liu.seSearch for publications in DiVA
Change search
Link to record
Permanent link

Direct link
BETA
Pihl, Mikael
Publications (10 of 14) Show all publications
Ludvigsson, J., Chéramy, M., Axelsson, S., Pihl, M., Åkerman, L. & Casas, R. (2014). GAD-treatment of children and adolescents with recent-onset Type 1 diabetes preserves residual insulin secretion after 30 months. Diabetes/Metabolism Research Reviews, 30(5), 405-414
Open this publication in new window or tab >>GAD-treatment of children and adolescents with recent-onset Type 1 diabetes preserves residual insulin secretion after 30 months
Show others...
2014 (English)In: Diabetes/Metabolism Research Reviews, ISSN 1520-7552, E-ISSN 1520-7560, Vol. 30, no 5, p. 405-414Article in journal (Refereed) Published
Abstract [en]

BACKGROUND: This study aimed to analyse data from two different studies (Phase II and Phase III) regarding the safety and efficacy of treatment with alum formulated glutamic acid decarboxylase GAD65 (GAD-alum), 30 months after administration to children and adolescents with Type 1 diabetes (T1D).

METHODS: The Phase II trial was a double-blind, randomized placebo-controlled study, including 70 children and adolescents which were followed for 30 months. Participants received a subcutaneous injection of either 20 µg of GAD-alum or placebo at baseline and one month later. During a subsequent larger European Phase III trial including three treatment arms, participants received two or four subcutaneous injections of either 20 µg of GAD-alum and/or placebo at baseline, 1, 3 and 9 months. The Phase III trial was prematurely interrupted at 15 months, but of the 148 Swedish patients, a majority completed the 21 months follow-up and 45 patients completed the trial at 30 months. Both studies included GADA-positive patients with fasting C-peptide ≥0.10 nmol/l. We have now combined the results of these two trials.

RESULTS: There were no treatment related adverse events. In patients treated with 2 GAD-alum doses, stimulated C-peptide AUC had decreased significantly less (9 m: p < 0.037; 15 m p < 0.032; 21 m p < 0.003 and 30 m p < 0.004) and a larger proportion of these patients were also able to achieve a peak stimulated C-peptide >0.2 nmol/l (p < 0.05), as compared to placebo.

CONCLUSION: Treatment with two doses of GAD-alum in children and adolescents with recent-onset T1D shows no adverse events and preserves residual insulin secretion. This article is protected by copyright. All rights reserved.

Place, publisher, year, edition, pages
Wiley-Blackwell, 2014
Keywords
arrays; celiac disease; children; gene expression; gluten-free diet; IL-17; mucosa; Th17
National Category
Medical and Health Sciences
Identifiers
urn:nbn:se:liu:diva-108613 (URN)10.1002/dmrr.2503 (DOI)000339416900007 ()24302596 (PubMedID)
Available from: 2014-07-01 Created: 2014-07-01 Last updated: 2017-12-05Bibliographically approved
Axelsson, S., Cheramy, M., Åkerman, L., Pihl, M., Ludvigsson, J. & Casas, R. (2013). Cellular and Humoral Immune responses in Type 1 Diabetic patients participating in a Phase III GAD-alum Intervention Trial. Diabetes Care, 36(11), 3418-3424
Open this publication in new window or tab >>Cellular and Humoral Immune responses in Type 1 Diabetic patients participating in a Phase III GAD-alum Intervention Trial
Show others...
2013 (English)In: Diabetes Care, ISSN 0149-5992, E-ISSN 1935-5548, Vol. 36, no 11, p. 3418-3424Article in journal (Refereed) Published
Abstract [en]

OBJECTIVEGAD formulated in aluminum hydroxide (GAD-alum) has previously been shown to induce preservation of residual insulin secretion in recent-onset type 1 diabetes, but recent phase II and III GAD-alum trials failed to reach primary outcomes. The European phase III study was therefore closed after 15 months, and only a minority of patients completed the 30 months of follow-up.RESEARCH DESIGN AND METHODSThis study aimed to characterize cellular and humoral responses in the Swedish patients (n = 148) participating in the phase III trial, receiving four (4D) or two (2D) GAD-alum doses or placebo. Serum GAD(65) antibody (GADA) levels, GADA IgG1-4 subclass distribution, cytokine secretion, and proliferative responses in peripheral blood mononuclear cells (PBMCs) were analyzed.RESULTSThe GAD(65)-induced cytokine profile tended to switch toward a predominant Th2-associated profile over time both in the 2D and 4D group. The groups also displayed increased GADA levels and PBMC proliferation compared with placebo, whereas GADA IgG subclass distribution changed in 4D patients.CONCLUSIONSBoth 2D and 4D patients displayed GAD(65)-specifc cellular and humoral effects after GAD-alum treatment, but at different time points and magnitudes. No specific immune markers could be associated with treatment efficacy.

Place, publisher, year, edition, pages
American Diabetes Association, 2013
National Category
Clinical Medicine
Identifiers
urn:nbn:se:liu:diva-99798 (URN)10.2337/dc12-2251 (DOI)000326274100013 ()23863909 (PubMedID)
Available from: 2013-10-21 Created: 2013-10-21 Last updated: 2017-12-06Bibliographically approved
Pihl, M., Axelsson, S., Cheramy, M., Reijonen, H., Ludvgisson, J. & Casas, R. (2013). GAD-alum treatment induces GAD-specific CD4 T cells in a phase III clinical trial.
Open this publication in new window or tab >>GAD-alum treatment induces GAD-specific CD4 T cells in a phase III clinical trial
Show others...
2013 (English)Manuscript (preprint) (Other academic)
Abstract [en]

Glutamic Acid Decarboxylase (GAD)65 formulated in aluminium hydroxide (GAD-alum preserved insulin secretion in a phase II clinical trial in recent onset type 1 diabetes. GADalum treated patients up-regulated FOXP3 upon antigen recall at 21 and 30 months after treatment. A 4-year follow-up of the study revealed increased frequencies of both CD25+CD127+ and CD25hiCD127lo cells in treated patients after antigen recall. A subsequent european phase III trial was closed after 15 months after failing to reach primary outcome. We monitored antigen recall induced frequencies of memory, effector and regulatory T cells throughout the phase III trial. Antigen recall induced mainly CD25+CD127+, CD45RO+ and non-suppressive FOXP3loCD45RA- cells in GAD-alum treated patients. In addition, a population of activated FSChiSSChi cells was observed, enriched in CD25+CD127+, CD45RO+ and proliferating cells. GAD65-specific T cells determined by tetramer staining were induced by antigen recall in GAD-alum treated patients and were more frequent in the FSChiSSChi population. Additional doses of GAD-alum increased frequencies of CD25+CD127+, CD45RO+ and FSChiSSChi cells but had no effect on frequencies of CD25hiCD127lo. Our findings indicate that antigen recall after GAD-alum treatment primarily induces memory and activated T cells. In particular, GAD65-specific cells were mainly of a memory or activated phenotype. Additional doses of GAD-alum mainly affect memory T cell frequency and T cell activation.

National Category
Medical and Health Sciences
Identifiers
urn:nbn:se:liu:diva-98251 (URN)
Available from: 2013-10-04 Created: 2013-10-04 Last updated: 2013-10-04
Pihl, M., Verma, D., Fredrikson, M., Söderkvist, P., Ludvgisson, J. & Casas, R. (2013). Polymorphisms in NALP3 inflammasome components NLRP3 and CARD8 affect C-peptide secretion in type 1 diabetes.
Open this publication in new window or tab >>Polymorphisms in NALP3 inflammasome components NLRP3 and CARD8 affect C-peptide secretion in type 1 diabetes
Show others...
2013 (English)Manuscript (preprint) (Other academic)
Abstract [en]

Interleukin-1β has long been known to have potential roles in type 1 diabetes (T1D) pathogenesis. Production of active Iinterleukin-1β is dependent on the action of a caspase activating protein complex called NALP3 inflammasome. The NALP3 inflammasome is composed of NALP3/Cryopyrin, ASC and CARD8. Polymorphisms in the NLRP3 and CARD8 genes have been linked to several autoinflammatory diseases. The NALP3 inflammasome is crucial for adjuvanticity of aluminium hydroxide, which is used as adjuvant in clinical trials of glutamic acid decarboxylase (GAD)-alum in T1D. Our aim was to investigate the effect of common polymorphisms of NLRP3 on T1D susceptibility as well as on GAD-alum treatment efficacy. The single nucleotide polymorphisms NLRP3 Q705K, CARD8 C10X and an SNP downstream of the NLRP3 gene, rs10733113, were genotyped using a Taqman genotyping assay. The A allele of CARD8 C10X was associated with a lower stimulated insulin secretion 3 months after diagnosis in males. Patients with at least one G allele at rs10733113 were more likely to produce auto-antibodies against two or more of the islet antigens GAD, Insulin or IA-2. None of the genotyped SNPs had any significant influence on efficacy of GAD-alum treatment, but individuals with at least one rs10733113 G allele treated with placebo had lower residual insulin secretion than those with the AA genotype at 9, 15 and 21 months after start of treatment.

National Category
Medical and Health Sciences
Identifiers
urn:nbn:se:liu:diva-98248 (URN)
Available from: 2013-10-04 Created: 2013-10-04 Last updated: 2013-10-04Bibliographically approved
Pihl, M., Åkerman, L., Axelsson, S., Chéramy, M., Hjorth, M., Mallone, R., . . . Casas, R. (2013). Regulatory T cell phenotype and function 4 years after GAD–alum treatment in children with type 1 diabetes. Clinical and Experimental Immunology, 172(3), 394-402
Open this publication in new window or tab >>Regulatory T cell phenotype and function 4 years after GAD–alum treatment in children with type 1 diabetes
Show others...
2013 (English)In: Clinical and Experimental Immunology, ISSN 0009-9104, E-ISSN 1365-2249, Vol. 172, no 3, p. 394-402Article in journal (Refereed) Published
Abstract [en]

Glutamic acid decarboxylase (GAD)65 formulated with aluminium hydroxide (GAD-alum) was effective in preserving insulin secretion in a Phase II clinical trial in children and adolescents with recent-onset type 1 diabetes. In addition, GAD-alum treated patients increased CD4+CD25hi forkhead box protein 3+ (FoxP3+) cell numbers in response to in-vitro GAD65 stimulation. We have carried out a 4-year follow-up study of 59 of the original 70 patients to investigate long-term effects on the frequency and function of regulatory T cells after GAD-alum treatment. Peripheral blood mononuclear cells were stimulated in vitro with GAD65 for 7 days and expression of regulatory T cell markers was measured by flow cytometry. Regulatory T cells (CD4+CD25hiCD127lo) and effector T cells (CD4+CD25CD127+) were further sorted, expanded and used in suppression assays to assess regulatory T cell function after GAD-alum treatment. GAD-alum-treated patients displayed higher frequencies of in-vitro GAD65-induced CD4+CD25+CD127+ as well as CD4+CD25hiCD127lo and CD4+FoxP3+ cells compared to placebo. Moreover, GAD65 stimulation induced a population of CD4hi cells consisting mainly of CD25+CD127+, which was specific of GAD-alum-treated patients (16 of 25 versus one of 25 in placebo). Assessment of suppressive function in expanded regulatory T cells revealed no difference between GAD-alum- and placebo-treated individuals. Regulatory T cell frequency did not correlate with C-peptide secretion throughout the study. In conclusion, GAD-alum treatment induced both GAD65-reactive CD25+CD127+ and CD25hiCD127lo cells, but no difference in regulatory T cell function 4 years after GAD-alum treatment.

Place, publisher, year, edition, pages
Wiley-Blackwell, 2013
Keywords
CD4 T cells (T helper, Th0, Th1, Th2, Th3, Th17), diabetes, immune regulation, regulatory T cells (Treg), therapy/immunotherapy
National Category
Medical and Health Sciences
Identifiers
urn:nbn:se:liu:diva-93379 (URN)10.1111/cei.12078 (DOI)000318073000004 ()
Note

Funding Agencies|Swedish Research Council|K2008-55x-20652-01-3|Swedish Child Diabetes Foundation (Barndiabetesfonden)||Medical Research Council of Southeast Sweden||JDRF|1-2008-106|Ile-de-France CODDIM||Inserm Avenir Program||

Available from: 2013-05-31 Created: 2013-05-31 Last updated: 2017-12-06Bibliographically approved
Pihl, M. (2013). Reign in Blood: Immune Regulation in Type 1 Diabetes. (Doctoral dissertation). Linköping: Linköping University Electronic Press
Open this publication in new window or tab >>Reign in Blood: Immune Regulation in Type 1 Diabetes
2013 (English)Doctoral thesis, comprehensive summary (Other academic)
Abstract [en]

Type 1 Diabetes (T1D) is an autoimmune disease resulting in insulin deficiency as a result ofautoimmune destruction of pancreatic β-cells. Preserving β-cell function in patients with T1D would be of great benefit since patients with sustained endogenous insulin secretion are known to suffer less from secondary complications due to hyperglycemia. Glutamic acid decarboxylase 65 (GAD65) is a major autoantigen targeted by self-reactive lymphocytes in T1D, and has been used in several attempts at treating T1D by inducing tolerance to β-cell antigens. We showed positive clinical effects of GAD65 formulated with aluminium hydroxide (GAD-alum) on preservation of C-peptide secretion in a phase II clinical trial. Unfortunately, a phase III clinical trial in a larger population failed to confirm this finding. Regulatory T cells (Treg) are instrumental in maintaining peripheral tolerance to self-antigens. Deficiencies in Treg function are thought to influence the pathogenesis of autoimmune diseases, including T1D. One proposed mechanism of achieving tolerance to β-cell antigens in T1D is the induction of antigen-specific Treg through immunomodulation. The general aim of this thesis was to study immune regulation in T1D, the role of Treg and immunomodulatory effects of GAD-alum treatment in particular. Our hypothesis was that Treg biology is altered in T1D and pre-diabetes, and that an induction of GAD65-specific Treg contributes to the clinical efficacy of GAD-alum treatment. We demonstrated that T cells expressing Treg-associated markers were increased in number in patients with recent-onset T1D, as well as in children with high risk of developing T1D. We found that antigen recall 4 years after GAD-alum treatment induced cells with both regulatory and effector phenotypes in GAD-alum treated patients. Furthermore there was no effect on Treg-mediated suppression in GAD-alum treated patients, while patients with T1D, regardless of treatment, exhibited deficient Treg-mediated suppression of Teff that was intrinsic to the Treg population. We followed patients participating in a phase III trial of GAD-alum, and using an extended antibody panel we demonstrated that antigen recall induced mainly Teff cells in treated patients, along  with increased frequencies of memory T cells, non-suppressive CD45RA-FOXP3lo cells and increased GAD65-induced proliferation of mainly Teff and memory T cells. Finally we examined whether SNPs in genes encoding inflammasome components contributed to T1D risk, but found no effects of variant alleles on the risk of developing T1D, or on the efficacy of GAD-alum treatment. We show small effects on C-peptide secretion and autoantibody positivity in patients with T1D. In conclusion, we find that while Treg are deficient in patients with T1D, induction of Treg is an unlikely mechanism of action of GAD-alum treatment.

Place, publisher, year, edition, pages
Linköping: Linköping University Electronic Press, 2013. p. 113
Series
Linköping University Medical Dissertations, ISSN 0345-0082 ; 1377
National Category
Medical and Health Sciences
Identifiers
urn:nbn:se:liu:diva-98250 (URN)10.3384/diss.diva-98250 (DOI)978-91-7519-533-9 (ISBN)
Public defence
2013-11-08, Berzeliussalen, Campus US, Linköpings universitet, Linköping, 09:00 (English)
Opponent
Supervisors
Available from: 2013-10-04 Created: 2013-10-04 Last updated: 2019-12-08Bibliographically approved
Ludvigsson, J., Hjorth, M., Chéramy, M., Axelsson, S., Pihl, M., Forsander, G., . . . Casas, R. (2011). Extended evaluation of the safety and efficacy of GAD treatment of children and adolescents with recent-onset type 1 diabetes: a randomised controlled trial. DIABETOLOGIA, 54(3), 634-640
Open this publication in new window or tab >>Extended evaluation of the safety and efficacy of GAD treatment of children and adolescents with recent-onset type 1 diabetes: a randomised controlled trial
Show others...
2011 (English)In: DIABETOLOGIA, ISSN 0012-186X, Vol. 54, no 3, p. 634-640Article in journal (Refereed) Published
Abstract [en]

The aim of this study was to investigate the safety and efficacy of alum formulated glutamic acid decarboxylase GAD(65) (GAD-alum) treatment of children and adolescents with type 1 diabetes after 4 years of follow-up. Seventy children and adolescents aged 10-18 years with recent onset type 1 diabetes participated in a phase II, double-blind, randomised placebo-controlled clinical trial. Patients identified as possible participants attended one of eight clinics in Sweden to receive information about the study and for an eligibility check, including a medical history. Participants were randomised to one of the two treatment groups and received either a subcutaneous injection of 20 mu g of GAD-alum or placebo at baseline and 1 month later. The study was blinded to participants and investigators until month 30. The study was unblinded at 15 months to the sponsor and statistician in order to evaluate the data. At follow-up after 30 months there was a significant preservation of residual insulin secretion, as measured by C-peptide, in the group receiving GAD-alum compared with placebo. This was particularly evident in patients with andlt; 6 months disease duration at baseline. There were no treatment-related serious adverse events. We have now followed these patients for 4 years. Overall, 59 patients, 29 who had been treated with GAD-alum and 30 who had received placebo, gave their informed consent. One patient in each treatment group experienced an episode of keto-acidosis between months 30 and 48. There were no treatment-related adverse events. The primary efficacy endpoint was the change in fasting C-peptide concentration from baseline to 15 months after the prime injection for all participants per protocol set. In the GAD-alum group fasting C-peptide was 0.332 +/- 0.032 nmol/l at day 1 and 0.215 +/- 0.031 nmol/l at month 15. The corresponding figures for the placebo group were 0.354 +/- 0.039 and 0.184 +/- 0.033 nmol/l, respectively. The decline in fasting C-peptide levels between day 1 and month 1, was smaller in the GAD-alum group than the placebo group. The difference between the treatment groups was not statistically significant. In those patients who were treated within 6 months of diabetes diagnosis, fasting C-peptide had decreased significantly less in the GAD-alum group than in the placebo-treated group after 4 years. Four years after treatment with GAD-alum, children and adolescents with recent-onset type 1 diabetes continue to show no adverse events and possibly to show clinically relevant preservation of C-peptide. ClinicalTrials.gov NCT00435981 The study was funded by The Swedish Research Council K2008-55X-20652-01-3, Barndiabetesfonden (The Swedish Child Diabetes Foundation), the Research Council of Southeast Sweden, and an unrestricted grant from Diamyd Medical AB.

Place, publisher, year, edition, pages
Springer Science Business Media, 2011
Keywords
C-peptide, Children, GAD-alum treatment, Immune modulation, Type 1 diabetes
National Category
Medical and Health Sciences
Identifiers
urn:nbn:se:liu:diva-66310 (URN)10.1007/s00125-010-1988-1 (DOI)000286987000021 ()
Note
The original publication is available at www.springerlink.com: Johnny Ludvigsson, Maria Hjorth, Mikael Chéramy, Stina Axelsson, Mikael Pihl, G Forsander, N -O Nilsson, B-O Samuelsson, T Wood, J Aman, E Ortqvist and Rosaura Casas, Extended evaluation of the safety and efficacy of GAD treatment of children and adolescents with recent-onset type 1 diabetes: a randomised controlled trial, 2011, DIABETOLOGIA, (54), 3, 634-640. http://dx.doi.org/10.1007/s00125-010-1988-1 Copyright: Springer Science Business Media http://www.springerlink.com/ Available from: 2011-03-11 Created: 2011-03-11 Last updated: 2011-03-24
Pihl, M., Chéramy, M., Mjösberg, J., Ludvigsson, J. & Casas, R. (2011). Increased expression of regulatory T cell-associated markers in recent-onset diabetic children. Open Journal of Immunology, 1(3), 57-64
Open this publication in new window or tab >>Increased expression of regulatory T cell-associated markers in recent-onset diabetic children
Show others...
2011 (English)In: Open Journal of Immunology, ISSN 2162-450X, E-ISSN 2162-4526, Vol. 1, no 3, p. 57-64Article in journal (Refereed) Published
Abstract [en]

CD4+CD25hi T cells are thought to be crucial for the maintenance of immunological tolerance to self antigens. In this study, we investigated the frequencies of these cells in the early stage of type 1 diabetes, as well as in a setting of possible pre-diabetic autoimmunity. Hence, the expression of FOXP3, CTLA-4, and CD27 in CD4+ CD25hi T cells was analyzed using flow cytometry in 14 patients with recent onset type 1 diabetes, in 9 at-risk individuals, and 9 healthy individuals with no known risk for type 1 diabetes. Our results show there were no differences in the frequency of CD4+CD25hi cells between groups. However, compared to controls, recent-onset type 1 diabetic patients had higher expression of FOXP3, CTLA-4, and CD27 in CD4+ CD25hi cells from peripheral blood. The median fluorescence intensity of FOXP3 was significantly higher in CD4+CD25hi cells from patients with type 1 diabetes than from controls. Furthermore, a positive correlation between the frequency of FOXP3+ cells and the median fluorescence intensity of FOXP3 was observed among patients with type 1 diabetes. These data suggest that the frequency of CD4+CD25hi FOXP3+ T cells in the periphery is not decreased but rather increased at onset of type 1 diabetes. Thus, functional deficiencies rather than reduced numbers of CD4+CD25hi cells could contribute to the development of type 1 diabetes. 

Place, publisher, year, edition, pages
Irvine, CA. USA: Scientific Research Publishing, 2011
Keywords
Regulatory T cells; Type 1 Diabetes; Autoantibodies
National Category
Medical and Health Sciences
Identifiers
urn:nbn:se:liu:diva-75890 (URN)10.4236/oji.2011.13007 (DOI)
Available from: 2012-03-15 Created: 2012-03-15 Last updated: 2017-12-07
Axelsson, S., Chéramy, M., Hjorth, M., Pihl, M., Åkerman, L., Martinuzzi, E., . . . Casas, R. (2011). Long-Lasting Immune Responses 4 Years after GAD-Alum Treatment in Children with Type 1 Diabetes. PLoS ONE, 6(12)
Open this publication in new window or tab >>Long-Lasting Immune Responses 4 Years after GAD-Alum Treatment in Children with Type 1 Diabetes
Show others...
2011 (English)In: PLoS ONE, ISSN 1932-6203, E-ISSN 1932-6203, Vol. 6, no 12Article in journal (Refereed) Published
Abstract [en]

A phase II clinical trial with glutamic acid decarboxylase (GAD) 65 formulated with aluminium hydroxide (GAD-alum) has shown efficacy in preserving residual insulin secretion in children and adolescents with recent-onset type 1 diabetes (T1D). We have performed a 4-year follow-up study of 59 of the original 70 patients to investigate long-term cellular and humoral immune responses after GAD-alum-treatment. Peripheral blood mononuclear cells (PBMC) were stimulated in vitro with GAD(65). Frequencies of naive, central and effector memory CD4+ and CD8+ T cells were measured, together with cytokine secretion, proliferation, gene expression and serum GAD(65) autoantibody (GADA) levels. We here show that GAD-alum-treated patients display increased memory T-cell frequencies and prompt T-cell activation upon in vitro stimulation with GAD(65), but not with control antigens, compared with placebo subjects. GAD(65)-induced T-cell activation was accompanied by secretion of T helper (Th) 1, Th2 and T regulatory cytokines and by induction of T-cell inhibitory pathways. Moreover, post-treatment serum GADA titres remained persistently increased in the GAD-alum arm, but did not inhibit GAD(65) enzymatic activity. In conclusion, memory T- and B-cell responses persist 4 years after GAD-alum-treatment. In parallel to a GAD(65)-induced T-cell activation, our results show induction of T-cell inhibitory pathways important for regulating the GAD(65) immunity.

Place, publisher, year, edition, pages
Public Library of Science, 2011
National Category
Medical and Health Sciences
Identifiers
urn:nbn:se:liu:diva-74156 (URN)10.1371/journal.pone.0029008 (DOI)000298366600057 ()
Note
Funding Agencies|Swedish Research Council|K2008-55x-20652-01-3|Swedish Child Diabetes Foundation (Barndiabetesfonden)||Medical Research Council of Southeast Sweden||Juvenile Diabetes Research Foundation (JDRF)|1-2008-106|Ile-de-France CODDIM||Inserm Avenir Program||Available from: 2012-01-20 Created: 2012-01-20 Last updated: 2017-12-08
Casas, R., Hjorth, M., Axelsson, S., Chéramy, M., Pihl, M. & Ludvigsson, J. (2009). Specific immunomodulatory effect of GAD(65) in type 1 diabetics. In: in DIABETOLOGIA, vol 52 (pp. S194-S194). , 52
Open this publication in new window or tab >>Specific immunomodulatory effect of GAD(65) in type 1 diabetics
Show others...
2009 (English)In: in DIABETOLOGIA, vol 52, 2009, Vol. 52, p. S194-S194Conference paper, Published paper (Refereed)
Abstract [en]

n/a

National Category
Medical and Health Sciences
Identifiers
urn:nbn:se:liu:diva-20610 (URN)
Available from: 2009-09-16 Created: 2009-09-15 Last updated: 2009-09-16
Organisations

Search in DiVA

Show all publications