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Biomedical subjects

P G Gell

Publications and source records attributed to P G Gell.

At least 19 recordsLinked to original sources
PubMed1985

Production of cell-mediated immune response to herpes simplex virus by immunization with anti-idiotypic heteroantisera.

Three BALB/c monoclonal antibodies capable of neutralizing herpes simplex virus type 1 (HSV-1) were used to prepare rabbit anti-idiotypic antisera. Affinity-purified antibodies from four of these rabbits were used to immunize mice by repeated subcutaneous injection over a period of 6 to 7 weeks: the mice were then challenged with HSV-1 subcutaneously in the ear pinna. Measurement of ear swelling showed that prior administration of anti-idiotypic serum could generate dose-dependent delayed-type hypersensitivity responses.

Animals↗
PubMed1983

Membrane phenotype of murine effector and suppressor T cells involved in delayed hypersensitivity and protective immunity to herpes simplex virus.

The membrane phenotype of T cells involved in delayed hypersensitivity (DH), protective immunity, and suppression of delayed hypersensitivity to herpes simplex virus (HSV) has been determined. T cells from immune lymph nodes transferring DH and antiviral immunity to normal recipients were characterized as Lyt 1+2-. There appeared to be no detectable antiviral role for Lyt 1-2+ cells in the transferred cell suspension. Splenic T cells suppressing the induction of DH to HSV were characterized as being both Lyt 1+2- and Lyt 1-2+ 4 weeks after their induction. At earlier times, i.e., after 7 days, the suppression was mediated solely by the Lyt 1+2- population. Thereafter, a progressive increase in the contribution of the Lyt 1-2+ suppressor was observed. Both the early and later phases of suppression were due to I-J positive cells. The nature of the two suppressor cell types is discussed in relation to suppressor cell "cascades" and to the pathogenesis of herpes simplex virus infection.

Animals↗
PubMed1982

Inhibition of herpes simplex virus multiplication by activated macrophages: a role for arginase?

Proteose-peptone-activated mouse macrophages can prevent productive infection by herpes simplex virus in neighboring cells in vitro whether or not those cells belong to the same animal species. The effect does not require contact between the macrophages and the infected cells, may be prevented by adding extra arginine to the medium, and may be reversed when extra arginine is added 24 h after the macrophages. Arginase activity was found both intracellularly and released from the macrophages. The extracellular enzyme is quite stable; 64% activity was found after 48 h of incubation at 37 degrees C in tissue culture medium. No evidence was found that the inefficiency of virus replication in macrophages was due to self-starvation by arginase. As might be predicted macrophages can, by the same mechanism, limit productive infection by vaccinia virus.

Animals↗
PubMed1981

Tolerance and immunity in mice infected with herpes simplex virus: studies on the mechanism of tolerance to delayed-type hypersensitivity.

Tolerance to delayed-type hypersensitivity is produced in mice following an intravenous injection of herpes simplex virus. This form of tolerance is produced early on, following simultaneous injections of virus subcutaneously and intravenously, and is long lasting (greater than 100 days). The early tolerance mechanism is resistant to high doses of cyclophosphamide and is not transferable by serum or spleen cells taken after 7 days. However, spleen cells taken at 14 days onwards inhibit the induction of delayed hypersensitivity when transferred to normal syngeneic recipients. These cells are T lymphocytes and are specific for the herpes type used in the induction.

Animals↗
PubMed1981

Tolerance and immunity in mice infected with herpes simplex virus: simultaneous induction of protective immunity and tolerance to delayed-type hypersensitivity.

Unresponsiveness to delayed type hypersensitivity was induced in mice following an intravenous injection of herpes simplex virus. The principal tolerogens used were thymidine kinase-deficient virus mutants which grow poorly in vivo; u.v.-inactivated and to a lesser extent formalin-inactivated virus were also tolerogenic. The tolerance induced was specific for the virus type. Despite the tolerance to delayed hypersensitivity, anti-viral immunity is present as determined by the rapid inactivation of infectious virus. The mechanism of tolerance to herpes virus and the importance of these observations for the pathogenesis of viral disease is discussed.

Animals↗
PubMed1980

Cell-mediated immunity in herpes simplex virus-infected mice: suppression of delayed hypersensitivity by an antigen-specific B lymphocyte.

Lymph node cells, regional to the site of infection with herpes simplex virus type 1 (HSV-1), when taken 1 to 9 months p.i. and transferred to HSV-1 immune recipients, suppressed the delayed type hypersensitivity (DTH) reaction to the virus. The suppressive activity was specific for HSV-1 and was transferred by a thy-1.2-negative, Ig-positive, lymphocyte population. Anti-HSV-1 serum did not suppress the HSV-1-induced DTH response. Contralateral lymph nodes contained little or no suppressor cell activity but in infected, adult thymectomized mice, these lymph node cells were as effective as the draining node in transferring suppression. The significance of these observations for the pathogenesis of herpes infections is discussed.

Animals↗
PubMed1979

Immune responsiveness and oral immunization.

The effects on the immune response of daily feeding of 30 mg of human serum albumin to rats have been studied. Feeding for periods of 17-20 days consistently resulted in a specific systemic hyporesponsiveness evident on subsequent parenteral immunogen challenge. Local secretory sites such as the major salivary glands were not made hyporesponsive as evidenced by the salivary antibody titres and the enumeration of glandular plaque-forming cells. The levels and classes of antibodies present in the secretions and sera were identified by passive haemagglutination, and a sensitive red-cell-linked antigen-antiglobulin reaction. By the use of radioimmunoassay and haemagglutination inhibition assays it was possible to quantitate the amount of antigen appearing in the circulation at varying times after feeding. It was shown in the use of oesophagectomised rats that absorption of small amounts of intact protein occurs from undefined sites in the oral cavity. Attempts were made to transfer the specific systemic hyporesponsiveness to syngeneic animals using spleen cell and serum transfers.

Administration, Oral↗
PubMed1976

Induction of specific anti-guinea pig T cell sera in rabbits.

In an attempt to increase the specificity of antisera raised in rabbits against strain 2 guinea pig thymocytes and brain, the rabbits were screened for titres of natural antibodies to thymocytes and other lymphocytes. Although unimmunized rabbits commonly had moderate titres of cytotoxic antibodies to guinea pig thymocytes, occasional animals had low titres to thymocytes and moderate titres to bone marrow cells. Intravenous immunization of this latter group of rabbits with thymocytes led to the production of high titred anti-thymocyte sera which were easily made specific for thymus-derived lymphocytes (T cells) by absorption with L2 C lymphoma, a bone marrow-derived lymphoma of strain 2 guinea pigs. Sera raised against guinea pig brain in complete Freund's adjuvant which had high titres of antibodies to both thymocytes and bone marrow cells could be made specific for T cells only with great difficulty. The cytotoxic activity of the anti-T cell serum could be absorbed by strain 2 thymocytes and brain homogenates, while high dilutions of this serum inhibited the formation of spontaneous rosettes between guinea pig lymphoid cells and normal rabbit erythrocytes.

Absorption↗
PubMed1976

Separation by column chromatography of cells active in delayed-onset hypersensitivities.

Lymph node cells from guinea-pigs contact sensitive to 1-thiocyamo-2,4-dinitrobenzene have been fractionated by affinity chromatography over modified polyacrylamide beads. Cells mediating lymphokine release in response to active sensitizer were depleted only by chromatography over dinitrophyenyl (DNP) containing substrates and could be specifically eluted with DNP-glycine. DNP rosette-forming cells (RFC) were equally well depleted by chromatography using either DNP or trinitrophenyl containing materials but could not be eluted from the columns by DNP-glycine. While the antigen receptors of cells mediating the release of macrophage agglutination factor in response to DNP-containing antigens and of DNP-RFC were found to be hapten-specific, their specificity was shown to differ using chromatography over trinitrophenyl containing polyacrylamide.

Animals↗