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Biomedical subjects

K Strigård

Publications and source records attributed to K Strigård.

16 recordsLinked to original sources
PubMed2001

Incidence of GM-CSF antibodies in cancer patients receiving GM-CSF for immunostimulation.

We have assessed the immunogenicity profile of GM-CSF in patients with either colorectal carcinoma (CRC) at different stages of disease or with multiple myeloma who were given recombinant human GM-CSF (Escherichia coli-derived) combination therapy. Metastatic CRC patients received a colon carcinoma-reactive antibody and high doses of GM-CSF (425--500 microg/day for 10 days), while other CRC patients and those with myeloma received low doses of GM-CSF (75--80 microg/day for 4 days) as an adjuvant along with appropriate tumor antigens. We found that 55% of the patients (11/20) given high doses of GM-CSF developed GM-CSF-reactive antibodies in comparison with an incidence of only 16% (4/25) in patients given low doses of GM-CSF. None of the patients developed neutralizing antibodies and so the biological effects of GM-CSF were not compromised. A majority of patients (80%) (36/45) also developed antibodies to E. coli proteins that were present as trace contaminants in the GM-CSF product. Treatment with recombinant GM-CSF products, therefore, may induce antibodies against this cytokine depending on the regimen and the amounts used. In this study, multiple immunizations with low doses of GM-CSF was associated with a low incidence of GM-CSF antibodies, which did not neutralize the effect of the cytokine. This therapeutic strategy was effective in inducing adjuvant-type effects and needs to be explored in further clinical trials with this cytokine.

Antibodies↗
PubMed1998

Pharmacological administration of granulocyte/macrophage-colony-stimulating factor is of significant importance for the induction of a strong humoral and cellular response in patients immunized with recombinant carcinoembryonic antigen.

Eighteen colorectal carcinoma patients without macroscopic disease after surgery were immunized using recombinant (r) human (h) carcinoembryonic antigen (CEA) with (n=9) or without (n=9) the addition of soluble granulocyte/macrophage-colony-stimulating factor (GM-CSF). The dose of rhCEA per immunization was 100 microg (n=6), 316 microg (n=6) or 1000 microg (n=6). rhCEA was given s.c. on day 1 and 80 microg/day of GM-CSF s.c. on days 1-4. The schedule was repeated six times during a period of 9 months. All patients in the GM-CSF group developed a strong rhCEA-dose-dependent IgG antibody response while only one-third of the non-GM-CSF patients mounted a weak antibody response. All patients (9/9) in the GM-CSF group developed a strong rhCEA-specific proliferative T cell response as well as type I T cells (interferon gamma secretion). In 45% of the patients also a weak type II T cell response (interleukin-4 secretion) was evoked. Both MHC-class-I- and -II restricted rhCEA-specific T cells were noted. A specific cellular response (proliferation and/or cytokine secretion) against native hCEA could be found in 8/9 patients in the GM-CSF group, although at a significantly lower level than against rhCEA. In the non-GM-CSF group a weak rhCEA-specific T cell response was induced. Three patients had a proliferative response, 4 patients type I T cells and 6 patients type II T cells. No signs of autoimmune reactions were noted. Local pharmacological administration of GM-CSF seemed to be a prerequisite for the induction of a strong immunity against baculovirus-produced hCEA protein. However, the cellular response against native CEA was of a significantly lower magnitude.

Adjuvants, Immunologic↗
PubMed1998

Muscle strength and endurance after surgery for primary hyperparathyroidism.

OBJECTIVE: To evaluate the effect of surgery on muscular strength and endurance in patients with primary hyperparathyroidism (HPT). DESIGN: Prospective open study. SETTING: University hospital, Sweden. SUBJECTS: Nine patients undergoing HPT surgery and nine matched patients undergoing thyroid resection who acted as controls. INTERVENTIONS: Concentric and eccentric endurance was evaluated with a test comprising 100 repeatedly executed muscle action at 90 degrees.s-1. Blood samples obtained before and after operation were analysed for calcium, phosphate, thyroid stimulating hormone (TSH), and parathyroid hormone (PTH) concentrations. MAIN OUTCOME MEASURES: Peak torque during maximum voluntary concentric and eccentric muscle actions at 90 degrees.s-1 before, three months and one year after operation. RESULTS: There were no differences in concentric and eccentric peak torque before and after operation either within or between groups. Concentric and eccentric endurance were similar in the HPT group and controls before as well as after operation. The return of calcium and PTH concentrations to their reference ranges after parathyroidectomy did not correlate with changes in concentric and eccentric peak torque. CONCLUSIONS: The subjective improvement in muscle endurance which is often encountered in patients with HPT after operation is not associated with an objective increase in muscle strength or endurance as measured by isokinetic muscle performance.

Calcium↗
PubMed1996

Pregnancy and Guillain-Barré syndrome: a nationwide register cohort study.

In this study, we determined the relationship between Guillain-Barré syndrome (GBS) and pregnancy. By taking advantage of several nationwide registers and the availability of personal identification numbers, we calculated person-years for Swedish females aged 15-49 years in the following categories: (1) neither pregnant nor postpartum; (2) pregnant; (3) in the first month postpartum, or (4) in the first 3 months postpartum during 1973-1983. For these women, we determined the corresponding exposure status of hospital-registered GBS cases. Medical records were examined for GBS cases hospitalized during the 2-week period postpartum and 1-month period after the last menstruation. Poisson regression analysis yielded age-adjusted relative risks (RRs) of 0.86 (95% CI 0.40-1.84) for pregnant women, and 1.47 (0.54-3.99) and 2.21 (0.55-8.94) for females during the 3-month and the 30-day period after delivery. The risk for GBS seems to be lower during pregnancy and increases after delivery.

Adolescent↗
PubMed1992

Hyperparathyroidism associated with treatment of manic-depressive disorders by lithium.

OBJECTIVE: To clarify the association between treatment of affective psychiatric disorders with lithium, and the development of secondary hyperparathyroidism. DESIGN: Retrospective review of medical records, 1973-89. SUBJECTS: 17 patients with affective psychiatric disorders who were treated with lithium (n = 6) or with tricyclic antidepressant, or neuroleptic, drugs (n = 11) all of whom were operated on for hyperparathyroidism. MAIN OUTCOME MEASURE: Duration of lithium therapy and parathyroid histology. RESULTS: Parathyroid hyperplasia was present in 5 patients who had taken lithium during a median period of 13 years. A parathyroid adenoma was found in one patient treated with lithium for three years. Ten of the 11 patients who had been treated with tricyclic antidepressant, or neuroleptic drugs had a parathyroid adenoma and the remaining one had an adenoma as an underlying cause of hyperparathyroidism. CONCLUSION: Hyperparathyroidism in patients who have undergone long term treatment with lithium is associated with parathyroid hyperplasia. This indicates that lithium may exert a chronic stimulus that results in secondary hyperparathyroidism.

Adenoma↗
PubMed1990

Oestrogen treatment reduces duration of experimental allergic neuritis in rats and suppresses T cell responses to myelin.

The effects of oestrogen and pregnancy on the disease course of experimental allergic neuritis (EAN) in rats were investigated. Pregnant rats were totally protected from EAN and long term 17-beta-oestradiol treatment significantly shortened the disease duration. Lymph node cells from oestrogen treated rats had a suppressed proliferative response when stimulated with myelin or PPD, both when the response was measured immediately after cell preparation and after 72 h cell culture in vitro. Serum levels of IgG antibodies against myelin, P2 or PPD did not differ between treated and non-treated rats although oestrogen treated rats had significantly higher levels of total IgG. Immunohistochemical stainings of nerve roots showed less intensive invasion of T lymphocytes in the oestrogen treated group while immunoreactivity to both class I and II major histocompatibility complex antigens did not differ in between the groups. These findings show that oestrogen ameliorates EAN and suggest that this effect is mediated by suppression of T cell dependent immunity. Factors in addition to oestrogen may be operative during pregnancy when a total protection from EAN is obtained.

Animals↗
PubMed1989

Distribution of plasma cells secreting antibodies against nervous tissue antigens during experimental allergic encephalomyelitis enumerated by a nitrocellulose immunospot assay.

The B cell response to central nervous system (CNS) myelin and myelin basic protein, as well as total numbers of IgG secreting cells, was studied in acute experimental allergic encephalomyelitis using a nitrocellulose immunospot assay. The method was able to detect single plasma cells secreting antibodies. Cells secreting antibodies against myelin antigens were detected in regional lymph node cell suspension by day 5 post-immunization (p.i.). At that time no anti-myelin antibodies were detected free in serum. Later, at day 15 p.i., specific antibody secreting cells were found in bone marrow and spleen indicating a generalization of the immune response. The B cell response became partly sequestered to the target of immune attack since an increased number of IgG secreting cells was detected among mononuclear cells recovered from the CNS. Studies of cellular secretion of antibodies rather than free levels in body fluids may be a more accurate reflection of the in vivo B cell response. These findings may be generally considered in studies of B cell mediated immunity in neuroinflammatory diseases.

Animals↗
PubMed1989

In vivo monoclonal antibody treatment with Ox19 (anti-rat CD5) causes disease relapse and terminates P2-induced immunospecific tolerance in experimental allergic neuritis.

The role of CD5+ lymphocytes in the recovery phase and on immunospecific protection against experimental allergic neuritis (EAN) was examined in Lewis rats by in vivo treatment with Ox19, a mouse anti-rat CD5 monoclonal antibody. Animals pretreated with the peripheral nerve basic protein P2 and thereby rendered resistant to the disease showed clinical signs of EAN after intraperitoneal (i.p.) Ox19 injection given at the same time as the rechallenge with neuritogenic doses of myelin in Freund's complete adjuvant. Non-pretreated rats recovered from signs of EAN developed a clinical relapse after i.p. Ox19 injections. Taken together, these data suggest an important regulatory role of the CD5 receptor in the immune response.

Animals↗
PubMed1989

In vivo treatment of rats with monoclonal antibodies against gamma interferon: effects on experimental allergic neuritis.

To elucidate the role of gamma interferon in experimental allergic neuritis (EAN) a mouse monoclonal antibody (DB-1) directed against rat gamma interferon was used to treat rats during different phases of the development of experimental allergic neuritis (EAN). The effects of this treatment were followed by clinical evaluation, and in some instances by immunohistochemical analysis of lymphoid organs and affected nerves for presence of MHC class II antigens and various T cell subsets. DB-1 treatment given after onset of clinical symptoms (Day 15 after immuniozation with myelin) shortened disease duration, compared with non-treated EAN controls. Affected nerves of DB-1 treated animals showed reduced expression of MHC class II antigens and lower numbers of T lymphocytes within the affected nerves. In contrast, when DB-1 treatment was given on the day of immunization (Day 0), the disease duration increased, and when given before onset of the disease (Day 9) the clinical course was not significantly affected. The results support an important role for gamma interferon in the pathogenesis of EAN.

Animals↗
PubMed1988

Modulation of experimental allergic neuritis in rats by in vivo treatment with monoclonal anti T cell antibodies.

Monoclonal antibodies (MCA) to different T lymphocyte cell surface antigens have been used to treat rats during different phases of the development of experimental allergic neuritis (EAN). The effects of this treatment were followed by clinical evaluation and in some instances by immunohistochemical analysis of lymphoid organs and affected nerves of the antibody-treated rats. Several MCA, W3/13 (pan T cell reactive), W3/25 (anti-rat CD4), Ox 8 (anti-rat CD8) as well as Ox 6 (anti-Ia) partly prevented clinical signs of EAN when given shortly before expected onset of disease, whereas W3/13 and Ox 8 given at the height of disease did not further affect disease development. However, Ox 19 (anti-rat CD5) given at the same time as immunization partly prevented clinical signs of EAN, while Ox 19 given shortly before expected onset of disease or during height of disease drastically exaggerated disease symptoms. Immunohistochemical studies after Ox 8 or Ox 19 treatment showed a complete absence of staining for the respective antibodies, while staining was preserved with the other MCA. It is concluded that: (1) Ox 8 positive "suppressor/cytotoxic" T lymphocytes do not exert any suppressive effects on EAN during the now investigated phases of disease, and that (2) anti T lymphocyte antibodies (here Ox 19) may exert opposite effects on autoimmune disease when given at different phases of disease development. This may have implications for potential therapeutic trials of MCA therapy for putative autoimmune demyelinating diseases in man.

Animals↗
PubMed1988

Elimination of CD8+ T cells in vivo does not break induced immunospecific tolerance to experimental allergic neuritis in rats.

The role of CD8+ T 'cytotoxic/suppressor' T cells in induced immunospecific tolerance and during recovery after actively induced disease was examined by means of elimination of CD8+ cells from Lewis rats using in vivo treatment by Ox8 monoclonal antibodies, in experimental allergic neuritis (EAN). Animals depleted of CD8+ T cells after recovery from EAN did not show any clinical signs of relapse. Other animals were pretreated with the peripheral nerve basic protein P2 and thereby rendered resistant to disease induction with a potentially neuritogenic emulsion. The elimination of CD8+ T cells did not result in EAN here either. Thus, the CD8+ T-cell population does not seem to participate in the suppression of this autoimmune disease under these experimental conditions.

Animals↗
PubMed1987

T-lymphocyte subsets, functional deficits, and morphology in sciatic nerves during experimental allergic neuritis.

Conduction velocities, demyelination, "macrophage/dendritic" cells, different sets of T-lymphocytes, and immunoglobulins were estimated in sciatic nerves during various phases of experimental allergic neuritis in Lewis rats. Demyelination was minimal day 15 postimmunization (p.i.) when conduction velocity already was reduced, somewhat more pronounced day 17 p.i. when nerve conduction was blocked, and most pronounced day 23 p.i. when nerve conduction partially had recovered. This suggests a dissociation between the degree of demyelination and the functional deficits. Decrease of sciatic nerve conduction velocities coincided with endoneurial appearance of T-lymphocytes and "macrophage/dendritic" cells, as well as endoneurial immunoglobulins, day 15 p.i. Later partial functional recovery occurred in parallel with the disappearance of T-cells. The degree of functional deficits thus correlated with the number of endoneurial T-lymphocytes. T-cells may, directly or indirectly, initiate several of the disease components in experimental allergic neuritis, including the nerve conduction deficit.

Animals↗