Trond Sundby Halstensen

• Kvamme, Jan-Magnus; Sørbye, Sveinung; Florholmen, Jon & Halstensen, Trond S. (2022). Population-based screening for celiac disease reveals that the majority of patients are undiagnosed and improve on a gluten-free diet. Scientific Reports. ISSN 2045-2322. 12(1). doi: 10.1038/s41598-022-16705-2. Fulltekst i vitenarkiv
• Petronijevic, Sanja; Stig, Solveig & Halstensen, Trond S. (2021). Epitope mapping of anti-amelogenin IgG in untreated celiac children. European Journal of Oral Sciences. ISSN 0909-8836. 129(2), s. 1–13. doi: 10.1111/eos.12770. Fulltekst i vitenarkiv
• Halstensen, Trond S. (2020). Ancestral Wheat Types Release Fewer Celiac Disease Related T Cell Epitopes than Common Wheat upon Ex Vivo Human Gastrointestinal Digestion. Foods. ISSN 2304-8158.
• Petronijevic, Sanja; Stig, Solveig & Halstensen, Trond S. (2020). Epitope mapping of anti-amelogenin IgA in coeliac disease. European Journal of Oral Sciences. ISSN 0909-8836. 128(1), s. 27–36. doi: 10.1111/eos.12672.
• Asledottir, Tora; Rehman, Rashida; Mamone, Gianfranco; Picariello, Gianluca; Devold, Tove Gulbrandsen & Vegarud, Gerd Elisabeth [Vis alle 11 forfattere av denne artikkelen] (2020). Ancestral wheat types release fewer celiac disease related t cell epitopes than common wheat upon ex vivo human gastrointestinal digestion. Foods. ISSN 2304-8158. 9:, s. 1–12. doi: 10.3390/foods9091173. Fulltekst i vitenarkiv
• Prydz, Kristian; Halstensen, Trond S.; holen, Halvor Lauvstad & aasheim, Hans-Christian (2018). Ephrin-B3 binds both cell-associated and secreted proteoglycans. Biochemical and Biophysical Research Communications - BBRC. ISSN 0006-291X. 503(4), s. 2212–2217. doi: 10.1016/j.bbrc.2018.06.140.
• Petronijevic, Sanja; Stig, Solveig; Gao, Jian & Halstensen, Trond S. (2016). Amelogenin specific IgA and IgG in children with untreated coeliac disease. European Journal of Oral Sciences. ISSN 0909-8836. 124, s. 526–533. doi: 10.1111/eos.12314.
• Attramadal, Cecilie Gjøvaag; Kumar, Sheeba; Gao, Jian; Boysen, Morten Ebbe; Halstensen, Trond Sundby & Bryne, Magne (2016). Low mast cell density predicts poor prognosis in oral squamous cell carcinoma and reduces survival in head and neck squamous cell carcinoma. Anticancer Research. ISSN 0250-7005. 36(10), s. 5499–5506. doi: 10.21873/anticanres.11131.
• Gao, Jian; Ulekleiv, Camilla Husvik & Halstensen, Trond Sundby (2016). Epidermal growth factor (EGF) receptor-ligand based molecular staging predicts prognosis in head and neck squamous cell carcinoma partly due to deregulated EGF- induced amphiregulin expression. Journal of Experimental & Clinical Cancer Research. ISSN 1756-9966. 35(1). doi: 10.1186/s13046-016-0422-z.
• Gao, Jian; Zhao, Sen & Halstensen, Trond Sundby (2016). Increased interleukin-6 expression is associated with poor prognosis and acquired cisplatin resistance in head and neck squamous cell carcinoma. Oncology Reports. ISSN 1021-335X. 35(6), s. 3265–3274. doi: 10.3892/or.2016.4765. Fulltekst i vitenarkiv
• Attramadal, Cecilie Gjøvaag; Halstensen, Trond Sundby; Dhakal, Hari Prasad; Ulekleiv, Camilla Husvik; Boysen, Morten Ebbe & Nesland, Jahn M [Vis alle 7 forfattere av denne artikkelen] (2015). High nuclear SOX2 expression is associated with radiotherapy response in small (T1/T2) oral squamous cell carcinoma. Journal of Oral Pathology & Medicine. ISSN 0904-2512. 44(7), s. 515–522. doi: 10.1111/jop.12261.
• Halstensen, Trond Sundby (2013). Cøliaki er mye vanligere enn du tror. Indremedisineren. ISSN 1891-1617. 5(4), s. 28–30.
• Sjåheim, Tone Bjørg; Bjørtuft, Øystein; Drabløs, P.-A.; Kongerud, Johny & Halstensen, Trond Sundby (2013). Increased Bronchial Density of CD25+Foxp3+ Regulatory T Cells in Occupational Asthma: Relationship to Current Smoking. Scandinavian Journal of Immunology. ISSN 0300-9475. 77(5), s. 398–404. doi: 10.1111/sji.12035. Vis sammendrag

  To identify activated T cell subset in the asthmatic bronchia, we developed a triple-colour immunohistofluorescence labelling technique on cryo-section to discriminate activated CD4+CD25+ T cells, (effector T cells) from Foxp3+ regulatory T cells (Treg). Additional coexpression of activation and proliferation markers was also examined in situ. Bronchial biopsies were taken from 20 aluminium potroom workers (12 smokers) with asthma (>12% reversibility), 15 non-asthmatic potroom workers (7 smokers) and 10 non-smoking, non-exposed controls. Non-smoking asthmatics had significantly higher subepithelial density of both Tregs, effector T cells, activated (HLA-DR+) CD8+ and activated CD4+ T cells. Moreover, both Tregs, effector T cells and CD8+ T cells proliferated in the non-smoking asthmatics, only. Although smoking asthmatics had no asthma-associated increase in bronchial T cell, both had a significantly increase in effector T cell to Treg ratios. The significantly increased bronchial density of Tregs, effector T cells, proliferative T cells and activated CD8+ T cells in non-smoking asthmatics clearly showed that both the effector T cells and the inhibitory Treg system were activated in asthma.

• Husvik, Camilla; Khuu, Cuong; Bryne, Magne & Halstensen, Trond Sundby (2009). PGE2 Production in Oral Cancer Cell Lines is COX-2 Dependent. Journal of Dental Research. ISSN 0022-0345. 88(2), s. 164–169. doi: 10.1177/0022034508329519.
• Husvik, Camilla; Bryne, Magne & Halstensen, Trond Sundby (2009). Epidermal growth factor-induced cyclooxygenase-2 expression in oral squamous cell carcinoma cell lines is mediated through extracellular signal-regulated kinase 1/2 and p38 but is Src and nuclear factor-kappa B independent. European Journal of Oral Sciences. ISSN 0909-8836. 117(5), s. 528–535.
• Husvik, Camilla; Bryne, Magne & Halstensen, Trond Sundby (2009). c-Jun N-terminal kinase negatively regulates epidermal growth factor-induced cyclooxygenase-2 expression in oral squamous cell carcinoma cell lines. European Journal of Oral Sciences. ISSN 0909-8836. 117(6), s. 663–668.
• Husvik, Camilla; Khuu, Cuong; Bryne, Magne & Halstensen, Trond Sundby (2009). PGE(2) Production in Oral Cancer Cell Lines is COX-2-dependent. Journal of Dental Research. ISSN 0022-0345. 88(2), s. 164–169. doi: 10.1177/0022034508329519.
• Sletten, GB; Halvorsen, Ragnhild; Egaas, E & Halstensen, Trond Sundby (2007). Memory T cell proliferation in cow's milk allergy after CD25+ regulatory T cell removal suggests a role for casein-specific cellular immunity in IgE-mediated but not in non-IgE-mediated cow's milk allergy. International Archives of Allergy and Immunology. ISSN 1018-2438. 142(13), s. 190–198.
• Sletten, Gaynour B Gordon; Halvorsen, Ragnhild; Egaas, E & Halstensen, Trond Sundby (2007). Casein-specific immunoglobulins in cow's milk allergic patient subgroups reveal a shift to IgA dominance in tolerant patients. Pediatric Allergy and Immunology. ISSN 0905-6157. 18, s. 71–80. doi: 10.1111/j.1399-3038.2006.00489.x.
• Sjåheim, Tone Bjørg; Kongerud, Johny; Bjortuft, O; Drablos, PA; Malterud, D. & Halstensen, Trond Sundby (2006). Reduced bronchial CD4+T-cell density in smokers with occupational asthma. European Respiratory Journal. ISSN 0903-1936. 28, s. 1138–1144.
• Brandtzæg, Per; Carlsen, Hege Synnøve & Halstensen, Trond Sundby (2006). The B-cell system in inflammatory bowel disease. Advances in Experimental Medicine and Biology. ISSN 0065-2598. 579, s. 149–167.
• Sletten, GBG; Halvorsen, Ragnhild; Egaas, E & Halstensen, Trond Sundby (2006). Changes in humoral responses to beta-lactoglobulin in tolerant patients suggest a particular role for IgG(4) in delayed, non-IgE-mediated cow's milk allergy. Pediatric Allergy and Immunology. ISSN 0905-6157. 17, s. 435–443.
• Sjåheim, Tone Bjørg; Halstensen, Trond Sundby; Lund, May Brit; Bjørtuft, Øystein; Drablos, PA & Malterud, D [Vis alle 7 forfattere av denne artikkelen] (2004). Airway inflammation in aluminium potroom asthma. Occupational and Environmental Medicine. ISSN 1351-0711. 61, s. 779–785.
• Halstensen, Trond Sundby (2003). Bronchial mast cells are the dominating LTC4S expressing leukocyte in aspirin-tolerant asthma. American Journal of Respiratory Cell and Molecular Biology. ISSN 1044-1549. 29(6), s. 683–694.
• Heldal, Kari; Halstensen, Anne S.; Thorn, J; Djupesland, Per Gisle; Wouters, I & Eduard, Wijnand [Vis alle 7 forfattere av denne artikkelen] (2003). Upper airway inflammation in waste handlers exposed to bioaerosols. Occupational and Environmental Medicine. ISSN 1351-0711. 60(6), s. 444–450.
• Heldal, Kari; Halstensen, Anne S.; Thorn, J; Eduard, Wijnand & Halstensen, Trond Sundby (2003). Airway inflammation in waste handlers exposed to bioaerosols assessed by induced sputum. European Respiratory Journal. ISSN 0903-1936. 4(4), s. 641–645.
• Farstad, Inger Nina; Johansen, Finn Eirik; Vlatkovic, L.; Jahnsen, Jørgen; Scott, Helge & Fausa, Olav [Vis alle 9 forfattere av denne artikkelen] (2002). Heterogeneity of intraepithelial lymphocytes in refractory sprue: potential implications of CD30 expression. Gut. ISSN 0017-5749. 51, s. 372–378.
• Askling, Johan; Linet, Martha; Gridley, Gloria; Halstensen, Trond Sundby; Ekström, Karin & Ekbom, Anders (2002). Cancer incidence in a population-based cohort of individuals hospitalized with celiac disease or dermatitis herpetiformis. Gastroenterology. ISSN 0016-5085. 123(5), s. 1726–1729. Vis sammendrag

  BACKGROUND & AIMS: Studies of cancer risk in celiac disease (CD) or dermatitis herpetiformis (DH) indicate increased risks for malignant lymphoma and occasionally other neoplasms, but are characterized by small numbers, lack of systematic cancer assessment, and subjects identified from referral institutions. METHODS: By using Swedish population-based inpatient and cancer registry data, we followed-up 12,000 subjects with CD or DH, and evaluated cancer incidence by using standardized incidence ratios (SIR). RESULTS: Adults (but not children and adolescents) with CD had an elevated overall risk for cancer (SIR = 1.3) that declined with time and eventually reached unity. Elevated risks were found for malignant lymphomas, small-intestinal, oropharyngeal, esophageal, large intestinal, hepatobiliary, and pancreatic carcinomas. The excess occurrence of malignant lymphomas was confined to adults, decreased with time of follow-up evaluation, and decreased over successive calendar periods. Decreased risks were found for breast cancer. Subjects with DH had a slightly increased overall cancer risk (SIR = 1.2) owing to excesses of malignant lymphoma and leukemia, but no increases of gastrointestinal carcinomas. CONCLUSIONS: Albeit increased, the relative risks for lymphomas and gastrointestinal cancers in this study are lower (and declining) than in most previous reports. The overall cancer risk is only moderately increased, and nonelevated during childhood and adolescence

• Steinsvoll, Svein E B; Halstensen, Trond Sundby & Schenck, Karl (1999). Extensive expression of TGF-1 in chronically-inflamed periodontal tissue. Journal of Clinical Periodontology. ISSN 0303-6979. 26, s. 366–373.
• Myint, Maung Maung; Odden, Kåre; Schreurs, Olav Joseph F; Halstensen, Trond Sundby & Schenck, Karl (1999). The gingival plasma cell infiltrate in HIV-positive patients with periodontitis is disorganized. Journal of Clinical Periodontology. ISSN 0303-6979. 26, s. 358–365. Vis sammendrag

  Patients infected with the human immunodeficiency virus (HIV) are highly susceptible to chronic marginal periodontitis (CMP) and the lesion is generally characterized by abundant plasma cell infiltration. HIV-induced reduction of CD4+ T cells may indirectly affect local production of immunoglobulins (Ig). Gingival biopsies taken from 10 HIV+ and 12 HIV- control patients with CMP were washed, fixed in ethanol and embedded in paraffin. Sections were examined after immunohistochemical staining with monoclonal antibodies against IgA, IgA1-2, IgG, IgG1-4, IgM and IgE. Ig-containing cells were counted in 3 separate connective tissue zones (subjacent to pocket epithelium, central zone and subjacent to oral epithelium). HIV+ patients showed a remarkably increased density of all Ig-containing cells in the connective tissue zone subjacent to the oral epithelium (p<0.05) and a lower % of IgG2+ cells in the entire gingival section (p<0.05). In HIV+ patients, the density of IgG-containing cells in the gingiva was strongly correlated with the serum IgG concentration. The altered topical distribution might imply impaired restriction of the inflammatory lesion, additional antigenic challenges by unusual microorganisms in the oral cavity, or be secondary to HIV-induced dysregulation of the B-cell system.

• Brandtzæg, Per; Halstensen, Trond Sundby; Huitfeldt, Henrik & Valnes, K (1997). Immunofluorescence and immunoenzyme histochemistry. I Johnstone, AP & Turner, MW (Red.), Immunochemistry 2 ¿ A Practical Approach. Oxford University Press, Oxford. s. 71–130.
• Helgeland, Lars; Vaage, John Torgils; Rolstad, Bent; Halstensen, Trond Sundby; Midtvedt, Tore & Brandtzæg, Per (1997). Regional phenotypic specialization of intraepithelial lymphocytes in the rat intestine does not depend on microbial colonization. Scandinavian Journal of Immunology. ISSN 0300-9475. 46, s. 349–357.
• Schreurs, Olav Joseph F; Halstensen, Trond Sundby; Dembic, Zlatko; Bogen, Bjarne & Schenck, Karl (1997). TUNEL combined with staining for epithelial cellmarker permits unambiguous localization of apoptic cells in murine thymus. Biochemica. ISSN 0946-1310. 4, s. 19–21.
• Berstad, Audun Elnæs; Brandtzæg, Per; Stave, R & Halstensen, Trond Sundby (1997). Epithelium related deposition of activated complement in Helicobacter pylori associated gastritis. Gut. ISSN 0017-5749. 40, s. 196–203.
• Farstad, Inger Nina; Halstensen, Trond Sundby; Kvale, Dag; Fausa, Olav & Brandtzæg, Per (1997). Topographic distribution of homing receptors on B and T cells in human gut-associated lymphoid tissue. Relation of L-selectin and integrin _a4_b7 to naive and memory phenotypes. American Journal of Pathology. ISSN 0002-9440. 150, s. 187–199.
• Berstad, Audun Elnæs; Brandtzæg, Per; Stave, R & Halstensen, Trond Sundby (1997). Epithelium related deposition of activated compliment in Heliobacter pylori-associated gastritis. Gut. ISSN 0017-5749. 40, s. 196–203.
• Nilssen, Dag Egil; Muller, Fredrik; Øktedalen, O.; Frøland, Stig Sophus; Fausa, Olav & Halstensen, Trond Sundby [Vis alle 7 forfattere av denne artikkelen] (1996). Intraepithelial gamma/delta cells in duodenal mucosa are related to the immune state and survival time in AIDS. Journal of Virology. ISSN 0022-538X. 70(6), s. 3545–3550.
• Andersen, Rune; Hosaka, Junro; Halstensen, Trond Sundby; Stordahl, Arvid; Tverdal, A. & Aabakken, Lars [Vis alle 7 forfattere av denne artikkelen] (1996). The X-ray contrast medium iodixanol detects increased colonic permeability equally well as 51 Cr-lbeled ethylendiaminetetraacetic acid in experimental colitis of rats. Scandinavian Journal of Gastroenterology. ISSN 0036-5521. 31, s. 140–146.
• Nilssen, Dag Egil; Fredrik, M; Øktedalen, O.; Frøland, Stig Sophus; Fausa, Olav & Halstensen, Trond Sundby [Vis alle 7 forfattere av denne artikkelen] (1996). Intraepithelial gamma/delta T Cells in Duodenal Mucosa Are Related to the Immune State and Survival Time in AIDS. Journal of Virology. ISSN 0022-538X. s. 3545–3550.
• Rugtveit, K.; Scott, Helge; Halstensen, Trond Sundby; Norstein, J. & Brandtzæg, Per (1996). Expression of the L1 antigen (calprotectin) by tissue macrophages reflects recent recruitment from peripheral blood rather than upregulation of local synthesis: implications for rejection diagnosis in formalin-fixed kidney specimens. Journal of Pathology. ISSN 0022-3417. 180, s. 194–199.

Se alle arbeider i Cristin

• Florholmen, Jon; Sørbye, Sveinung & Halstensen, Trond Sundby (2022). Stor norsk studie avdekker cøliaki hos mange som ikke visste de hadde det - Intervju Jan-Magnus Kvamme. https://forskning.no/.
• Halstensen, Trond S. (2021). Epitope mapping of anti-amelogenin IgG in untreated celiac children. European Journal of Oral Sciences. ISSN 0909-8836.
• Halstensen, Trond S. (2021). Population‑based screening for celiac disease reveals that the majority of patients are undiagnosed and improve on a gluten‑free diet. Scientific Reports. ISSN 2045-2322.
• Kvamme, Jan-Magnus; Halstensen, Trond S.; Sørbye, Sveinung Wergeland & Florholmen, Jon (2021). Tema: Forekomst av udiagnostisert cøliaki i Tromsø- undersøkelsen: Hva er betydning av glutenfri diett i denne gruppen?
• Petronijevic, Sanja; Stig, Solveig & Halstensen, Trond S. (2017). IgA and IgG anti-amelogenin antibodies in untreated celiac children.
• Petronijevic, Sanja; Gao, Jian; Stig, Solveig & Halstensen, Trond Sundby (2016). IgA and IgG anti-amelogenin antibodies in untreated celiac disease.
• Petronijevic, Sanja; Solveig, Stig & Halstensen, Trond Sundby (2016). Immune reactivity to amelogenin in celiac disease.
• Petronijevic, Sanja; Stig, Solveig & Halstensen, Trond Sundby (2015). IgA anti-amelogenin antibodies in celiac disease patients.
• Petronijevic, Sanja; Stig, Solveig & Halstensen, Trond Sundby (2015). IgA anti-amelogenin levels in pediatric celiac patients.
• Petronijevic, Sanja; Stig, Solveig & Halstensen, Trond Sundby (2014). The role of anti-amelogenin antibodies in enamel defects pathogenesis in celiac disease .
• Halstensen, Trond Sundby (2013). Voksendiagnostiserte cøliakere Anbefales å vaksineres mot lungebetennelsesbakterien: pneumokokk. glutenFRI, Norsk cøliakiforening. s. 21–21.
• Halstensen, Trond Sundby (2013). Cøliaki hos eldre. glutenFRI, Norsk cøliakiforening. s. 4–6.
• Halstensen, Trond Sundby (2012). Hva er forskjellen på cøliaki og glutenintoleranse? glutenFRI, Norsk cøliakiforening. s. 29–31.
• Halstensen, Trond Sundby (2008). Gluten i Vin? Cøliakinytt. 31(4), s. 15–15.
• Halstensen, Trond Sundby (2008). Cøliaki og osteoporose. Cøliakinytt. 31(4), s. 27–27.
• Halstensen, Trond Sundby (2008). Cøliaki likevel? Cøliakinytt. 31(2), s. 12–12.
• Husvik, Camilla; Khuu, Cuong; Bryne, Magne & Halstensen, Trond Sundby (2007). Basal and EGF-induced PGE2 production in oral cancer cell lines is COX-2 dependent.
• Sjåheim, Tone Bjørg; Kongerud, Johny; Bjørtuft, O & Halstensen, Trond Sundby (2007). Mucosal regulatory T cells in nonsmoking and smoking asthmatics.
• Husvik, Camilla; Khuu, Ngoc Ky Cuong; Bryne, Magne & Halstensen, Trond Sundby (2006). EGF induced PGE2 production in OSCC cell lines is COX-2 dependent.
• Husvik, Camilla; Bryne, Magne & Halstensen, Trond Sundby (2006). EGFR signalling and COX-2 in oral cancer.
• Husvik, Camilla; Bryne, Magne & Halstensen, Trond Sundby (2006). PGE2 production in OSCC cell lines is COX-2 dependent.
• Husvik, Camilla; Bryne, Magne & Halstensen, Trond Sundby (2006). EGFR signalling and COX-2 in oral cancer.
• Halstensen, Trond Sundby; Corthay, Alexandre & Westgaard, Arne (2005). Immunologiens dag 29. april 2005 - populærvitenskapelig konferanse i universitetets aula. [Internett]. Norsk Selskap for Immunologi - www.norwegianimmunology.org. Vis sammendrag

  Den europeiske immunologiforeningen EFIS innstiftet "Day of Immunology", som ble markert for første gang den 29. april 2005. Norsk Selskap for Immunologi (NSI) var ansvarlig for arrangementene i Norge.

• Halstensen, Trond Sundby; Westgaard, Arne & Corthay, Alexandre (2005). NSI's Annual General Meeting 2005. [Internett]. Abstraktbok utgitt i papirform.
• Liu, Yixin; Ek, Johan & Halstensen, Trond Sundby (2002). Immunohistochemical detection of CD25+ regulatory T cells in tonsils and inflammed mucosa. Vis sammendrag

  The interleukin-2 (IL-2) receptor alfa-chain, CD25 is expressed on activated T cells. These cells were previously believed to represent activated inflammatory effector T cells. However, it was recently shown that CD25+ T cells in the peripheral blood represented suppressor T cells that inhibited T cell activation in an antigen unspecific manner. These regulatory T cells are CD4+ CD25high T cells that translocate intracytoplasmatic CTLA-4+ upon activation. The CTLA-4 molecule can then bind CD80/CD86 on the antigen presenting cell, preventing these molecules to interact with CD28 on activated effector T cells. The CD25+ CD4+ regulatory T cells, moreover, inhibit immune responses by producing IL-10 and expression of activated membrane bound TGF-beta. Removals of these CD25+CD4+ regulatory T cells from mice induce autoimmune phenomenon and diseases, whereas cell transfer ameliorated experimental induced autoimmune diseases. The small intestine of patients with celiac disease contains an increased percentage of CD25+ CD4+ T cells that has been identified as antigen specific Th1 cells with high IFN-gamma production. In order to examine the distribution and location of CD25+ regulatory (CTLA-4+) T cells (CD3+) in celiac disease and tonsils we performed multicolor immunohistofluorescence staining for CTLA-4 in combinations with CD3 and CD25, CD4 or CD28. Results Trippel labeling for CTLA-4, CD25+ on T cells (CD3+), revelled that CTLA-4+ T cells were located both in the follicular and in the T cell area of the tonsils, but only few (<1%) expressed CD25.: This was strikungly different from the situation in celiac disease. The percentage of CD25+ lamina propria CD3+ T cells increased from median 4% in the controls (range 1-8%) to 13 percentage in celiac disease (range 2-29%). Surprisingly many of these CD25+ T cells expressed CTLA-4 intracellularly in the controls (median 60%, range 36-100). Although there was an increased density of of CD25+ CTLA-4neg effector T cells in celiac disease, the density of regulatory CD25+ CTLA-4+ T cells increased as well. Thus, almost half (44%) of the CD25+ T ells in the celiac lesion may have represented T- regulative cells rather than effector T cells as they coexpressed CTLA-4 (range 30-85%). A similar percentage of T cells expressed intracytoplasmic CTLA-4 in controls (median 8%, range 7-15%) and celiac disease (median 12%, range 5-49%). Although, most of these cells did not coexpress CD25 in controls (median 19%, 14-58%), it increased to 33% in the celiac disease (range 30-40%). Conclution These results showed that activated (CD25+) T cells in the celiac disease may represent not only effector T cells but also CD25+ CD4+ CTLA-4+ regulatory T cells.

• Cai, Y.; Bjermer, L & Halstensen, Trond Sundby (2002). Bronchial Prostaglandin D2 Synthase Expressing Mast Cells in Asthma. Vis sammendrag

  Introduction: Activated mast cell produce prostaglandin D2 (PGD2) that attracts and activates eosinophil through two different PGD2-receptors, CRTH2 and PD, respectively. PGD2 is also potent inducer of smooth muscle contraction and an important trigger of the asthmatic response. Mast cells express PGD2 synthase (PGD2S), which catalyze the conversion of PGH2 to PGD2. All mast cells are believed to produce PGD2 upon activation. However, multi-color immunohistochemical examination of bronchial mucosa revealed two different pattern of mast cells expression and a large fraction of non-expression mast cells. Methods: Bronchial biopsies (n=84) from 29 asthmatic patients (treated, n=15; untreated, n=12 and bronchial allergen challenged, n=2) and from 9 controls were processed. Immunohistochemical staining of cryo-sections (n=101) were performed with mAb to PGD2 synthases in combination with antiserum to LTC4 synthases. Antiserum to LTC4 synthases was similar combined with mAbs to tryptase, CD117, CD68, CD3, HLA-DR, EG2 and COX-2. Eosinophil granulocyte was also identified with diffraction contrast microscopy (DIC). Results: PGD2S were only observed in LTC4 synthase positive cells that on separate experiments was shown to be COX-2+, CD117+, tryptase+ mast cells. However, not all mast cells expressed PGD2S, and there were no significant difference in the fraction of mast cells that expressed strong immunoreactivity for PGD2S (39% and 36% in controls and asthma, respectively). Some mast cells had a cytoplasmic weak granular immunoreactivity for PGD2S (20-17%). Almost half of the bronchial mast cells (46-44%) did not express PGD2S at all. The few intraepithelial mast cells that were observed were predominantly PGD2S (78-62%), with few weak PGD2S expressing cells (0-10%). Although the density of PGD2S expressing mast cells in untreated asthma was similar to controls, the treated asthma had significantly lower density of PGD2S expressing mast cells than untreated asthma. Conclution: In contrast to common believes only half of the bronchial mast cells expressed prostaglandin D2 synthase and thus are able to produce the bronchospastic and eosinophil-activating prostaglandin D2. The fraction of PGD2S expressing mast cells was similar in controls and asthma, the density of such cells was significantly reduced in treated as compared to untreated asthma and controls. The expression of PGD2S divided the mast cell population into two almost equal groups that presumably produce different signals upon activation.

• Blikshavn, Thomas; Buanæs, J.A.; Dølvik, Sverre & Halstensen, Trond Sundby (2001). Increased subepithelial complement activation in nasal polyps from patients with aspirin-induced asthma. Vis sammendrag

  Patients with aspirin-induced asthma (AIA) have a non-allergic eosinophilic inflammation in the respiratory tract that is associated with severe asthma and recurrent nasal polyposis. Biopsies from newly formed nasal polyps (n = 10) and adjacent mucosal specimens (n = 20) from untreated patients with AIA, and mucosal specimens from non-AIA patients undergoing nasal surgery (n = 10) were immunohistochemically examined for in situ complement activation. Monoclonal antibodies (mAbs) to activation neoepitopes in the C3c part of C3b, and to the C9 part of the terminal complement complex (TCC) were used in combination with mAbs to the complement inhibitory proteins CD59 and S-protein (vitronectin). All polyp specimens displayed an intense subepithelial TCC immunoreactivity, which was significantly increased (p < 0.05) compared to both adjacent nasal mucosa from the same patients, and to nasal mucosa from the non-AIA control mucosa. Subepithelial C3b immunoreactivity was in most cases scant and weak. Subepithelial and vascular TCC colocalized with S-protein, but not with CD59. CD59 was expressed on surface epithelium and strongly on endothelium in most vessels. Newly formed nasal polyps in patients with AIA contain an increased amount of subepithelial TCC deposition. Thus, subepithelial complement activation may contribute to the local inflammation and polyp formation.

• Koren, Margaret; Sjaaheim, T.; Bjørtuft, Øystein; Kongerud, Johny & Halstensen, Trond Sundby (2001). T Cell Subsets in bronchial biopsies from aluminum potroom workers with and without occupational asthma. Vis sammendrag

  Bronchial biopsies were obtained from potroom workers with (n=16) and without asthma, (n=8). A multi-colour immunohistochemical examination of mucosal T cell phenotypes was performed by combining monoclonal antibodies (mab) to CD3d with mabs to CD4, CD8 or T-cell receptor g/d(TCR g/d) and antiserum to keratin to visualize the epithelium. The mucosal T cells were counted pr. grid and the density of cells calculated. Although the density of lamina propria CD8+ve T cells (CD3+ve) tended to be higher in the asthmatics (median 216 cells/mm2; range 72-335) than in the non-asthmatic workers (186 cells/mm2, range 45-447) there were no significant difference. Similar, the slightly decreased density of lamina propria CD4+ve T cells in the asthmatics (107 cells/mm2 , range 39-261) was not significantly different from the non-asthmatic potrooms workers (137 cells/mm2, range 52-211). Few of the lamina propria T cells expressed TCRg/d chain both in the asthmatics (median 0.35%, range 0-4%) and in the non-asthmatic workers (median 2%, range 0-11%). Although the density of intraepithelial CD8+ve T cells/mm basal lamina was slightly higher in the asthmatics (median 31/mm, range 6-183) than the non-asthmatic workers (median 19 /mm, range 6-57) the difference was not significant. Likewise, the asthmatics contained slightly more CD4+ve intraepithelial T cells/mm basal membrane (median 9, range 4-48), but it was not significantly different from the controls (median 5 range 4-17). Also the slightly decreased percentage of intraepithelial TCR g/d+ve T cells in the asthmatics (median 2%, range 0-11) was not significant different from the controls (3 %, range 0-5). Thus, the bronchial mucosa in occupational potroom asthmatics contained a similar density CD4+ve, CD8+ve and TCRg/d+ve lamina propria and intraepithelial T cells as the non-asthmatic workers. The increased percentage of CD4+ lamina propria T cells reported for atopic asthma was not observed in this asthmatic group, suggesting that other immunopathological, mechanisms are involved in potroom asthmatics than in traditional atopic asthma.

• Cai, Y.; Bjermer, L & Halstensen, Trond Sundby (2001). Bronchial mucosa in COPD contain more LeukotrieneC4-synthase (LTC4S) expressing mast cells than asthmatics or controls. Vis sammendrag

  Bronchial production of leukotriene-C4 (LTC4) induces bronchial hyperactivity and asthmatic symptoms. Eosinophilic granulocytes (Eos) may be the dominant cellular source of the LTC4 producing enzyme Leukotriene-C4-synthase (LTC4S) because single colour immunohistochemical examination of GMA-embedded bronchial biopsies from patients with aspirin induced asthma (AIA) and non-AIA asthma identified Eos as the dominant LTC4S+ve cells. A total of 30 bronchial biopsies from 17 patients with non-AIA asthma, 23 biopsies from 14 patients with chronic obstructive pulmonary disease (COPD) and 15 biopsies from 8 controls were processed. Cryosections (n=75) were examined with multi-colour immunohistochemical staining for LTC4S, in combination with mAbs to cyclooxygenase-2 (COX2), and mast cells (mAb AA1). Eos were identified with diffraction interface contrast (DIC) microscopy. The density of LTC4+ve cells/mm2 lamina propria (LP) was calculated. LTC4S was observed in smooth muscle cells and in mononuclear cells. The bronchial LP from controls contained a median of 50 LTC4S+ve cells pr mm2 (range 35-79/mm2), increasing to 75 cells/mm2 in COPD (range 5-118/mm2; p<0,05) compared to a median of only 44/mm2 in asthma (range 4-81/mm2). The majority of the LTC4S+ve cells were tryptase+ve mast cells (mAb AA1+ve) both in asthma (median 89%; range 63-100%), COPD (median 91%; range 33-97%) and controls (median 93; range 83-100%). Moreover, almost all LTC4S+ve cells co-expressed COX2 (median 100% in all groups). There were no increased density of Eos in any of the groups and data from 32 sections revealed that only 26% of the 57 Eos observed in the asthmatic and 16% of the 44 Eos observed in 26 sections from COPD, expressed LTC4S. Thus, mast cells and smooth muscular cells (not Eos) were the major cellular source of LTC4S both in asthma and COPD. Moreover, the bronchial mucosa from patients with COPD contained significantly higher density of LTC4S+ve COX2+ve mast cells, than asthmatic patients or controls.

• Sjaaheim, T.; Koren, Margaret; Bjørtuft, Øystein; Kongerud, Johny & Halstensen, Trond Sundby (2001). T Cell Subsets in bronchial biopsies from aluminum potroom workers with and without occupational asthma. Vis sammendrag

  The immunopathology of occupational asthma in potroom workers is unknown. Bronchial biopsies were obtained from potroom workers with asthma (n=14), other asthmatics (n=7) and controls (n=9). Methods: a double immunofluorescent staining method was performed by monoclonal antibodies (mab) to CD3 in combination with mab to CD4, CD8 or T cell receptor &#61543;&#61540;. Results: The percentage of CD8+ lamina propria T cells were significantly (p<0,05) increased in potroom asthma (median 55%, range 33-78) compared to the other asthmatic group (median 41%, range 18-62) but not different from the controls (median 55%, range 36-67). The percentage of the CD4+ T cells in lamina propria were significantly higher in "traditional" asthma (median 57%, range 41-79) than in potroom asthma (median 40%, range 23-55). The bronchial epithelium in potroom asthma workers contained significantly decreased percentage of CD8+ intraepithelial T cells (median 68% range 52-85) compared to both the "traditional" asthmatics (median 83%, range 66-91) and controls (median 86%, range 53-95). The percentages of TCR &#61543;/&#61540;+ intraepithelial or lamina propria T cells were not different. Conclusions. The bronchial mucosa in occupational potroom asthmatics showed a different distribution of T cell subsets compared to non-occupational asthmatics. Thus, potroom asthma may involve other immunpathological mechanisms than traditional asthma.

• Halvorsen, Ragnvald; Paulsen, Berit Smestad & Halstensen, Trond Sundby (1999). Betenkning fra Allergigruppa i SNTs Vitenskapskomite ang. overvåkingsfunksjon når det gjelder forekomst av gluten i såkalte glutenfrie produkter. [Radio]. Statens Næringsmiddeltilsyn.
• Halvorsen, Ragnvald; Paulsen, Berit Smestad & Halstensen, Trond Sundby (1999). Vurdering av betegnelsen hypoallergen på morsmelkerstatninger. [Radio]. Statense Næringsmiddelstilsyn.
• Halvorsen, Ragnvald; Paulsen, Berit Smestad & Halstensen, Trond Sundby (1999). Matallergier og -intoleranser Innspill til SNTs plandokumenter. [Radio]. Statens Næøringsmiddeltilsyn.
• Steinsvoll, Svein E B; Halstensen, Trond Sundby & Schenck, Karl (1997). TGF-b1 is upregulated in several cell types in inflamed periodontal tissues.
• Steinsvoll, Svein E B; Halstensen, Trond Sundby & Schenck, Karl (1997). Cell types expressing TGF&#61538;1 in inflamed gingiva.
• Halstensen, Trond Sundby; Viken, H.D.; Rønningen, Kjersti Skjold; Fausa, Olav; Kett, Kjell & Ek, Johan [Vis alle 9 forfattere av denne artikkelen] (1997). The proportion of intestinal TCR KL intraepithelial lymphocytes in coeliac disease is independent of HLA-DQ2.
• Halstensen, Trond Sundby; Viken, H.D.; Rønningen, Kjersti Skjold; Fausa, Olav & Kett, Kjell (1997). The increased percentage of intestinal TCRgama/delta intraepithelial lymphocytes (IEL) in coeliac diseases in independent of HLA-DQ2.
• Steinsvoll, Svein E B; Halstensen, Trond Sundby & Schenck, Karl (1997). TGF&#61538;1 is upregulated in macrophages in gingiva from patients with periodontitis.
• Steinsvoll, Svein E B; Halstensen, Trond Sundby & Schenck, Karl (1996). Increased prevalence of gingival TGF-b1 producing cells in patients with periodontitis.
• Steinsvoll, Svein E B; Halstensen, Trond Sundby & Schenck, Karl (1996). TGF-&#61538;1 Containing Cells in Gingiva from Patients with Periodontitis.
• Sjåheim, Tone Bjørg; Halstensen, Trond Sundby & Kongerud, Johny (2008). Immunopathology of occupational asthma in aluminium potroom workers. Unipub forlag. ISSN 978-82-8072-757-2.
• Henriksen, Tore; Eggesbø, Merete; Guldberg, Mette; Halstensen, Trond Sundby; Henriksen, Christine & Honningdal, Ernst H. [Vis alle 8 forfattere av denne artikkelen] (1996). Matvareallergi/-intoleranse. Folkehelsa, SNT, NAAF, Statens Ern.råd.

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