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H Kirchner

Publications and source records attributed to H Kirchner.

At least 361 records · Page 20Linked to original sources
PubMed1984

Concanavalin A-induced interferon gamma production by murine spleen cells and T cell lines. Lack of correlation with Lyt 1,2 phenotype.

Concanavalin A(Con A)-induced interferon-gamma (IFN gamma) production by resting or preactivated murine spleen cells negatively selected with monoclonal antibodies specific for Lyt 1,2 antigens plus complement (C) and by interleukin 2(IL-2)-dependent T cell lines of different Lyt phenotype was studied. The data show that most of the IFN-gamma produced upon stimulation of resting spleen cells was a product of Lyt 1+2+ cells. Lyt 1-2+ cells were negative for IFN gamma production. When spleen cells that had been preactivated for 3 days with Con A were restimulated with Con A, Lyt 1+2+, Lyt 1+2- as well as Lyt 1-2+ cells produced IFN gamma in a relationship of approximately 5:3:1. In both cases the picture remained unaltered independently when the supernatants were harvested after 1, 3 or 5 days. Furthermore, two IL-2 dependent T cell lines were studied in regard to Con A-induced IFN gamma production. Line 1.3 was Thy 1+, Lyt 1-2+, whereas line 20.9. was Thy 1+, Lyt 1+2-. Both lines produced initially high titers of IFN gamma upon stimulation with Con A. After prolonged passage in vitro, however, they progressively lost the capacity to produce IFN gamma.

Animals↗
PubMed1984

Characterization of lymphokine-mediated activation of macrophages for antigen presentation: studies with long-term cultured bone marrow-derived macrophages and cloned T cells.

In cultures of bone marrow (BM) supplemented with L cell-derived colony-stimulating factor a pure population of macrophages (M phi) differentiates, which can be further propagated with a doubling time of 3.8 days. "Young" BMM phi obtained on day 8 of culture were shown to act as antigen-presenting cells inducing the antigen-specific proliferation of the cloned T cell line ST2/K.9, whereas "old" M phi had lost this ability. However, at any time tested (up to 132 days) the presentation function of old BMM phi could be completely restored by pulsing the cells with lymphokines (LK). A duration of 11 hr for the LK-pulse was sufficient to trigger the M phi to exert an optimal presentation function. This activity could be maintained when the LK-treatment was prolonged (tested up to 17 days). Activation was accompanied by a deceleration of growth. The LK effective in M phi activation were found to be contained in the supernatants of T cell lines stimulated by antigen or mitogen, and could be substituted by a low dose (5-10 units/ml) of recombinant interferon-gamma. In direct comparison LK-triggered BMM phi presented antigen as efficiently as peritoneal exudate M phi activated in vivo by ConA. Moreover, primed lymph node T cells responded to antigen-presenting BMM phi in a similar way as ST2/K.9 T cells. Therefore, these findings obtained with long-term cultured cells can be expected to reflect a physiological mechanism for the amplification of the immune response.

Animals↗
PubMed1984

Protection of mice against infection with mouse hepatitis virus type 3 by injection of silica.

Injection of silica did not brake the resistance against MHV3 conferred to C57BL/6 mice by injection of C. parvum. However, silica itself had a marked protective effect against MHV3 infection that was maximal when injecting 1 mg 2 hrs before virus infection. The protective effect of silica was observed in a number of inbred mouse strains that differ in their relative resistance to MHV3 infection. No viral titers were observed in the spleen and liver of mice which had received MHV3 plus silica, whereas high titers were observed in the virus-infected controls. Injection of silica caused a marked decrease in the number of esterase-positive macrophages in the peritoneal wash-out population, that may be compatible with the possibility that the cause of the protection is the depletion of target cells for the viral infection. This latter effect, however, was short-lived and 24-48 hrs after injection of silica, high numbers of esterase-positive cells were again observed. This may explain why only little protection was observed when silica was administered 2 days before virus infection.

Adjuvants, Immunologic↗
PubMed1984

Induction of interferon gamma in mouse spleen cells by culture supernatants of mycoplasma arthritidis.

Factor(s) in the supernatant of cultured mycoplasma arthritidis (MAS) represented potent inducers of interferon (IFN) in cultures of mouse spleen cells. Responding mouse strains included A/J, BALB/c, CBA, C3H, and DBA/2 whereas spleen cells of C57BL/6 and C57BL/10 mice were nonresponders. Interferon production was controlled by the I region of the H-2 locus. Treatment of CBA spleen cells by anti-thy-1 antibody plus C abolished IFN production. A similar effect was seen when CBA spleen cells were freed of macrophages by passage through Sephadex G-10 columns. Pure macrophages themselves, however, were not producing IFN when treated by MAS. Macrophage-depleted CBA spleen cells could be reconstituted to produce IFN by the addition of 2-ME. Interferon induction by CBA spleen cells was independent of lymphoproliferation as evidenced by experiments utilizing mitomycin C. The IFN induced by MAS represented IFN gamma (gamma), since it was acid-labile and neutralized by a specific antiserum.

Animals↗
PubMed1984

Lymphoproliferation induced in mouse spleen cells by Mycoplasma arthritidis mitogen. Reversal of the defect of nonresponder mice.

Spleen cells of various mouse strains (e.g. BALB/c, C311, and CBA) reacted towards MAS (a mitogen derived from supernatants of cultured Mycoplasma arthritidis) with a marked lymphoproliferative response. This reactivity was T-cell-dependent. It was reduced by 90% after removal of macrophages by passage of the spleen cells through Sephadex G-10 columns. Addition of 2-mercaptoethanol (2-ME) to macrophage-depleted CBA spleen cells completely restored the response to MAS. Spleen cells of C57BL/6 and C57BL/10 mice were unreactive to MAS, even in the presence of macrophages, and this non-reactivity was controlled by the I-region of H-2. Other mouse strains that, similarly to C57BL/6, lack the expression of I-E on the cell surface (that is, mice of the haplotype H-2f, H-2q, and H-2s) were also non-responsive to MAS. However, the addition of 2-ME to spleen cells of non-responder mice resulted in high lymphoproliferative responses to MAS, which were as high as those of CBA spleen cells. The reaction of C57BL/6 spleen cells to MAS in the presence of 2-ME again was T-cell-dependent, as shown by data with spleen cells of homozygous nude mice and spleen cells treated by anti-thy-1 and C. A macrophage dependency of this response was also evident. When C57BL/6 spleen cells were vigorously freed of accessory cells by the use of nylon wool columns, the MAS response could no longer be restored by 2-ME.

Animals↗
PubMed1984

Lymphoproliferative responses of spleen cells of inbred rat strains to Mycoplasma arthritidis mitogen.

A potent mitogen for T lymphocytes of various species has recently been isolated from the supernatant of cultured Mycoplasma arthritidis organisms (MAS). In the mouse, reactivity to this mitogen has been observed to be controlled by the I-E subregion of the major histocompatibility complex. We have analysed the responses of spleen cells from several inbred rat strains covering practically all known haplotypes of the major histocompatibility complex of the rat (RT1). Unlike in the mouse, all of these responded well to MAS, except for the BN rat strain, which is a low responder to all T-cell mitogens, including phytohaemagglutinin and concanavalin A. This unresponsiveness, however, appeared to be unrelated to the RT1 haplotype, since LEW.1N rats carrying the same RT1n haplotype as BN animals responded well. Mice of the strain C57BL/6 are non-responders to MAS, but--as previously shown--their spleen cell responses can be reconstituted by the addition of 2-mercaptoethanol. No such reconstitution was observed for the low responsiveness of BN rat spleen cells. Stimulation with MAS induced high titres of interferon (presumably gamma interferon) in spleen cells from all rat strains tested. Spleen cells from BN rats produced lower interferon activities than those from other strains.

Animals↗
PubMed1984

[Lymphokine production in vitro by blood lymphocytes from patients with a defective or hyperactive immune system].

Blood lymphocytes from 8 patients with common variable immunodeficiency (CVID), 5 patients with signs of polyclonal activation of the immune system (1 SLE, 3 AILAP, 1 NHL) and 6 patients with various granulomatous diseases were examined for their capacity to produce lymphokines in vitro. Lymphocytes from 16 healthy individuals served as controls. To induce interleukin-2 (IL-2) and gamma-interferon (gamma-IFN) production lymphocytes were stimulated for 24 hrs with ConA or PHA or for 72 hrs with ConA + PMA + urea. alpha-IFN production was induced with Herpes simplex virus I (HSV) and the mycoplasma infected murine leukemia line L1210. Cell-free culture supernatants were harvested and IL-2 activity was determined by means of its growth promoting activity for a murine T-cell line (M-2). IFN activities were measured in a conventional virus plaque reduction assay. Besides lymphokine production the isolated cells were also examined for lymphocyte markers, mitogen responsiveness and NK activity. As compared to the control group, CVID lymphocytes exhibited a slightly enhanced IFN production and a moderately reduced IL-2 production. Three day preincubation in FCS containing medium enhanced the IL-2 production of control and patient lymphocytes. By contrast, preincubation of lymphocytes in medium supplemented with autologous serum no longer enhanced IL-2 production of CVID lymphocytes whereas it still did so for control lymphocytes. A striking finding was the impairment of IL-2 and IFN production in cultures of lymphocytes from patients with a polyclonally activated immune system. Notably lymphocytes from the three patients with angioimmunoblastic lymphadenopathy (AILAP) failed to produce significant amounts of lymphokines. Patients with granulomatous diseases (3 Morbus Behçet, 1 tuberculosis, 2 chronic granulomatous diseases) showed little alterations of their lymphokine production capacity. The results are compared with other lymphocyte parameters and are discussed in view of recent reports in the literature on lymphokine production in various diseases.

Adult↗
PubMed1984

Replication of herpes simplex virus in human T lymphocytes: characterization of the viral target cell.

Herpes simplex virus (HSV) replicated in mitogen-stimulated human T cells. Virus replication was obtained in highly enriched mitogen-stimulated T cells of the OKT 3+, OKT 4+, or OKT 8+ subtype, in stimulated B cells, and in macrophages precultured for 7 days. In contrast, no virus replication was obtained in unstimulated T or B cells, in macrophages grown in culture for 1 day, in Null/NK cells, or in granulocytes. Infectious center assays revealed that below 1% of the infected T cell subpopulations supported virus replication, whereas up to 42% of infected B cells and 80% of macrophages cultured for 1 wk were able to replicate HSV. By indirect double immunofluorescence studies, complement-mediated mass cytolysis, and positive selection experiments, it was shown that only T cells expressing Ia antigen actively replicated the virus. T cells activated in the mixed lymphocyte culture and with UV-inactivated HSV were also susceptible to HSV infection. Several human leukocyte cell lines were tested for their ability to support virus replication and were tested for a correlation with the expression of Ia antigen. Only cell lines expressing Ia antigen on more than about 5% of the total population produced new progeny virus. Ia-expressing T cells that spontaneously replicated HSV without any mitogenic prestimulation were found to occur in variable numbers in human cord blood. It is suggested, that such T cells, permissive for HSV replication, might contribute to an outspread of viral infection in vivo.

Antibodies, Viral↗
PubMed1984

[Clinical course and therapy of acquired anal incontinence].

43 patients suffering from anal incontinence underwent surgical correction. The late results up to 14 years after surgery are described. Continence was evaluated by inquiries and by manometric readings of the recto-anal stress profile. Prevailing surgical procedures were reconstruction of the anal sphincter (n = 23) and pedicled transplantation of the M. gracilis (n = 10). Both methods yielded satisfactory late results.

Adult↗
PubMed1983

Production of colony-stimulating factors by Hodgkin cell lines.

This work was performed with L 428, a cell line established in 1978 from a patient with Hodgkin's disease. These in vitro cells represent counterparts of in vivo Hodgkin and Sternberg-Reed cells. L 428 and its derived sublines produce a significant amount of colony-stimulating factor (CSF) compared to standard preparations of CSF (fetal liver conditioned medium). Hodgkin-cell-derived conditioned medium, tested in cord-blood assays and in semi-solid agar systems, induced myeloproliferation predominantly. Production of CSF is independent of fetal calf serum concentration in the cultures. L 428-conditioned medium could provide an excellent source for characterization and purification of granulocyte CSF.

Cell Line↗
PubMed1983

Interferon-gamma production by Listeria monocytogenes-specific T cells active in cellular antibacterial immunity.

Cultures of peritoneal exudate T lymphocyte-enriched cells (PETLEC) from Listeria monocytogenes-immune mice, antigen-presenting cells (APC) and heat-killed L. monocytogenes produced high amounts of interferon-gamma (IFN-gamma). High IFN titers were also observed after stimulation of L. monocytogenes-immune cell cultures with the T cell mitogens concanavalin A and phytohemagglutinin. L. monocytogenes-immune PETLEC produced several fold higher IFN titers than normal cell cultures in response to mitogen and antigen. Under both circumstances, APC were required for optimum responses. L. monocytogenes-immune PETLEC participating in IFN production were Lyt 1+23-. IFN-gamma was also produced in cultures of cloned L. monocytogenes-specific T cells. Since the same T cell clone showed antigen-specific proliferative responses and interleukin production in vitro, and could adoptively mediate delayed-type hypersensitivity and anti-listerial protection in vivo, it is suggested that IFN production is a function of specific T cells active in cellular antibacterial immunity.

Animals↗
PubMed1983

Bone-marrow derived macrophages as targets for the replication of mouse hepatitis virus type 3.

Bone-marrow (BM) derived macrophages are sensitive target cells for replication of mouse hepatitis virus type 3 (MHV3). These cells can be grown in large numbers and the percentage of defined macrophages increased until day 10 when 100% of the cells represented macrophages. MHV3 replicated within these cells to high titers and caused the formation of multi-nucleated giant cells. This effect was seen with very low virus inocula in BM macrophages of C57BL/6 mice that are highly susceptible to in vivo infection with MHV3 whereas macrophages from resistant A/J mice did not show a cytopathic effect at these virus doses. 1000-fold higher virus doses, however, caused the cytopathic effect in macrophages of both C57BL/6 and A/J mice.

Animals↗
PubMed1983

Herpes simplex virus - induced interferon production and activation of natural killer cells in SM/J mice. Relation to antiviral resistance.

We have studied the susceptibility of SM/J mice to intraperitoneal (i.p.) infection with herpes simplex virus type 1 (HSV) and have searched for correlations of susceptibility with the activation of Natural Killer (NK) cells and with local induction of interferon. SM/J were exceedingly susceptible to virus infection as they could be killed by less than 10 plaque forming units (PFU). The NK cell system of these mice, as measured by the activity of spleen cells against YAC-1 lymphoma cells, was hyperreactive, which is in agreement with previous findings of others. The peritoneal exudate cells (PEC) of uninfected mice had no activity. However, 18 h after i.p. injection of HSV NK cell activity was detected in the PEC population, which was at least as high as that in C57BL/6 mice that are resistant to HSV infection. Thus it appears as if the NK cell system does not play a major role in antiviral resistance in our experimental system. In contrast, from our previous work it would rather appear that the magnitude of the early local interferon response is important for resistance. The current data obtained in SM/J mice are in accordance with this, in that these highly susceptible mice are deficient in their early interferon response. Homozygous beige mice were found to be as resistant to infection with HSV as C57BL/6 mice. While the NK cell activity in their PEC population after injection of HSV was low, the titers of locally induced interferon were as high as those in the controls.

Animals↗
PubMed1983

Production of interferon-gamma in the syngeneic mixed lymphocyte reaction.

Cocultures of nylon wool-separated, non-adherent (T enriched) mouse spleen cells with mitomycin C-treated adherent cells resulted in the production of antiviral activity in the culture supernatants. This antiviral activity was defined as interferon gamma (IFN-gamma) because of its lability at pH 2 and the susceptibility to inactivation by anti mouse IFN-gamma antibodies. Treatment of non-adherent cells with anti-Thy 1.2 or anti-Lyt 1.2 antibody plus complement abolished IFN production. In contrast, anti-Lyt 2.2 plus complement treatment had no effect on IFN production. Abrogation of IFN production was also seen when anti-Ia antibodies were added. IFN could be observed in the SMLR, regardless of the H-2 haplotype of the mouse strains with the exception of NZB mice. Addition of hydrophilic polymers such as polyethyleneglycol or DEAE-dextran enhanced IFN production.

Animals↗
PubMed1983

Induction of interferon gamma in leucocyte cultures of the peripheral blood of mice.

The present report summarizes a number of approaches to elicit the production of interferon gamma (IFN-gamma) in leucocytes derived from the peripheral blood of mice. Only moderate titers were observed when the blood cells were obtained from untreated mice. Significantly higher IFN production in response to phytohemagglutinin (PHA) or Concanavalin A (Con A) was observed when mice were tested after pretreatment with B. pertussis organisms, which caused a marked lymphocytosis. Additionally, two restimulation approaches are presented which are based on preactivation of peripheral leucocytes with Con A (plus in one case with T cell growth factor) and subsequent restimulation with different mitogens. These techniques allow to obtain high yields of IFN-gamma in lymphocyte cultures derived from the peripheral blood of mice.

Animals↗