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Biomedical subjects

J Korlak

Publications and source records attributed to J Korlak.

At least 19 recordsLinked to original sources
PubMed1999

Phenotyping analysis of peripheral blood leukocytes in patients with multiple sclerosis.

Multiple sclerosis (MS) is a central nervous disease thought to be elicited by an autoimmune process. Many studies in recent years have concentrated on finding the alterations in the peripheral blood immune profile in MS patients that would reflect disease activity. In the present study, we investigated surface antigen expression on lymphocytes and granulocytes from MS patients and control subjects. We have studied 29 patients suffering from relapsing-remitting or relapsing-progressive forms of MS. The disease was diagnosed in all patients at least 12 months before inclusion into the study. All patients had no attack at the study entry date or within a previous month. The control group included 29 age-matched subjects. Phenotyping of peripheral blood leukocytes was carried out with different fluorescence-conjugated murine monoclonal antibodies. The analysis was performed with three-color flow cytometry. The following antigens were determined [cluster of definition (CD)]: leukocyte common antigen (LCA) (B220, T 200, Ly-5), CD45; LPS-R (lipopolysaccharide receptor), CD14; found on all T cells, CD3; LFA-2 (lymphocyte function associated antigen, T 11), CD2; coreceptor for MHC class II molecules, found on helper T cells, CD4; coreceptor for MHC class I molecules, found on suppressor/cytotoxic T cells, CD8; B4, found on all human B cells, CD19; NCAM (neural cell adhesion molecule), CD56; integrin beta2 subunit, associated with CD11a (CD11a/CD18, LFA-1, alphaLbeta2) and CD11b (CD11b/CD18, Mac-1,CR3, alphaMbeta2), CD18; alphaL, alpha subunit of integrin LFA-1 (alphaLbeta2, CD11a/CD18), CD11a; alphaM, alpha subunit of integrin Mac-1 (CR3, alphaMbeta2, CD11b/CD18), CD11b; ICAM-1 (intercellular adhesion molecule), CD54; H-CAM, Hermes antigen, Pgp-1, CD44; AIM (activation inducer molecule), early activation antigen, CD69; T-cell receptor gammadelta, TCR gammadelta. In the MS group, we have found a significant increased expression of CD54 and CD44 antigens on lymphocytes, and higher percentage CD54(+) and CD11a+CD54(+) lymphocytes out of all lymphocytes compared with the control group. We have also found a significant increased expression of CD11a, CD18 and CD54 antigens on granulocytes, and higher percentage CD11b+CD18(+) granulocytes out of all granulocytes in MS patients compared with control. Higher levels of expression of the adhesion molecules may reflect the activation state of leukocytes in MS patients.

Adult↗
PubMed1998

Increased expression of adhesion molecule CD18 (LFA-1beta) on the leukocytes of peripheral blood in patients with acute ischemic stroke.

OBJECTIVES: The aim of this study was to investigate whether adhesion molecules play a role in acute ischemic stroke. MATERIAL AND METHODS: Using immunofluorescence phenotyping and flow cytometry, the expression of leukocyte adhesion molecules CD54, CD11a, CD11b and CD18 in peripheral blood were measured within 12 h after onset of ischemia in 20 patients with stroke. Follow-up measurements were performed at 7 and 30 days after ictus. RESULTS: CD18 immunofluorescence was significantly increased on the leukocytes within 12 h after onset in patients with stroke compared with the age-matched control group (20 patients with other neurological diseases). Follow-up measurement of CD18 revealed normal results as found in the control group. CONCLUSION: Our data support the idea that adhesion molecules are involved in tissue injury in ischemic stroke.

Aged↗
PubMed1996

Gamma delta + T cells in Wilson's disease.

Little is currently known about the role of gamma delta + T cells in disease pathogenesis. We have demonstrated elevated levels of gamma delta + T cells in the peripheral blood and cerebrospinal fluid of patients with Wilson's disease compared with other neurological diseases. The percentage of V delta 1 +/ gamma delta + T cells was between 20% and 50% in all patient groups; gamma delta + T cells in blood correlated with copper concentrations. The antigen reactivity of gamma delta + T cells and how the antigens relate to the gamma delta + T cells found in WD remains unknown. It remains unclear whether there is a direct reason for the elevated gamma delta + T cells population found in WD. Immunohistochemistry of frozen autopsy material from brain and liver of WD patients could allow exact localization of gamma delta + T cells and heat shock proteins in future studies.

Adult↗
PubMed1996

Pargyline pretreatment prevents immunological changes induced by MPTP in mice.

The relationship between the central dopaminergic and the immune system is poorly understood. Experimental work suggest that damage of the nigrostriatal system may influence immunity. Immunological abnormalities have been described in Parkinson's disease and in a mouse model of this disorder induced by 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP). In this report, we present evidence that reduced numbers of L3T4 T cells in blood, and diminished primary antibody response to sheep erythrocytes in MPTP treated mice can be restored by pargyline pretreatment. Since pargyline prevents dopamine depletion in the striatum in MPTP treated animals, our data extend previous experimental observations and support a possible role for dopamine in immune regulation.

1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine↗
PubMed1993

Immunological changes in the MPTP-induced Parkinson's disease mouse model.

The role of the central dopaminergic system in modulating immune response is not completely established. We examined the influence of central dopamine depletion on selected parameters of immune functions in 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) treated and untreated mice. IgM antibody production of splenocytes to sheep red blood cells was reduced in MPTP-treated mice (P < 0.001). Proliferation of splenocytes in response to a wide range of mitogen concentrations (Concanavalin A, phytohaemagglutinin, lipopolysaccharide) was also significantly diminished in MPTP-treated mice. Production of migration inhibition factor (MIF) was diminished only in low mitogen concentration. Our results obtained in the experimental model of Parkinson's disease provide evidence that the damage of the central dopaminergic pathways induces alterations of some immune functions in mice.

1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine↗
PubMed1991

The immunological status in Parkinson's disease.

It has been suggested that patients with idiopathic Parkinson's disease have altered functions of the immune system. We determined certain immunological parameters in groups of Parkinson's disease patients who have been i) treated and ii) not been treated, with levodopa. Changes in the immune functions were observed to be more profound in Parkinson's disease patients than in age-matched controls. Treatment with levodopa induced an increase in interleukin-1 synthesis, and in IgM and IgA levels in plasma, which suggest a possible selective action on cells of the immune system.

Age Factors↗
PubMed1989

Interleukin 1 and 2 production by peripheral blood mononuclear cells in subacute sclerosing panencephalitis and exacerbation of multiple sclerosis.

Il-1 and Il-2 production by peripheral blood mononuclear cells was studied in 10 patients with SSPE and 15 patients in the acute stage of MS. Both SSPE and MS cells in vitro released spontaneously high amounts of Il-1, and could not be further stimulated to synthesis of Il-1 by latex. The Il-2 production was decreased in both processes but in MS after the recovery from the acute stage the production of Il-2 increased. The role of the observed changes in both Il-1 and Il-2 secretion in the pathogenesis of SSPE and MS is unknown.

Adult↗
PubMed1983

Subacute sclerosing panencephalitis: influence of the clinical course and treatment with isoprinosine on non-specific cell-mediated and humoral immunity.

Cell-mediated and humoral immunity were studied in 30 patients with subacute sclerosing panencephalitis (SSPE). Marked changes in cell-mediated immunity were observed, manifested as a decrease in total lymphocyte count, decrease of proportion of T cells forming late E rosettes, depression in lymphocyte blastogenesis, production of migration inhibition factor and delayed-type skin reactivity. The humoral immune responses was not so markedly changed and only increased levels of serum IgG, IgM and the C3c fragment of complement were noticed. The changes in immunity were more pronounced in patients with a more advanced stage of the disease. 19 patients were investigated 3 times at 7-week intervals during treatment with isoprinosine. In the group of patients (10 cases) whose clinical status was rapidly deteriorating, a marked decline of cell-mediated immunity was observed. In the group of patients showing a stationary course of the disease, cellular immunity was improving. The mechanism of the disturbances of non-specific immunity in SSPE and the influence of isoprinosine on the immune answer are discussed.

Adolescent↗
PubMed1982

Sensitization of cerebrospinal fluid and peripheral blood lymphocytes to myelin basic protein in multiple sclerosis.

Cerebrospinal fluid (CSF) and peripheral blood (PB) lymphocyte sensitization to rabbit myelin basic protein (MBP) in 44 multiple sclerosis (MS) patients, 21 patients with other neurological diseases (OND) and 14 persons with neurosis was studied with the antigen-active rosette forming cells (Ag-ARFC) assay. The frequency of sensitization of CSF lymphocytes to MBP in groups of MS patients in the relapse stage and the chronic progressive stage was higher than in the group of MS patients in the stable stage and the OND patients. None of the healthy subjects showed a positive reaction with MBP. In BP there were no differences in the incidence of sensitization to MBP between patients in various stages of the disease, but it was higher than in the group of patients with OND and neuroses. In the patients who had suffered from MS for less than 4 years, sensitization to MBP was more common in CSF lymphocytes than in BP lymphocytes. The results suggest that primary sensitization to MBP occurs in CSF, and is probably secondary to myelin damage. However at present it is difficult to determine the extent to which sensitization of CSF and PB lymphocytes to MBP play a role in further demyelination processes.

Adolescent↗
PubMed1981

Differences between lymphocyte subsets of the cerebrospinal fluid in subacute sclerosing panencephalitis and acute aseptic meningitis.

In CSF of patients with acute aseptic meningitis (AAM) an increase in the percentage of total and active T lymphocytes was observed, whereas in SSPE a decrease in T cells was noted. In SSPE there was the increase in the relative number of lymphocytes bearing "avid" FcIgG receptor and decrease in alpha-naphthyl nonspecific esterase-positive cells, but in AAM the cell proportions were not disturbed. The changes in the peripheral blood lymphocytes subsets were less evident. The results seem to suggest that in AAM there is a strong T response in CSF with well preserved proportions of T-cell subsets, while in SSPE a low T-cell level may be accompanied by disturbances in T-cell function.

Acute Disease↗
PubMed1980

Lymphocyte subpopulations in the cerebrospinal fluid and peripheral blood in multiple sclerosis.

Subpopulations of lymphocytes in the CSF and peripheral blood were studied in 30 patients with MS, 16 with other neurological diseases (OND) and 15 control subjects without any neurological abnormalities. In patients with relapse of MS, the absolute numbers of total lymphocytes, alpha-naphthyl acid esterase (ANAE) positive, E-rosette forming and bearing the "avid" FcIgG receptor lymphocytes were significantly increased in the CSF as compared with stable or slowly progressive MS patients, patients with other OND and control subjects. The relative number of ANAE-positive cells was higher, and "avid"FcIgG receptor bearing cells lower in the CSF of all patients with MS than in the two other groups. The significance of the finding is unclear. The imbalance between lymphocyte subpopulations may reflect a primary defect in MS, or may be secondary, due to the presence of circulating immune complexes. In peripheral blood no substantial differences in lymphocyte behavior were observed between MS patients and other groups.

Adolescent↗
PubMed1979

Immunological observations on patients with acute cerebral vascular disease.

Cell-mediated and humoral immunity was studied in 74 patients with acute cerebral vascular disease. During the first two days after the onset of disease marked changes of cell-mediated immunity were observed, manifested as a decrease in total lymphocyte count in the peripheral blood, decrease in number of T lymphocytes, depression in lymphocyte blastogenesis and production of the migration inhibition factor, and a delayed-type skin reactivity. The changes were most evident in patients with severe lesions of brain tissue resulting from primary cerebral haemorrhage and cerebral infarction with fatal outcome. In the group of patients with cerebral infarction with improvement of neurological symptoms the immunological changes were not so pronounced as in the two above-mentioned groups, the smallest changes being found in patients with subarachnoid haemorrhage. We suppose that the depression in the immunne function was caused by severe stress during the course of disease. Impairment of the immune function may increase susceptibility to infection. The humoral immune response was not so evidently changed, and the observed increase of IgA in the sera was probably present before the stroke. In cases with good clinical course some improvement in the immunological parameters was observed, but full recovery did not occur until 3 weeks after the onset of disease.

Adult↗
PubMed1979

The immune response during aging.

Complex studies were carried out on humoral and cell mediated immunity among persons over 60 years of age and persons aged 18-40. Humoral immune responses were not profoundly disturbed in the group of older persons. The level of isoagglutinins was lower in older subjects, but the level of immunoglobulins and antibodies to widespread bacterial and virus antigens (S. typhi O, Kunin's CA, Parainfluenza types I, II and III) was the same in both groups. Cell mediated immunity was more greatly changed. Response to PPD in skin tests, lymphocyte stimulation tests, and the migration inhibition test was reduced in older subjects. Also, in this group, PHA in lymphocyte stimulation tests and the number of E- rosette forming cells was lower than among younger adults. However, responses to other antigens in skin tests, lymphocyte stimulation tests, migration inhibition tests (Candida albicans, SK-SD, Trichophyton) and responses to other stimulants of the lymphocyte stimulation tests (Con A, PWM) were well preserved in older subjects.

Adolescent↗
PubMedDate not supplied

[Presence of immune complexes in ischemic stroke].

There is increasing evidence that inflammatory responses play an important role in the pathogenesis of atherosclerosis and cerebral infarct. The aim of this study was to determine the amount of immunocomplexes (i.c.) in patients with stroke in the early period of the disease. Studies were performed on 35 subjects. The concentration of immunocomplexes was determined with the precipitation method (3.5% polyethylenoglikol was used). Increased concentration of i.c. was found in patients with cerebral infarct (after 12 hours and 7 days). It suggests, that i.c. could be one of the markers for systemic inflammation and be important in the patogenesis of atherosclerosis and stroke.

Adult↗
PubMedDate not supplied

[Secretion of tumor necrosis factor alpha (TNF-alpha) by peripheral blood monocytes in patients with multiple sclerosis and subacute sclerosis panencephalitis].

TNF alpha production by peripheral blood monocytes was studied in seventeen patients with a recent exacerbation of MS, thirteen with remission of MS and fourteen patients with SSPE. Monocytes from both MS groups spontaneously secreted high amounts of TNF alpha in vitro. Addition of lipopolisaccharide could not stimulate further synthesis of TNF alpha. In SSPE spontaneous and stimulated TNF alpha release did not differ from that in the control group. The observed changes in TNF alpha release in MS patients could play a role in the pathogenesis of the disease.

Cells, Cultured↗