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2. Effects of Gluten Intake on Risk of Celiac Disease: A Case-Control Study on a Swedish Birth Cohort

Author

Rewers, Marian, Bautista, Kimberly, Baxter, Judith, Bedoy, Ruth, Felipe-Morales, Daniel, Frohnert, Brigitte I., Gesualdo, Patricia, Hoffman, Michelle, Karban, Rachel, Liu, Edwin, Norris, Jill, Samper-Imaz, Adela, Steck, Andrea, Waugh, Kathleen, Wright, Hali, She, Jin-Xiong, Schatz, Desmond, Hopkins, Diane, Steed, Leigh, Thomas, Jamie, Adams, Janey, Silvis, Katherine, Haller, Michael, Gardiner, Melissa, McIndoe, Richard, Sharma, Ashok, Williams, Joshua, Foghis, Gabriela, Anderson, Stephen W., Robinson, Richard, Ziegler, Anette G., Beyerlein, Andreas, Bonifacio, Ezio, Hummel, Michael, Hummel, Sandra, Foterek, Kristina, Kersting, Mathilde, Knopff, Annette, Koletzko, Sibylle, Peplow, Claudia, Roth, Roswith, Stock, Joanna, Strauss, Elisabeth, Warncke, Katharina, Winkler, Christiane, Toppari, Jorma, Simell, Olli G., Adamsson, Annika, Hyöty, Heikki, Ilonen, Jorma, Jokipuu, Sanna, Kallio, Tiina, Kähönen, Miia, Knip, Mikael, Koivu, Annika, Koreasalo, Mirva, Kurppa, Kalle, Lönnrot, Maria, Mäntymäki, Elina, Multasuo, Katja, Mykkänen, Juha, Niininen, Tiina, Nyblom, Mia, Rajala, Petra, Rautanen, Jenna, Riikonen, Anne, Romo, Minna, Simell, Satu, Simell, Tuula, Simell, Ville, Sjöberg, Maija, Stenius, Aino, Särmä, Maria, Vainionpää, Sini, Varjonen, Eeva, Veijola, Riitta, Virtanen, Suvi M., Vähä-Mäkilä, Mari, Åkerlund, Mari, Lernmark, Åke, Agardh, Daniel, Aronsson, Carin Andrén, Ask, Maria, Bremer, Jenny, Carlsson, Ulla-Marie, Cilio, Corrado, Ericson-Hallström, Emelie, Fransson, Lina, Gard, Thomas, Gerardsson, Joanna, Bennet, Rasmus, Hansen, Monica, Hansson, Gertie, Harmby, Cecilia, Hyberg, Susanne, Johansen, Fredrik, Jonasdottir, Berglind, Larsson, Helena Elding, Forss, Sigrid Lenrick, Lundgren, Markus, Månsson-Martinez, Maria, Markan, Maria, Melin, Jessica, Mestan, Zeliha, Rahmati, Kobra, Ramelius, Anita, Rosenquist, Anna, Salami, Falastin, Sibthorpe, Sara, Sjöberg, Birgitta, Swartling, Ulrica, Amboh, Evelyn Tekum, Trulsson, Erika, Törn, Carina, Wallin, Anne, Wimar, Åsa, Åberg, Sofie, Hagopian, William A., Killian, Michael, Crouch, Claire Cowen, Skidmore, Jennifer, Ayres, Stephen, Dunson, Kayleen, Hervey, Rachel, Johnson, Corbin, Lyons, Rachel, Meyer, Arlene, Mulenga, Denise, Scott, Elizabeth, Stabbert, Joshua, Tarr, Alexander, Uland, Morgan, Willis, John, Becker, Dorothy, Franciscus, Margaret, Smith, MaryEllen Dalmagro-Elias, Daftary, Ashi, Klein, Mary Beth, Yates, Chrystal, Krischer, Jeffrey P., Abbondondolo, Michael, Austin-Gonzalez, Sarah, Baethke, Sandra, Brown, Rasheedah, Burkhardt, Brant, Butterworth, Martha, Clasen, Joanna, Cuthbertson, David, Eberhard, Christopher, Fiske, Steven, Garcia, Dena, Garmeson, Jennifer, Gowda, Veena, Heyman, Kathleen, Laras, Francisco Perez, Lee, Hye-Seung, Liu, Shu, Liu, Xiang, Lynch, Kristian, Malloy, Jamie, McCarthy, Cristina, McLeod, Wendy, Meulemans, Steven, Shaffer, Chris, Smith, Laura, Smith, Susan, Sulman, Noah, Tamura, Roy, Uusitalo, Ulla, Vehik, Kendra, Vijayakandipan, Ponni, Wood, Keith, Yang, Jimin, Ballard, Lori, Hadley, David, Akolkar, Beena, Bourcier, Kasia, Briese, Thomas, Johnson, Suzanne Bennett, Triplett, Eric, Andrén Aronsson, Carin, and Norris, Jill M.

Published
2016
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3. Joint modeling of longitudinal autoantibody patterns and progression to type 1 diabetes: results from the TEDDY study

Author

Köhler, Meike, Beyerlein, Andreas, Vehik, Kendra, Greven, Sonja, Umlauf, Nikolaus, Lernmark, Åke, Hagopian, William A., Rewers, Marian, She, Jin-Xiong, Toppari, Jorma, Akolkar, Beena, Krischer, Jeffrey P., Bonifacio, Ezio, Ziegler, Anette-G., Rewers, Marian, Bautista, Kimberly, Baxter, Judith, Bedoy, Ruth, Felipe-Morales, Daniel, Driscoll, Kimberly, Frohnert, Brigitte I., Gesualdo, Patricia, Hoffman, Michelle, Karban, Rachel, Liu, Edwin, Norris, Jill, Samper-Imaz, Adela, Steck, Andrea, Waugh, Kathleen, Wright, Hali, Toppari, Jorma, Simell, Olli G., Adamsson, Annika, Ahonen, Suvi, Hyöty, Heikki, Ilonen, Jorma, Jokipuu, Sanna, Kallio, Tiina, Karlsson, Leena, Kähönen, Miia, Knip, Mikael, Kovanen, Lea, Koreasalo, Mirva, Kurppa, Kalle, Latva-aho, Tiina, Lönnrot, Maria, Mäntymäki, Elina, Multasuo, Katja, Mykkänen, Juha, Niininen, Tiina, Niinistö, Sari, Nyblom, Mia, Rajala, Petra, Rautanen, Jenna, Riikonen, Anne, Riikonen, Mika, Rouhiainen, Jenni, Romo, Minna, Simell, Tuula, Simell, Ville, Sjöberg, Maija, Stenius, Aino, Leppänen, Maria, Vainionpää, Sini, Varjonen, Eeva, Veijola, Riitta, Virtanen, Suvi M., Vähä-Mäkilä, Mari, Åkerlund, Mari, Lindfors, Katri, She, Jin-Xiong, Schatz, Desmond, Hopkins, Diane, Steed, Leigh, Thomas, Jamie, Adams, Janey, Silvis, Katherine, Haller, Michael, Gardiner, Melissa, McIndoe, Richard, Sharma, Ashok, Williams, Joshua, Young, Gabriela, Anderson, Stephen W., Jacobsen, Laura, Ziegler, Anette G., Beyerlein, Andreas, Bonifacio, Ezio, Hummel, Michael, Hummel, Sandra, Foterek, Kristina, Janz, Nicole, Kersting, Mathilde, Knopff, Annette, Koletzko, Sibylle, Peplow, Claudia, Roth, Roswith, Scholz, Marlon, Stock, Joanna, Warncke, Katharina, Wendel, Lorena, Winkler, Christiane, Lernmark, Åke, Agardh, Daniel, Aronsson, Carin Andrén, Ask, Maria, Bremer, Jenny, Carlsson, Ulla-Marie, Cilio, Corrado, Ericson-Hallström, Emelie, Fransson, Lina, Gard, Thomas, Gerardsson, Joanna, Bennet, Rasmus, Hansen, Monica, Hansson, Gertie, Hyberg, Susanne, Johansen, Fredrik, Jonsdottir, Berglind, Larsson, Helena Elding, Lindström, Marielle, Lundgren, Markus, Månsson-Martinez, Maria, Markan, Maria, Melin, Jessica, Mestan, Zeliha, Ottosson, Karin, Rahmati, Kobra, Ramelius, Anita, Salami, Falastin, Sibthorpe, Sara, Sjöberg, Birgitta, Swartling, Ulrica, Amboh, Evelyn Tekum, Törn, Carina, Wallin, Anne, Wimar, Åsa, Åberg, Sofie, Hagopian, William A., Killian, Michael, Crouch, Claire Cowen, Skidmore, Jennifer, Carson, Josephine, Dalzell, Maria, Dunson, Kayleen, Hervey, Rachel, Johnson, Corbin, Lyons, Rachel, Meyer, Arlene, Mulenga, Denise, Tarr, Alexander, Uland, Morgan, Willis, John, Becker, Dorothy, Franciscus, Margaret, Smith, MaryEllen Dalmagro-Elias, Daftary, Ashi, Klein, Mary Beth, Yates, Chrystal, Krischer, Jeffrey P., Abbondondolo, Michael, Austin-Gonzalez, Sarah, Avendano, Maryouri, Baethke, Sandra, Brown, Rasheedah, Burkhardt, Brant, Butterworth, Martha, Clasen, Joanna, Cuthbertson, David, Eberhard, Christopher, Fiske, Steven, Garcia, Dena, Garmeson, Jennifer, Gowda, Veena, Heyman, Kathleen, PerezLaras, Francisco, Lee, Hye-Seung, Liu, Shu, Liu, Xiang, Lynch, Kristian, Malloy, Jamie, McCarthy, Cristina, Meulemans, Steven, Parikh, Hemang, Shaffer, Chris, Smith, Laura, Smith, Susan, Sulman, Noah, Tamura, Roy, Uusitalo, Ulla, Vehik, Kendra, Vijayakandipan, Ponni, Wood, Keith, Yang, Jimin, Ballard, Lori, Hadley, David, McLeod, Wendy, Akolkar, Beena, Yu, Liping, Miao, Dongmei, Bingley, Polly, Williams, Alistair, Chandler, Kyla, Rokni, Saba, Williams, Claire, Wyatt, Rebecca, George, Gifty, Grace, Sian, Erlich, Henry, Mack, Steven J., Ke, Sandra, Mulholland, Niveen, Bourcier, Kasia, Briese, Thomas, Johnson, Suzanne Bennett, Triplett, Eric, TEDDY study group, Ancillary Studies, Diet, Genetics, Human Subjects/Publicity/Publications, Immune Markers, Infectious Agents, Laboratory Implementation, Maternal Studies, Psychosocial, Quality Assurance, Steering, Study Coordinators, Celiac Disease, Clinical Implementation, and Quality Assurance Subcommittee on Data Quality

Published
2017
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4. Diagnostic methods for and clinical pictures of polyomavirus primary infections in children, Finland

Author

Chen, Tingting, Tanner, Laura, Simell, Ville, Hedman, Lea, Makinen, Marjaana, Sadeghi, Mohammadreza, Veijola, Riitta, Hyoty, Heikki, Ilonen, Jorma, Knip, Mikael, Toppari, Jorma, Simell, Olli, Soderlund-Venermo, Maria, and Hedman, Klaus

Subjects
Conjunctivitis -- Diagnosis -- Methods -- Health aspects, Children -- Methods -- Health aspects, Skin -- Methods -- Health aspects, Immunoglobulin G -- Methods -- Health aspects, Health
Abstract

Two novel human polyomaviruses can cause skin diseases that are predominant in immunosuppressed persons. Merkel cell polyomavirus (MCPyV) is associated with Merkel cell carcinoma, which is an uncommon aggressive skin [...]

Published
2014
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5. Association of human bocavirus 1 infection with respiratory disease in childhood follow-up study, Finland

Author

Meriluoto, Mira, Hedman, Lea, Tanner, Laura, Simell, Ville, Makinen, Marjaana, Simell, Satu, Mykkanen, Juha, Korpelainen, Jan, Ruuskanen, Olli, Ilonen, Jorma, Knip, Mikael, Simell, Olli, Hedman, Klaus, and Soderlund-Venermo, Maria

Subjects
Medical research -- Health aspects, Respiratory tract diseases -- Health aspects, DNA -- Health aspects, Viral antibodies -- Health aspects, Infection in children -- Health aspects, Infection -- Health aspects, Immunoglobulin G -- Health aspects, Children -- Diseases, Medicine, Experimental -- Health aspects, Lung diseases -- Health aspects, Immunoglobulins -- Health aspects, Conjunctivitis -- Health aspects, Enzymes -- Health aspects, Antibodies -- Health aspects, Health
Abstract

Human bocavirus 1 (HBoV1), a new member of the Bocavirus genus of the family Parvoviridae, was discovered in 2005 by large-scale sequencing in nasopharyngeal samples from children (1). HBoV1 DNA [...]

Published
2012
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6. Effects of Gluten Intake on Risk of Celiac Disease: A Case-Control Study on a Swedish Birth Cohort

Author

Aronsson, Carin Andrén, Lee, Hye-Seung, Koletzko, Sibylle, Uusitalo, Ulla, Yang, Jimin, Virtanen, Suvi M., Liu, Edwin, Lernmark, Åke, Norris, Jill M., Agardh, Daniel, Rewers, Marian, Bautista, Kimberly, Baxter, Judith, Bedoy, Ruth, Felipe-Morales, Daniel, Frohnert, Brigitte I., Gesualdo, Patricia, Hoffman, Michelle, Karban, Rachel, Liu, Edwin, Norris, Jill, Samper-Imaz, Adela, Steck, Andrea, Waugh, Kathleen, Wright, Hali, She, Jin-Xiong, Schatz, Desmond, Hopkins, Diane, Steed, Leigh, Thomas, Jamie, Adams, Janey, Silvis, Katherine, Haller, Michael, Gardiner, Melissa, McIndoe, Richard, Sharma, Ashok, Williams, Joshua, Foghis, Gabriela, Anderson, Stephen W., Robinson, Richard, Ziegler, Anette G., Beyerlein, Andreas, Bonifacio, Ezio, Hummel, Michael, Hummel, Sandra, Foterek, Kristina, Kersting, Mathilde, Knopff, Annette, Koletzko, Sibylle, Peplow, Claudia, Roth, Roswith, Stock, Joanna, Strauss, Elisabeth, Warncke, Katharina, Winkler, Christiane, Toppari, Jorma, Simell, Olli G., Adamsson, Annika, Hyöty, Heikki, Ilonen, Jorma, Jokipuu, Sanna, Kallio, Tiina, Kähönen, Miia, Knip, Mikael, Koivu, Annika, Koreasalo, Mirva, Kurppa, Kalle, Lönnrot, Maria, Mäntymäki, Elina, Multasuo, Katja, Mykkänen, Juha, Niininen, Tiina, Nyblom, Mia, Rajala, Petra, Rautanen, Jenna, Riikonen, Anne, Romo, Minna, Simell, Satu, Simell, Tuula, Simell, Ville, Sjöberg, Maija, Stenius, Aino, Särmä, Maria, Vainionpää, Sini, Varjonen, Eeva, Veijola, Riitta, Virtanen, Suvi M., Vähä-Mäkilä, Mari, Åkerlund, Mari, Lernmark, Åke, Agardh, Daniel, Ask, Maria, Bremer, Jenny, Carlsson, Ulla-Marie, Cilio, Corrado, Ericson-Hallström, Emelie, Fransson, Lina, Gard, Thomas, Gerardsson, Joanna, Bennet, Rasmus, Hansen, Monica, Hansson, Gertie, Harmby, Cecilia, Hyberg, Susanne, Johansen, Fredrik, Jonasdottir, Berglind, Larsson, Helena Elding, Forss, Sigrid Lenrick, Lundgren, Markus, Månsson-Martinez, Maria, Markan, Maria, Melin, Jessica, Mestan, Zeliha, Rahmati, Kobra, Ramelius, Anita, Rosenquist, Anna, Salami, Falastin, Sibthorpe, Sara, Sjöberg, Birgitta, Swartling, Ulrica, Amboh, Evelyn Tekum, Trulsson, Erika, Törn, Carina, Wallin, Anne, Wimar, Åsa, Åberg, Sofie, Hagopian, William A., Killian, Michael, Crouch, Claire Cowen, Skidmore, Jennifer, Ayres, Stephen, Dunson, Kayleen, Hervey, Rachel, Johnson, Corbin, Lyons, Rachel, Meyer, Arlene, Mulenga, Denise, Scott, Elizabeth, Stabbert, Joshua, Tarr, Alexander, Uland, Morgan, Willis, John, Becker, Dorothy, Franciscus, Margaret, Smith, MaryEllen Dalmagro-Elias, Daftary, Ashi, Klein, Mary Beth, Yates, Chrystal, Krischer, Jeffrey P., Abbondondolo, Michael, Austin-Gonzalez, Sarah, Baethke, Sandra, Brown, Rasheedah, Burkhardt, Brant, Butterworth, Martha, Clasen, Joanna, Cuthbertson, David, Eberhard, Christopher, Fiske, Steven, Garcia, Dena, Garmeson, Jennifer, Gowda, Veena, Heyman, Kathleen, Laras, Francisco Perez, Lee, Hye-Seung, Liu, Shu, Liu, Xiang, Lynch, Kristian, Malloy, Jamie, McCarthy, Cristina, McLeod, Wendy, Meulemans, Steven, Shaffer, Chris, Smith, Laura, Smith, Susan, Sulman, Noah, Tamura, Roy, Uusitalo, Ulla, Vehik, Kendra, Vijayakandipan, Ponni, Wood, Keith, Yang, Jimin, Ballard, Lori, Hadley, David, Akolkar, Beena, Bourcier, Kasia, Briese, Thomas, Johnson, Suzanne Bennett, and Triplett, Eric

Published
2016
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11. Correction: Vol. 18, No. 2

Author

Meriluoto, Mira, Hedman, Lea, Tanner, Laura, Simell, Ville, Makinen, Marjaana, Simell, Satu, Mykkanen, Juha, Korpelainen, Jan, Ruuskanen, Olli, Ilonen, Jorma, Knip, Mikael, Simell, Olli, Hedman, Klaus, and Soderlund-Venermo, Maria

Subjects
Health
Abstract

To the Editor: In our earlier assessment of the etiologic role of human bocavirus 1 (HBoVl) among 109 constitutionally healthy children, seroconversion measured by a standard IgG enzyme immunoassay (EIA) [...]

Published
2016

13. Association Between Early-Life Antibiotic Use and the Risk of Islet or Celiac Disease Autoimmunity.

Author

Kemppainen, Kaisa M., Vehik, Kendra, Lynch, Kristian F., Larsson, Helena Elding, Canepa, Ronald J., Simell, Ville, Koletzko, Sibylle, Liu, Edwin, Simell, Olli G., Toppari, Jorma, Ziegler, Anette G., Rewers, Marian J., Lernmark, Åke, Hagopian, William A., Jin-Xiong She, Akolkar, Beena, Schatz, Desmond A., Atkinson, Mark A., Blaser, Martin J., and Krischer, Jeffrey P.

Published
2017
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14. Identification of Non-HLA Genes Associated with Celiac Disease and Country-Specific Differences in a Large, International Pediatric Cohort.

Author

Sharma, Ashok, Liu, Xiang, Hadley, David, Hagopian, William, Liu, Edwin, Chen, Wei-Min, Onengut-Gumuscu, Suna, Simell, Ville, Rewers, Marian, Ziegler, Anette-G., Lernmark, Åke, Simell, Olli, Toppari, Jorma, Krischer, Jeffrey P., Akolkar, Beena, Rich, Stephen S., Agardh, Daniel, She, Jin-Xiong, and null, null

Subjects
CELIAC disease, HLA histocompatibility antigens, DISEASE incidence, DISEASE prevalence, AUTOANTIBODIES, PEDIATRICS
Abstract

Objectives: There are significant geographical differences in the prevalence and incidence of celiac disease that cannot be explained by HLA alone. More than 40 loci outside of the HLA region have been associated with celiac disease. We investigated the roles of these non-HLA genes in the development of tissue transglutaminase autoantibodies (tTGA) and celiac disease in a large international prospective cohort study. Methods: A total of 424,788 newborns from the US and European general populations and first-degree relatives with type 1 diabetes were screened for specific HLA genotypes. Of these, 21,589 carried 1 of the 9 HLA genotypes associated with increased risk for type 1 diabetes and celiac disease; we followed 8676 of the children in a 15 y prospective follow-up study. Genotype analyses were performed on 6010 children using the Illumina ImmunoChip. Levels of tTGA were measured in serum samples using radio-ligand binding assays; diagnoses of celiac disease were made based on persistent detection of tTGA and biopsy analysis. Data were analyzed using Cox proportional hazards analyses. Results: We found 54 single-nucleotide polymorphisms (SNPs) in 5 genes associated with celiac disease (TAGAP, IL18R1, RGS21, PLEK, and CCR9) in time to celiac disease analyses (10−4>P>5.8x10−6). The hazard ratios (HR) for the SNPs with the smallest P values in each region were 1.59, 1.45, 2.23, 2.64, and 1.40, respectively. Outside of regions previously associated with celiac disease, we identified 10 SNPs in 8 regions that could also be associated with the disease (P<10−4). A SNP near PKIA (rs117128341, P = 6.5x10−8, HR = 2.8) and a SNP near PFKFB3 (rs117139146, P<2.8x10−7, HR = 4.9) reached the genome-wide association threshold in subjects from Sweden. Analyses of time to detection of tTGA identified 29 SNPs in 2 regions previously associated with celiac disease (CTLA4, P = 1.3x10−6, HR = 0.76 and LPP, P = 2.8x10−5, HR = .80) and 6 SNPs in 5 regions not previously associated with celiac disease (P<10−4); non-HLA genes are therefore involved in development of tTGA. Conclusions: In conclusion, using a genetic analysis of a large international cohort of children, we associated celiac disease development with 5 non-HLA regions previously associated with the disease and 8 regions not previously associated with celiac disease. We identified 5 regions associated with development of tTGA. Two loci associated with celiac disease progression reached a genome-wide association threshold in subjects from Sweden. [ABSTRACT FROM AUTHOR]

Published
2016
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15. Reduced β-cell function in early preclinical type 1 diabetes.

Author

Koskinen, Maarit K., Helminen, Olli, Matomäki, Jaakko, Aspholm, Susanna, Mykkänen, Juha, Makinen, Marjaana, Simell, Ville, Vähä-Mäkilä, Mari, Simell, Tuula, Ilonen, Jorma, Knip, Mikael, Veijola, Riitta, Toppari, Jorma, and Simell, Olli

Subjects
DIABETES, INSULIN therapy, INSULIN resistance, BLOOD sugar, DISEASE susceptibility, DIAGNOSIS of diabetes
Abstract

Objective: We aimed to characterize insulin responses to i.v. glucose during the preclinical period of type 1 diabetes starting from the emergence of islet autoimmunity. Design and methods: A large population-based cohort of children with HLA-conferred susceptibility to type 1 diabetes was observed from birth. During regular follow-up visits islet autoantibodies were analysed. We compared markers of glucose metabolism in sequential intravenous glucose tolerance tests between 210 children who were positive for multiple (≥2) islet autoantibodies and progressed to type 1 diabetes (progressors) and 192 children testing positive for classical islet-cell antibodies only and remained healthy (non-progressors). Results: In the progressors, the first phase insulin response (FPIR) was decreased as early as 4-6 years before the diagnosis when compared to the non-progressors (P=0.001). The difference in FPIR between the progressors and non-progressors was significant (P<0.001) in all age groups, increasing with age (at 2 years: difference 50% (95% CI 28-75%) and at 10 years: difference 172% (95% CI 128-224%)). The area under the 10-min insulin curve showed a similar difference between the groups (P<0.001; at 2 years: difference 36% (95% CI 17-58%) and at 10 years: difference 186% (95% CI 143-237%)). Insulin sensitivity did not differ between the groups. Conclusions: FPIR is decreased several years before the diagnosis of type 1 diabetes, implying an intrinsic defect in β-cell mass and/or function. [ABSTRACT FROM AUTHOR]

Published
2016
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16. B-Cell Responses to Human Bocaviruses 1–4: New Insights from a Childhood Follow-Up Study.

Author

Kantola, Kalle, Hedman, Lea, Tanner, Laura, Simell, Ville, Mäkinen, Marjaana, Partanen, Juulia, Sadeghi, Mohammadreza, Veijola, Riitta, Knip, Mikael, Ilonen, Jorma, Hyöty, Heikki, Toppari, Jorma, Simell, Olli, Hedman, Klaus, and Söderlund-Venermo, Maria

Subjects
B cells, FOLLOW-up studies (Medicine), ANTIGEN analysis, POLYMERASE chain reaction, SERODIAGNOSIS, VIRUS diseases
Abstract

Human bocaviruses (HBoVs) 1–4 are recently discovered, antigenically similar parvoviruses. We examined the hypothesis that the antigenic similarity of these viruses could give rise to clinically and diagnostically important immunological interactions. IgG and IgM EIAs as well as qPCR were used to study ~2000 sera collected from infancy to early adolescence at 3–6-month intervals from 109 children whose symptoms were recorded. We found that HBoV1-4-specific seroprevalences at age 6 years were 80%, 48%, 10%, and 0%, respectively. HBoV1 infections resulted in significantly weaker IgG responses among children who had pre-existing HBoV2 IgG, and vice versa. Furthermore, we documented a complete absence of virus type-specific immune responses in six viremic children who had pre-existing IgG for another bocavirus, indicating that not all HBoV infections can be diagnosed serologically. Our results strongly indicate that interactions between consecutive HBoV infections affect HBoV immunity via a phenomenon called “original antigenic sin”, cross-protection, or both; however, without evident clinical consequences but with important ramifications for the serodiagnosis of HBoV infections. Serological data is likely to underestimate human exposure to these viruses. [ABSTRACT FROM AUTHOR]

Published
2015
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18. Bacteroides dorei dominates gut microbiome prior to autoimmunity in Finnish children at high risk for type 1 diabetes.

Author

Davis-Richardson, Austin G., Ardissone, Alexandria N., Dias, Raquel, Simell, Ville, Leonard, Michael T., Kemppainen, Kaisa M., Drew, Jennifer C., Schatz, Desmond, Atkinson, Mark A., Kolaczkowski, Bryan, Ilonen, Jorma, Knip, Mikael, Toppari, Jorma, Nurminen, Noora, Hyöty, Heikki, Veijola, Riitta, Simell, Tuula, Mykkänen, Juha, Simell, Olli, and Triplett, Eric W.

Subjects
DIABETES risk factors, BACTEROIDES, DISEASE incidence, DISEASE progression, AUTOIMMUNE diseases
Abstract

The incidence of the autoimmune disease, type 1 diabetes (T1D), has increased dramatically over the last half century in many developed countries and is particularly high in Finland and other Nordic countries. Along with genetic predisposition, environmental factors are thought to play a critical role in this increase. As with other autoimmune diseases, the gut microbiome is thought to play a potential role in controlling progression to T1D in children with high genetic risk, but we know little about how the gut microbiome develops in children with high genetic risk for T1D. In this study, the early development of the gut microbiomes of 76 children at high genetic risk for T1D was determined using high-throughput 16S rRNA gene sequencing. Stool samples from children born in the same hospital in Turku, Finland were collected at monthly intervals beginning at 4-6 months after birth until 2.2 years of age. Of those 76 children, 29 seroconverted to T1D-related autoimmunity (cases) including 22 who later developed T1D, the remaining 47 subjects remained healthy (controls). While several significant compositional differences in low abundant species prior to seroconversion were found, one highly abundant group composed of two closely related species, Bacteroides dorei and Bacteroides vulgatus, was significantly higher in cases compared to controls prior to seroconversion. Metagenomic sequencing of samples high in the abundance of the B. dorei/vulgatus group before seroconversion, as well as longer 16S rRNA sequencing identified this group as Bacteroides dorei. The abundance of B. dorei peaked at 7.6 months in cases, over 8 months prior to the appearance of the first islet autoantibody, suggesting that early changes in the microbiome may be useful for predicting T1D autoimmunity in genetically susceptible infants. The cause of increased B. dorei abundance in cases is not known but its timing appears to coincide with the introduction of solid food. [ABSTRACT FROM AUTHOR]

Published
2014
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19. Diagnostic Methods for and Clinical Pictures of Polyomavirus Primary Infections in Children, Finland.

Author

Tingting Chen, Tanner, Laura, Simell, Ville, Hedman, Lea, Mäkinen, Marjaana, Sadeghi, Mohammadreza, Veijola, Riitta, Hyöty, Heikki, Ilonen, Jorma, Knip, Mikael, Toppari, Jorma, Simell, Olli, Söderlund-Venermo, Maria, and Hedman, Klaus

Subjects
SERODIAGNOSIS, MERKEL cells, POLYOMAVIRUSES, POLYOMAVIRUS diseases, INFECTION in children, JUVENILE diseases
Abstract

We used comprehensive serodiagnostic methods (IgM, IgG, and IgG avidity) and PCR to study Merkel cell polyomavirus and trichodysplasia spinulosa-associated polyomavirus infections in children observed from infancy to adolescence. Comparing seroconversion intervals with previous and subsequent intervals, we found that primary infections with these 2 viruses were asymptomatic in childhood. [ABSTRACT FROM AUTHOR]

Published
2014
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20. Celiac Disease-Associated Antibodies in Children with Genetic Risk for both Type 1 Diabetes and Celiac Disease.

Author

Simell, Satu, Hoppu, Sanna, Hekkala, Anne, Simell, Tuula, StÅhlberg, Marja-Riitta, Viander, Markku, Yrjänäinen, Heta, Grönlund, Juhani, Markula, Perttu, Simell, Ville, Knip, Mikael, Ilonen, Jorma, Hyöyy, Heikki, and Simell, Olli

Subjects
CELIAC disease, IMMUNOGLOBULINS, CELIAC disease in children, DIABETES in children, TRANSGLUTAMINASES, GLUTEN
Abstract

Because celiac disease (CD) is a common partner of type 1 diabetes (T1D), the two diseases may share pathways in pathogenesis. In T1D Prediction and Prevention Study (DIPP) we examined serum samples from over 2000 children with HLA-conferred genetic T1D and CD susceptibility, born between 11/1994 and 12/2002. The samples were collected at 3- to 12-month intervals and examined for antibodies to tissue transglutaminase (TGA). If positive, all previous and forthcoming samples were also examined for endomysium (EMA), reticulin (ARA) and gliadin antibodies (AGA-IgA,AGA-IgG). Eighty one (ca 4%) of the 2000 children were TGA-positive. AGA-IgG emerged first at age 2.2 ± 1.7; 0.5-7.5 years (mean ± SD; range). TGA, EMA and ARA emerged slightly later (TGA at 3.5±1.9; 1.0-9.0 years; p<0.001). Very few TGA-positive children had symptoms of CD; most were symptom-flee. Because a majority of serum samples was collected before this CD study began, the children were continuously exposed to gluten until TGA positivity was retrospectively discovered using biobanked serum samples. Despite continued gluten exposure TGA, EMA, ARA, AGA-IgA and AGA-IgG positivity disappeared spontaneously in 47%, 36%, 37, 43% and 29% of the children, respectively. CD was diagnosed in 42 of 53 TGA positive children whose parents consented to biopsy. In conclusion, potential non-gluten factor(s) regulating onset of CD autoimmunity probably function before AGA-IgG emerges. In a large proportion of children CD-associated antibodies disappear spontaneously suggesting that regulatory immune phenomena often extinguish incipient CD without exclusion of gluten from the diet. [ABSTRACT FROM AUTHOR]

Published
2007

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