MSB-1, derived from a lymphoma induced by Marek's disease virus. The effector cell of suppression of both lymphoprolifrative functions appeared to be a macrophage because the suppressive activity of adherent cells could be abrogated by pretreatment with carrageenan but not with antisera specific to chicken T or B cells. The proportion of macrophages needed for effective suppression was substantially higher than the proportion of macrophages ordinarily present in spleen of normal, unstimulated chickens. This heretofore unrecognized suppressive capability of normal, presumably resting macrophages have been detected in certain infections.

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PubMed1980

Effect of neonatal thymectomy on pathogenesis of herpesvirus of turkeys in chickens.

Effect of immunosuppression on pathogenicity of herpesvirus of turkeys (HVT) in chickens was studied. In three experiments, newly hatched chickens of two genetic strains were surgically thymectmized and gamma-irradiated and then exposed to HVT. Lymphoid cells of thymectomized-irradiated chickens had reduced in vitro mitogenic response; this result indicated that the immunosuppressive regimen caused suppression of T cell function. The immunosuppressed chickens had more circulating HVT and had a slightly higher frequency of microsocpic lesions in peripheral nerves than the intact control chickens, although the intensity of lymphoproliferation remained very mild and no gross lesions or clinical disease was noted during the 5-week observation period. The absence of significant lesion development in an immunosuppressed host indicated that pathogenic potentials of HVT may be limited.

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