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Hjorth, Maria
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Boij, R., Mjosberg, J., Svensson Arvelund, J., Hjorth, M., Berg, G., Matthiesen, L., . . . Ernerudh, J. (2015). Regulatory T-cell Subpopulations in Severe or Early-onset Preeclampsia. American Journal of Reproductive Immunology, 74(4), 368-378
Öppna denna publikation i ny flik eller fönster >>Regulatory T-cell Subpopulations in Severe or Early-onset Preeclampsia
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2015 (Engelska)Ingår i: American Journal of Reproductive Immunology, ISSN 1046-7408, E-ISSN 1600-0897, Vol. 74, nr 4, s. 368-378Artikel i tidskrift (Refereegranskat) Published
Abstract [en]

Problem A deficiency in regulatory T (Treg) cells causing reduced immune regulatory capacity has been proposed in preeclampsia. Objective Utilizing recent advances in flow cytometry phenotyping, we aimed to assess whether a deficiency of Treg subpopulations occurs in preeclampsia. Method of study Six-color flow cytometry was used for Treg phenotyping in 18 preeclamptic women (one early-onset, one severe and 16 both), 20 women with normal pregnancy, and 20 non-pregnant controls. Results No differences were found in major Treg populations including CD127(low)CD25(+)/CD127(ow)FOXP3(+), resting (FOXP3(dim)CD45RA(+)), and activated (FOXP3(bright)CD45RA(-)) Treg cells, whereas preeclamptic women showed increased CTLA-4(+) and CCR4(+) proportions within resting/activated Treg populations. Corticosteroid treatment prior to blood sampling (n = 10) affected the distribution of Treg populations. Conclusions Although we found no major alterations in circulating Treg frequencies, differences in CTLA-4(+) and CCR4(+) frequencies suggest a migratory defect of Treg cells in preeclampsia. Corticosteroid treatment should be taken into account when evaluating Treg cells.

Ort, förlag, år, upplaga, sidor
WILEY-BLACKWELL, 2015
Nyckelord
Early-onset preeclampsia; preeclampsia; pregnancy; regulatory T cells
Nationell ämneskategori
Reproduktionsmedicin och gynekologi
Identifikatorer
urn:nbn:se:liu:diva-122528 (URN)10.1111/aji.12410 (DOI)000362664200009 ()26118401 (PubMedID)
Anmärkning

Funding Agencies|FORSS (Medical Research Council of Southeast Sweden); Futurum, academy for Health and Care Jonkoping County Council, Sweden

Tillgänglig från: 2015-11-09 Skapad: 2015-11-06 Senast uppdaterad: 2017-12-01
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
Öppna denna publikation i ny flik eller fönster >>Regulatory T cell phenotype and function 4 years after GAD–alum treatment in children with type 1 diabetes
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2013 (Engelska)Ingår i: Clinical and Experimental Immunology, ISSN 0009-9104, E-ISSN 1365-2249, Vol. 172, nr 3, s. 394-402Artikel i tidskrift (Refereegranskat) 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.

Ort, förlag, år, upplaga, sidor
Wiley-Blackwell, 2013
Nyckelord
CD4 T cells (T helper, Th0, Th1, Th2, Th3, Th17), diabetes, immune regulation, regulatory T cells (Treg), therapy/immunotherapy
Nationell ämneskategori
Medicin och hälsovetenskap
Identifikatorer
urn:nbn:se:liu:diva-93379 (URN)10.1111/cei.12078 (DOI)000318073000004 ()
Anmärkning

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||

Tillgänglig från: 2013-05-31 Skapad: 2013-05-31 Senast uppdaterad: 2017-12-06Bibliografiskt granskad
Axelsson, S., Hjorth, M., Ludvigsson, J. & Casas, R. (2012). Decreased GAD(65) -specific Th1/Tc1 phenotype in children with Type 1 diabetes treated with GAD-alum.. Diabetic Medicine, 29(10), 1272-1278
Öppna denna publikation i ny flik eller fönster >>Decreased GAD(65) -specific Th1/Tc1 phenotype in children with Type 1 diabetes treated with GAD-alum.
2012 (Engelska)Ingår i: Diabetic Medicine, ISSN 0742-3071, E-ISSN 1464-5491, Vol. 29, nr 10, s. 1272-1278Artikel i tidskrift (Refereegranskat) Published
Abstract [en]

Aim  The balance between T helper cell subsets is an important regulator of the immune system and is often examined after immune therapies. We aimed to study the immunomodulatory effect of glutamic acid decarboxylase (GAD) 65 formulated with aluminium hydroxide (GAD-alum) in children with Type 1 diabetes, focusing on chemokines and their receptors. Methods  Blood samples were collected from 70 children with Type 1 diabetes included in a phase II clinical trial with GAD-alum. Expression of CC chemokine receptor 5 (CCR5) and CCR4 was analysed on CD4+ and CD8+ lymphocytes after in vitro stimulation with GAD(65) using flow cytometry, and secretion of the chemokines CCL2, CCL3 and CCL4 was detected in peripheral blood mononuclear cell supernatants with Luminex. Results  Expression of Th1-associated CCR5 was down-regulated following antigen challenge, together with an increased CCR4/CCR5 ratio and CCL2 secretion in GAD-alum-treated patients, but not in the placebo group. Conclusion  Our results suggest that GAD-alum treatment has induced a favourable immune modulation associated with decreased Th1/Tc1 phenotypes upon antigen re-challenge, which may be of importance for regulating GAD(65) immunity. © 2012 The Authors. Diabetic Medicine © 2012 Diabetes UK.

Ort, förlag, år, upplaga, sidor
Wiley-Blackwell, 2012
Nyckelord
Type 1 diabetes, GAD(65), immunomodulation, chemokines, chemokine receptors
Nationell ämneskategori
Medicin och hälsovetenskap
Identifikatorer
urn:nbn:se:liu:diva-77745 (URN)10.1111/j.1464-5491.2012.03710.x (DOI)000308960400014 ()22587593 (PubMedID)
Anmärkning

funding agencies|Swedish Research Council|K2008-55x-20652-01-3|Swedish Child Diabetes Foundation (Barndiabetesfonden) Diamyd Medical||Medical Research Council of Southeast Sweden||

Tillgänglig från: 2012-05-28 Skapad: 2012-05-28 Senast uppdaterad: 2017-12-07
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
Öppna denna publikation i ny flik eller fönster >>Extended evaluation of the safety and efficacy of GAD treatment of children and adolescents with recent-onset type 1 diabetes: a randomised controlled trial
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2011 (Engelska)Ingår i: DIABETOLOGIA, ISSN 0012-186X, Vol. 54, nr 3, s. 634-640Artikel i tidskrift (Refereegranskat) 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.

Ort, förlag, år, upplaga, sidor
Springer Science Business Media, 2011
Nyckelord
C-peptide, Children, GAD-alum treatment, Immune modulation, Type 1 diabetes
Nationell ämneskategori
Medicin och hälsovetenskap
Identifikatorer
urn:nbn:se:liu:diva-66310 (URN)10.1007/s00125-010-1988-1 (DOI)000286987000021 ()
Anmärkning
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/ Tillgänglig från: 2011-03-11 Skapad: 2011-03-11 Senast uppdaterad: 2011-03-24
Hjorth, M., Axelsson, S., Ryden, A., Faresjo, M., Ludvigsson, J. & Casas, R. (2011). GAD-alum treatment induces GAD(65)-specific CD4(+)CD25(high)FOXP3(+) cells in type 1 diabetic patients. CLINICAL IMMUNOLOGY, 138(1), 117-126
Öppna denna publikation i ny flik eller fönster >>GAD-alum treatment induces GAD(65)-specific CD4(+)CD25(high)FOXP3(+) cells in type 1 diabetic patients
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2011 (Engelska)Ingår i: CLINICAL IMMUNOLOGY, ISSN 1521-6616, Vol. 138, nr 1, s. 117-126Artikel i tidskrift (Refereegranskat) Published
Abstract [en]

Type 1 diabetes results from autoimmune destruction of insulin producing pancreatic beta-cells. We have shown that treatment with alum-formulated glutamic acid decarboxylase 65 (GAD-alum) preserved residual insulin secretion and induced antigen-specific responses in children with recent onset type 1 diabetes. The aim of this study was to further investigate the immunomodulatory effect of GAD-alum, focusing on CD4(+)CD25(high) cells and their association to cytokine secretion. Samples obtained 21 and 30 months after the initial injection of GAD-alum or placebo were included in the present study. GAD(65)-stimulation enhanced the percentage of CD4(+)CD25(high)FOXP3(+) cells, but reduced the percentage of CD4(+)CD25(+) cells, in samples from the GAD-alum treated group. Further, the GAD(65)-induced secretion of IL-5, -10, and -13 correlated with the expression of CD4(+)CD25(high)FOXP3(+) cells, but inversely with CD4(+)CD25(+) cells. These new data suggest that GAD-alum treatment induced GAD(65)-specific T cells with regulatory features.

Ort, förlag, år, upplaga, sidor
Elsevier Science B.V., Amsterdam, 2011
Nyckelord
Type 1 diabetes, Immunotherapy, GAD(65), Antigen-specific cell, FOXP3, Cytokine
Nationell ämneskategori
Medicin och hälsovetenskap
Identifikatorer
urn:nbn:se:liu:diva-65953 (URN)10.1016/j.clim.2010.10.004 (DOI)000286714000015 ()
Tillgänglig från: 2011-02-28 Skapad: 2011-02-28 Senast uppdaterad: 2011-02-28
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)
Öppna denna publikation i ny flik eller fönster >>Long-Lasting Immune Responses 4 Years after GAD-Alum Treatment in Children with Type 1 Diabetes
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2011 (Engelska)Ingår i: PLoS ONE, ISSN 1932-6203, E-ISSN 1932-6203, Vol. 6, nr 12Artikel i tidskrift (Refereegranskat) 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.

Ort, förlag, år, upplaga, sidor
Public Library of Science, 2011
Nationell ämneskategori
Medicin och hälsovetenskap
Identifikatorer
urn:nbn:se:liu:diva-74156 (URN)10.1371/journal.pone.0029008 (DOI)000298366600057 ()
Anmärkning
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||Tillgänglig från: 2012-01-20 Skapad: 2012-01-20 Senast uppdaterad: 2017-12-08
Axelsson, S., Hjorth, M., Åkerman, L., Ludvigsson, J. & Casas, R. (2010). Early induction of GAD(65)-reactive Th2 response in type 1 diabetic children treated with alum-formulated GAD(65). Diabetes/Metabolism Research Reviews, 26(7), 559-568
Öppna denna publikation i ny flik eller fönster >>Early induction of GAD(65)-reactive Th2 response in type 1 diabetic children treated with alum-formulated GAD(65)
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2010 (Engelska)Ingår i: Diabetes/Metabolism Research Reviews, ISSN 1520-7552, E-ISSN 1520-7560, Vol. 26, nr 7, s. 559-568Artikel i tidskrift (Refereegranskat) Published
Abstract [en]

Background We have previously shown that two injections of 20 mu g alum-formulated glutamic acid decarboxylase 65 (GAD(65)) (GAD-alum; Diamyd (R)) in children with recent-onset type 1 diabetes lead to preservation of residual insulin secretion. In vitro cytokine production at the 15 months follow-up indicated immunomodulation. In the present study, we took advantage of peripheral blood mononuclear cells, cryopreserved during early follow-ups, to investigate whether the immunomodulatory effect of GAD-alum was apparent earlier after treatment, preceding the changes previously reported at 15 months.<p>Methods Peripheral blood mononuclear cells from 70 type 1 diabetic children, randomly assigned GAD-alum (n = 35) or placebo (n = 35), that had been frozen at baseline (n = 27) and after 1 (n = 58), 3 (n = 67) and 9 (n = 66) months, were stimulated in vitro with GAD(65), tyrosine phosphatase-like protein IA-2 peptide, insulin peptide, GAD-alum, alum formulation or phytohaemagglutinin. Interleukin (IL)-5, -6, -10, -12, -13, -17, tumour necrosis factor and interferon-gamma were measured in cell supernatants and serum samples using Luminex. Expression of FOXP3 and transforming growth factor-beta was determined by real-time reverse transcription polymerase chain reaction.</p><p>Results Already 1 month after the first injection, GAD(65)-induced IL-5 and IL-13 together with FOXP3 were enhanced in GAD-alum-treated patients compared to those with placebo. The in vitro response at 3 and 9 months was characterized by a broader range of cytokines in the treated group. Notably, only the T-helper 2-associated cytokines IL-5 and IL-13 together with FOXP3 increased continuously over time.</p><p>Conclusions Treatment with GAD-alum in type 1 diabetic children induced an early T-helper 2 immune enhanced response to GAD(65), followed by a wider spectrum of cytokines at 3 and 9 months. Copyright (C) 2010 John Wiley &amp; Sons, Ltd.</p>

Ort, förlag, år, upplaga, sidor
John Wiley and Sons, 2010
Nyckelord
GAD65, Immunotherapy, Th1/Th2 Immune Response, Immunomodulation, Cytokines
Nationell ämneskategori
Medicin och hälsovetenskap
Identifikatorer
urn:nbn:se:liu:diva-52141 (URN)10.1002/dmrr.1126 (DOI)000283399000007 ()
Tillgänglig från: 2009-12-07 Skapad: 2009-12-07 Senast uppdaterad: 2017-12-12
Hjorth, M. (2010). Immunological profile and aspects of immunotherapy in type 1 diabetes. (Doctoral dissertation). Linköping: Linköping University Electronic Press
Öppna denna publikation i ny flik eller fönster >>Immunological profile and aspects of immunotherapy in type 1 diabetes
2010 (Engelska)Doktorsavhandling, sammanläggning (Övrigt vetenskapligt)
Abstract [en]

Type 1 diabetes (T1D) is a chronic, autoimmune disease caused by a T cell mediated attack on the insulin producing pancreatic ß-cells. Even though reasonable quality of life can be acquired with modern insulin therapy, prevention of acute and late serious complications is facilitated by preservation of residual insulin secretion. Preventing β-cell destruction is therefore an important goal of T1D therapy. Characterisation of immunological changes in the course of T1D is essential for understanding the underlying pathogenic mechanisms and for evaluating the efficacy of therapeutic intervention.

 

This thesis aimed to study the immune profile in individuals at increased risk of T1D and in patients diagnosed with the disease. In addition, the immunological effects of treatment with the B vitamin, Nicotinamide, and by antigen-specific immunotherapy using GAD65, have been studied in high-risk individuals and in T1D patients, respectively.

We have found that individuals at high risk of T1D had an increased T helper (Th) 1 like immune profile, defined by high secretion of interferon (IFN) -γ. At the time of clinical onset of T1D, the Th1 dominance was diminished. We further demonstrate that children with newly diagnosed T1D had a suppressed Th1 like profile, detected by chemokine and chemokine receptor profile. This was accompanied by an induced population of CCR7+ and CD45RA+ naïve, CD8+cytotoxic T (Tc) cells and a reduced CD45RO+ memory Tc cell pool.

 

It has previously been shown that oral Nicotinamide had no clinical effect in prevention of T1D. However, we found that the treatment was associated with a decreased secretion of IFN-γ. We have previously shown that subcutaneous injections with GAD-alum in T1D children induced a better preservation of endogenous insulin secretion compared with placebo. Here, we demonstrate that the treatment induced an early antigen-specific Th2 and regulatory immune profile. After a few months, and still after more than two years, the recall response to GAD65 was characterised by a broader range of cytokines. GAD-alum treatment also induced a GAD65-specific CD4+CD25highFOXP3+ cell population and reduced the levels of CD4+CD25+ cells.

 

In conclusion, a Th1 like immune profile in pre-diabetic individuals indicates an imbalance of the immune system. At time of clinical onset, and in the period afterwards, reduction of the Th1 associated immune response could be an effect of a suppressed destructive process, selective recruitment of effector T cells to the pancreas or a defective immune regulation. The protective effect of GAD-alum in T1D children seems to be mediated by an early skewing of GAD65-induced responses towards a Th2 phenotype. Further, induction of GAD65-specific T cells with regulatory characteristics might be able to suppress autoreactive responses and inflammation in the pancreas.

Ort, förlag, år, upplaga, sidor
Linköping: Linköping University Electronic Press, 2010. s. 82
Serie
Linköping University Medical Dissertations, ISSN 0345-0082 ; 1161
Nationell ämneskategori
Immunologi
Identifikatorer
urn:nbn:se:liu:diva-52139 (URN)978-91-7393-467-1 (ISBN)
Disputation
2010-01-14, Berzeliussalen, Hälsouniversitetet, Campus US, Linköpings universitet, Linköping, 09:00 (Svenska)
Opponent
Handledare
Tillgänglig från: 2010-01-24 Skapad: 2009-12-07 Senast uppdaterad: 2010-01-25Bibliografiskt granskad
Hjorth, M., Axelsson, S., Ludvigsson, J. & Casas, R. (2009). GAD-alum treatment induces GAD-specific FOXP3+ cells in type 1 diabetic children. In: in DIABETOLOGIA, vol 52 (pp. S193-S193). , 52
Öppna denna publikation i ny flik eller fönster >>GAD-alum treatment induces GAD-specific FOXP3+ cells in type 1 diabetic children
2009 (Engelska)Ingår i: in DIABETOLOGIA, vol 52, 2009, Vol. 52, s. S193-S193Konferensbidrag, Publicerat paper (Refereegranskat)
Abstract [en]

n/a

Nationell ämneskategori
Medicin och hälsovetenskap
Identifikatorer
urn:nbn:se:liu:diva-20609 (URN)
Tillgänglig från: 2009-09-16 Skapad: 2009-09-15 Senast uppdaterad: 2009-09-16
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
Öppna denna publikation i ny flik eller fönster >>Specific immunomodulatory effect of GAD(65) in type 1 diabetics
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2009 (Engelska)Ingår i: in DIABETOLOGIA, vol 52, 2009, Vol. 52, s. S194-S194Konferensbidrag, Publicerat paper (Refereegranskat)
Abstract [en]

n/a

Nationell ämneskategori
Medicin och hälsovetenskap
Identifikatorer
urn:nbn:se:liu:diva-20610 (URN)
Tillgänglig från: 2009-09-16 Skapad: 2009-09-15 Senast uppdaterad: 2009-09-16
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