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Biomedical subjects

K Baklien

Publications and source records attributed to K Baklien.

At least 19 recordsLinked to original sources
PubMed2000

Early changes in peripheral blood T cell subsets induced by antiretroviral treatment of human immunodeficiency virus-1 positive individuals.

Human immunodeficiency virus (HIV)-1 infection causes a gradual decline in peripheral blood CD4+ T cells. Shortly after the primary infection, an expansion of the activated memory CD8+ T-cell pool is also observed paralleling increased levels of plasma viraemia. In the present study we investigated the immediate effects of zidovudine therapy on peripheral blood T-cell subsets during the first 3 weeks of therapy in a group of HIV-1 positive individuals receiving influenza vaccine. HIV-1 positive individuals who received vaccine, but no treatment, were included as controls. Both the number of CD4+ and CD8+ T cells increased during the first week of therapy in parallel with a decline in plasma viraemia. The majority of CD4+ T cells contributing to this expansion expressed CD28, CD45RO and Fas, whereas the expanded CD8+ T cells were predominantly CD28-, CD45RO+, CD38+, Fas+ and Fas+ (CD95). We propose that the increase in the number of activated memory T cells observed in peripheral blood immediately after the onset of antiretroviral treatment is most likely caused by the redistribution of cells from various lymphoid organs in response to decreased levels of viral load in these compartments. The degree of T-cell redistribution is probably dependent on the magnitude of virus suppression.

Adult↗
PubMed1998

[Chronic lymphatic leukemia. Immunophenotyping as an aid to correct diagnosis].

The purpose of the study was to examine the validity of the primary diagnosis in chronic lymphocytic leukemia based on clinical and morphological criteria, and to examine the role of immune phenotyping for correct diagnosis in an unselected population-based group of patients. Over a 2-year period leukemic cells from 222 of 235 patients in Norway with a recent clinical diagnosis of chronic lymphocytic leukemia (CLL) were immune phenotyped in order to find cases erroneously diagnosed as CLL. Median age was 72.5 years, and the ratio of men to women was 1.47. At the time of diagnosis, 77% of the patients were in Binet stage A and 23% in stage B or C. Immune phenotyping, in some patients followed by lymph node or bone marrow biopsy, showed a different diagnosis in 11 (5%) of 222 patients: prolymphocytic leukemia, four patients (three B-cell and one T-cell); morbus Waldenstrøm, one patient; T-cell CLL, one patient; hairy cell leukemia, one patient; mycosis fungoides, one patient; mantle cell lymphoma, one patient; monocytoid B-cell lymphoma, one patient and immunoblastic lymphoma one patient. In eight of these 11 patients, the clinical features or morphology, or both, were atypical for CLL, but this was not recognized at the time of diagnosis. Thus, immune phenotyping is valuable for correct diagnosis in a small subgroup of patients with chronic B- or T-cell leukemia, and it is essential in patients with modest lymphocytosis (lymphocytes < 10. 10(9)/1).

Adult↗
PubMed1996

Risk of toxoplasmic encephalitis in AIDS patients: indications for prophylaxis.

To establish the indications for primary prophylaxis against toxoplasmic encephalitis in the Norwegian HIV-positive population, we estimated the incidence of toxoplasmic encephalitis, and related the degree of immunodeficiency and the presence of IgG antibodies against Toxoplasma gondii (T. gondii) to the development of toxoplasmic encephalitis. This retrospective study includes all HIV-positive patients at our hospital from April 1983 to October 1994 (n = 705). A total of 238 patients had AIDS, which represents almost 90% of all AIDS patients in Oslo. Autopsy was done in over 70% of the patients who died during this period; 19 patients developed toxoplasmic encephalitis (8.0%). The median CD4 cell count was 75 x 10(6) cell/I (range 0-280) at the time of diagnosis of toxoplasmic encephalitis. T. gondii serology was studied in 698 (99.0%) of the patients, and was found positive for 17.8%. Of the patients with toxoplasmic encephalitis 18/19 had IgG antibodies against T. gondii and of the 40 AIDS patients who had anti-T. gondii IgG, 18 (45%) developed toxoplasmic encephalitis. We conclude that there is indication for prophylactic treatment of HIV positive patients who have IgG antibodies against T. gondii and who have fewer than 200 x 10(6) CD4 cells/I.

AIDS-Related Opportunistic Infections↗
PubMed1995

Intestinal B-cell isotype response in relation to local bacterial load: evidence for immunoglobulin A subclass adaptation.

BACKGROUND & AIMS: In experimental animals, the indigenous microbiota modulates mucosal immunity. In humans, such direct evidence is scarce. The aim of this study was to examine the effect of intestinal bacteria on the local immunoglobulin (Ig) response. METHODS: The numbers of IgA-, IgM-, and IgG-producing immunocytes per defined mucosal length unit were determined, and the local IgA subclass response was studied using immunohistochemistry in jejunal segments from adults with bacterial overgrowth and in sterile ileal urinary conduits from children. RESULTS: The ileal bladder mucosa showed atrophy, but the number of immunocytes only tended to be decreased. The jejunal segments with bacterial overgrowth showed minor histological changes; the numbers of IgA and IgG immunocytes were fairly normal, whereas the number of IgM immunocytes was significantly reduced (P < 0.05) (12 cells/U) compared with control mucosa (24 cells/U). The number of IgA2 immunocytes was significantly decreased (P < 0.01) in ileal conduits (7 cells/U or 30% of total IgA) but increased (P < 0.05) in jejunal segments with bacterial overgrowth (42 cells/U or 43% of total IgA) compared with normal ileum (15 cells/U or 40% of total IgA) and jejunum (24 cells/U or 23% of total IgA). CONCLUSIONS: An association exists between bacterial load and IgA subclass production. An increase in IgA2 may enhance mucosal protection and probably reflects immunomodulation caused by lipopolysaccharides.

Adolescent↗
PubMed1991

[Quantification of T-lymphocyte subpopulations. Immunological marker in human immunodeficiency virus infections].

The absolute number of CD4+ and CD8+ T cells was counted directly in the blood of 75 healthy controls and 223 individuals infected with human immunodeficiency virus (HIV). The HIV-seropositive individuals were also classified clinically according to the system recommended by the Centers for Disease Control. We observed a pattern of changes in the T cell subset counts of the patient group. This pattern could be defined by five T cell stages ranging from normal T cell subset values to values representing severe T cell immunodeficiency. A close correlation was observed between the immunological and clinical classification of the patients. Quantification of T cell subsets may provide useful information in the follow-up of individuals infected with HIV, particularly in assessing the indications for antiviral therapy, and its effects.

HIV Infections↗
PubMed1989

Antigenic specificity of human alveolar macrophages and blood monocytes studied by an immunofluorescence technique.

Lung alveolar macrophages (AM) and blood monocytes (BM) are part of the mononuclear phagocyte system (MPS) and have been shown to be composed of several functionally and biochemically distinct subsets. AM and BM were each fractionated into four subfractions by centrifugation over Percoll, 95 per cent of the monocytes having a higher buoyant density than the high-density AM fraction. Antigen distribution within the cell subfractions was studied by an immunofluorescence technique using a panel of ten monoclonal antibodies (MoAbs) reacting with separate antigenic determinants previously found on mononuclear phagocytes. Several antigens were present on both types of cells (Ki-M1, Ki-M6, Leu-M3, Leu-M5, 1D5, Dako-Ma, and HLA-DR), while other antigens were expressed exclusively on BM (MAS 072 and MAS 081) or on AM (Ki-M8). Ki-M1, Leu-M3, Leu-M5, and HLA-DR were expressed to a greater degree on the surface of AM (95-96 per cent of cells) than on BM (56-68 per cent), while an inverse relationship was noted for 1D5 antigen (present on 41 per cent of BM and 11 per cent of AM). Ki-M6 and Dako-Ma MoAbs recognized an intracellularly restricted antigen present in both AM and BM. Ki-M1, Ki-M8, MAS 072, MAS 081, Leu-M3, Leu-M5, 1D5, and HLA-DR were expressed both in the cytoplasm and at the cell surface. Some antigens (1D5, Leu-M3, MAS 072, MAS 081, and Dako-Ma) showed an uneven distribution among subsets of both AM and BM.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1987

Local immunoglobulin production is different in gastritis associated with dermatitis herpetiformis and simple gastritis.

The degree of inflammation and atrophy in gastric body mucosal specimens (n = 38) from 28 patients with dermatitis herpetiformis (DH) was graded histologically. Immunoglobulin (Ig) producing cells were enumerated by paired immunofluorescence staining in a 500 microns wide section area from the muscularis mucosae to the lumen (mucosal 'tissue unit'). The number of immunocytes of the three main classes (IgA, IgM, and IgG) was significantly raised with increasing degree of gastritis. All three classes were increased in specimens showing atrophy compared with those without atrophy. IgA cells predominated as in simple gastritis, but a striking difference was a marked increase of IgM cells in specimens with the most pronounced DH-associated gastritis. Relative class distribution of immunocytes within different mucosal zones showed that the percentage of IgA cells was significantly higher in the luminal than in the basal zone, whereas the contrary was true for IgG cells. IgM cells did not show any zonal preference. No relation was seen between small bowel and gastric lesions. The disproportionate increase of gastric IgM producing cells in DH might nevertheless reflect seeding of precursor cells of the secretory immune system generated in the proximal small intestine where the local IgM response is relatively pronounced.

Adolescent↗
PubMed1985

The human gastrointestinal secretory immune system in health and disease.

The main function of secretory IgA is to exert immune exclusion; that is, by intimate cooperation with innate non-specific defence mechanisms, it dampens down penetration of soluble antigens and inhibits epithelial colonisation of bacteria and viruses. Secretory IgM may exert a similar protective function in the gut as its local synthesis sometimes is markedly increased, especially in selective IgA deficiency. IgG should not be considered a secretory immunoglobulin because its external translocation depends on passive intercellular diffusion. By activating complement, antibodies of this isotype may cause increased mucosal permeability and tissue damage. IgG may thus contribute to persistent immunopathology in mucosal lesions. The same is true for IgE antibodies which, in atopic individuals, may be carried into the gut mucosa by mast cells and cause their degranulation with histamine release. Secretory IgA and secretory IgM are the products of two cell types: plasma cells synthesise IgA dimers and IgM pentamers which, by non-covalent association, become complexed with the secretory component (SC) which is synthesized by serous-type glandular cells. The adsorption of the Ig polymers to the SC-expressing epithelial cells depends on J chain-determined binding sites. This fact gives biological significance to the striking J chain expression shown by mucosal immunocytes regardless of the Ig class they produce. The immunocytes populating the gut mucosa apparently belong to relatively early memory B cell clones. The obvious functional goal of J chain expression at this stage of clonal differentiation is local generation of SC-binding IgA and IgM polymers. In various gut diseases, altered immune regulation results in a disproportionately increased number of J chain-negative IgG-producing cells in the mucosa. Such altered immunological homeostasis may contribute to perpetuation of inflammatory bowel diseases.

Adult↗
PubMed1982

Effect of immune complex-containing sera from patients with rheumatic diseases on thromboplastin activity of monocytes.

Monocytes isolated from peripheral blood of patients with various rheumatic diseases and circulating immune complexes (IC) developed a significantly higher thromboplastin (tissue factor) activity than normal cells when cultured in vitro without inducers, but normal cells responded more strongly with thromboplastin production upon stimulation with IC or phytohaemagglutinin (PHA). Sera from patients with rheumatic diseases and circulating IC induced a significant increase in the thromboplastin activity of normal monocytes. Lysozyme release from patient monocytes was significantly lower than the release from control cells when stimulated with IC. Patient sera contained higher amounts of lysozyme than normal sera, indicating lysozyme release in vivo. These data suggest that activation of monocytes in vivo by IC may take place. The increased expression of thromboplastin in monocytes/tissue macrophages may be important for the development of microvascular thrombosis and fibrin deposition seen in chronic inflammatory lesions.

Adolescent↗
PubMed1982

Purification and characterization of a nuclear SS-B antigen.

A nuclear SS-B antigen was isolated from a saline extract of acetone powder of rabbit thymus by precipitation with ammonium sulphate, affinity chromatography with Blue Sepharose CL-6B, and preparative agarose gel electrophoresis. The mol. wt of the antigen was 68,000. Its electrophoretic mobility was similar to that of pre-albumin, and the iso-electric point was around pH 4.0. The main amino acids of the antigen were glutamic acid, leucine, lysine and alanine. Both histidine and tyrosine were also found. The purified antigen precipitated with anti-SS-B sera but not with any other reference antisera. It resembled La and Ha antigens in susceptibility to proteolytic and nucleolytic enzymes and to heat. The purified SS-B antigen, however, had a higher molecular weight than did the Ha and La antigens. The molecule could not be split into subunits with mercaptoethanol or acid. Counter-electrophoresis showed antibodies to the SS-B antigen in sera from patients with rheumatic diseases, including rheumatoid arthritis, systemic lupus erythematosus and Sjögren's syndrome, but not in amy of the control sera.

Adult↗
PubMed1980

Immunoglobulin-producing cells in jejunal mucosa of children with coeliac disease on a gluten-free diet and after gluten challenge.

The jejunal Ig-producing cell populations in a group of 12 children with established coeliac disease (CD) in remission on a gluten-free diet were compared with those of a group of 10 patients in clinical relapse after gluten challenge. Quantification of the various immunocyte classes was performed by paired immunofluorescence staining in an individually defined mucosal tissue unit constituting a 6-micron-thick and 500-micron-wide block of tissue, including the mucosa at full height from the muscularis mucosae. In the treated group the percentage IgA/IgM/IgG cell ratios were, on the average, 82.6:12.9:4.5. There were no differences in these ratios or in the absolute immunocyte numbers when compared with a group of six control patients without CD. After gluten challenge the corresponding ratios were 77.2:17.2:5.6. The median cell number per mucosal tissue unit in the IgA, IgM, and IgG class was raised 2.1, 3.8 and 2.9 times, respectively. These increases were statistically significant. Moreover, there was a significant negative correlation between the time to clinical relapse and the number of IgG cells per tissue unit after challenge. This finding indicates that locally produced antibodies of the IgG class are especially involved in the pathogenesis of CD.

Antibody-Producing Cells↗
PubMed1980

Immunohistochemical studies of the immunoglobulin-producing cell systems of the human intestinal mucosa.

Since the reliability of immunohistochemical observations is highly dependent on the quality of the immunological reagents, the importance of purification, characterization and performances testing of the fluorochrome conjugates is discussed. The methods of tissue processing, immunohistochemical staining and differential enumeration of fluorescing cells used in our laboratory are described. The normal intestinal mucosa shows a striking preponderance (80-90%) of IgA immunocytes, and these cells produce J chains which are incorporated into dimeric IgA. The dimers are taken up by the columnar epithelial cells which produce "secretory component" (SC). Complexing of dimeric IgA with SC seems to explain the selective transport of IgA through the crypt epithelium. A similar transport mechanism operates for J-chain-containing pentameric IgM. Marked alterations of the intestinal immunocyte populations are seen associated with various bowel diseases. In coeliac disease and dermatitis herpetiformis, a numerical increase takes place for all Ig-producing cell classes--in relative terms most prominent for IgG and IgM cells. In ulcerative colitis and Crohn's disease, the IgG-cell response is very striking, In alpha-chain disease, the lamina propria is infiltrated with IgA cells that lack light-chain-producing capacity but show some ability to synthesize J chains; dimers of alpha chain are hence transported to the intestinal lumen but cannot function as antibodies. In patients with a complete and selective lack of IgA in serum, IgA-producing cells are absent from the intestinal mucosa, and there is a numerical increase of local IgG- and specially IgM-producing cells. Conversely, patients with a partial deficiency of serum IgA may show a fairly normal intestinal IgA-cell population, although the proportion of IgM-producing cells is often increased. The intestinal mucosa of patients with a generalized hypogrammaglobulinaemia is sometimes devoid of plasma cells, but rare Ig-producing immunocytes, especially of the IgM class, are often seen. Supported in part by the Norwegian Research Council for Science and the Humanities, Anders Jahres Fond, and Helga Sembs fond. We thank Ms. Evy Eriksen and Ms. Gummvor Oijordbakken for technical assistance, and Ms. Liv Støottum for typing the manuscript.

Adolescent↗
PubMed1979

Immunologic and gastrointestinal abnormalities in dermatitis herpetiformis.

Eighty patients with untreated dermatitis herpetiformis (DH) were studied. The final diagnosis was made after completion of immunofluorescence (IF) studies of the skin, iodine provocation tests and gastrointestinal investigations. IgA deposits in the skin and the HLA-DRw3 B-cell alloantigen can be demonstrated in nearly all cases of DH. Positive iodine provocation test and gastrointestinal abnormalities are present in about 78% of the cases. For diagnostic purposes tissue typing and intestinal biopsy is of value in addition to IF studies of the skin.

Adolescent↗