The prolonged and enhanced immune response in the non-obese diabetic mouse is dependent on genes in the Idd1/24, Idd12 and Idd18 regions

Sundström, Mia; Lejon, Kristina

doi:10.1016/j.jaut.2010.08.002

Cited by 5 publications

(8 citation statements)

References 44 publications

(34 reference statements)

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“…C1/Idd22 congenic mice, we confirmed our previous report that the TACI up‐regulation in NOD is linked to chromosome 1 and 8 (containing Idd5.1‐Idd5.4 and Idd22 , respectively), i.e. the TACI trait is not linked to the same genetic regions as the immune response trait . However, based on the fact that the immune response trait was assayed 21 days after immunization, versus the recent report that TACI is involved in the generation of long‐lived plasma cells (i.e.…”

Section: Discussionsupporting

confidence: 88%

“…As mentioned above, the increased TACI expression in the NOD mouse could contribute to a B-cell compartment that is prone to plasma cell differentiation and isotype switch. Indeed, we and others have reported that NOD mice display enhanced and prolonged immune responses [19][20][21] and genetic analysis of this trait revealed linkage to Idd1/24, Idd12 and Idd18.1 as well as chromosome 2. In this study, using NOD.C1/Idd22 congenic mice, we confirmed our previous report that the TACI up-regulation in NOD is linked to chromosome 1 and 8 (containing Idd5.1-Idd5.4 and Idd22, respectively), i.e.…”

Section: Discussionmentioning

confidence: 99%

“…It is also known that NOD B cells are naturally activated and secrete IgM and IgG of low avidity and broad specificity, with a V H gene usage typical for autoantibodies . Moreover, NOD mice exhibit various B‐cell‐related immune deviations when compared with non‐autoimmune‐disease‐prone mouse strains such as disordered V H gene utilization pattern, prolonged and enhanced immune responses and exaggerated immunoglobulin‐complex binding …”

Section: Introductionmentioning

confidence: 99%

“…15,16 Moreover, NOD mice exhibit various B-cell-related immune deviations when compared with non-autoimmune-disease-prone mouse strains such as disordered V H gene utilization pattern, prolonged and enhanced immune responses and exaggerated immunoglobulin-complex binding. [17][18][19][20][21][22] The transmembrane activator, calcium modulator and cyclophilin ligand interactor (TACI) is a receptor expressed on B cells and has regulatory effects on mouse B-cell development. TACI À/À mice display signs of autoimmunity with increased numbers of circulating and splenic B cells, increased B-cell proliferation and massive infiltration of lymphocytes in liver and kidney, indicating that TACI is an inhibitory receptor downregulating B-cell activation and expansion.…”

Section: Introductionmentioning

confidence: 99%

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Increased expression of TACI on NOD B cells results in germinal centre reaction anomalies, enhanced plasma cell differentiation and immunoglobulin production

et al. 2016

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B cells have an important pathogenic role in the development of type 1 diabetes in the non-obese diabetic (NOD) mouse. We have previously reported that NOD mice display an increased percentage of TACI -expressing B cells compared with C57BL/6 mice and this trait is linked to chromosomes 1 and 8. In this paper the genetic association of the transmembrane activator, calcium modulator and cyclophilin ligand interactor (TACI) trait was confirmed using double congenic NOD.B6C1/Idd22 mice. TACI ligation by a proliferation-inducing ligand (APRIL) has been shown to influence plasma cell differentiation, immunoglobulin production and isotype switch. Hence, the functional consequence of the up-regulation of TACI on NOD B cells was analysed both in vitro and in vivo. NOD B cells stimulated with APRIL showed an enhanced plasma cell differentiation and class switch to IgG and IgA compared with B cells from C57BL/6 mice. Moreover, flow cytometry analyses revealed that germinal centre B cells in NOD failed to down-regulate TACI. Availability of the TACI ligand B-cell activating factor (BAFF) has been shown to be a limiting factor in the germinal centre reaction. In line with this, upon immunization with 4-hydroxy-3-nitrophenylacetyl hapten-conjugated hen egg lysozyme, NOD mice produced higher titres of low-affinity antibodies compared with C57BL/6 mice. This observation was supported by the detection of increased levels of BAFF in NOD germinal centres after immunization compared with C57BL/6 by immunofluorescence. Our results support the hypothesis that increased TACI expression on NOD B cells contributes to the pathogenesis of type 1 diabetes in the NOD mouse.

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Section: Discussionsupporting

confidence: 88%

Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Increased expression of TACI on NOD B cells results in germinal centre reaction anomalies, enhanced plasma cell differentiation and immunoglobulin production

et al. 2016

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“…It has been demonstrated that B cells in the NOD are aberrant as to anomalies in natural antibody production, antigen presentation, immune response patterns and surface accumulation of immunoglobulins [9][10][11][19][20][21][22]. As in humans, anti-CD20 treatment in prediabetic NOD mice protects them from disease development [23].…”

Section: Introductionmentioning

confidence: 99%

Contribution of autoallergy to the pathogenesis in the NOD mice

et al. 2015

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The immunoglobulin isotype IgE is commonly associated with allergy. However, its involvement in autoimmune disease in general, and Type 1 diabetes (T1D) in particular, is still not completely clarified, nonetheless IgE has been observed in patients with T1D. In this article, we aimed to elucidate the contribution of IgE in the pathogenesis of the disease in a spontaneous model for T1D, i.e. the NOD mouse. We observed increased levels of IgE in splenic, lymph node and peripheral blood B cells in the NOD mice compared to the control C57BL/6 (B6) mice. No correlation was found between the IgE levels on B cells and those in the sera of these mice, indicating a B cell intrinsic property mediating IgE capture in NOD. Functionally, the B cells from NOD were similar to B6 in rescuing the IgE-mediated immune response via the low affinity receptor CD23 in a transgenic adoptive transfer system. However, the involvement of IgE in diabetes development was clearly demonstrated, as treatment with anti-IgE antibodies delayed the incidence of the diabetes in the NOD mice compared to the PBS treated group. Pancreas sections from a 13-week-old NOD revealed the presence of tertiary lymphoid structures with T cells, B cells, germinal centers and IgE suggesting the presence of autoantigen specific IgE. Our study provides an insight to the commonly overlooked immunoglobulin IgE and its potential role in autoimmunity.

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Autoimmunity in 2010

Selmi

2011

Autoimmunity Reviews

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The prolonged and enhanced immune response in the non-obese diabetic mouse is dependent on genes in the Idd1/24, Idd12 and Idd18 regions

Cited by 5 publications

References 44 publications

Increased expression of TACI on NOD B cells results in germinal centre reaction anomalies, enhanced plasma cell differentiation and immunoglobulin production

Increased expression of TACI on NOD B cells results in germinal centre reaction anomalies, enhanced plasma cell differentiation and immunoglobulin production

Contribution of autoallergy to the pathogenesis in the NOD mice

Autoimmunity in 2010

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