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Lejon, Kristina
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Publications (10 of 47) Show all publications
Kindstedt, E., Holm, C. K., Palmqvist, P., Sjöström, M., Lejon, K. & Lundberg, P. (2019). Innate lymphoid cells are present in gingivitis and periodontitis. Journal of Periodontology, 90(2), 200-207
Open this publication in new window or tab >>Innate lymphoid cells are present in gingivitis and periodontitis
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2019 (English)In: Journal of Periodontology, ISSN 0022-3492, E-ISSN 1943-3670, Vol. 90, no 2, p. 200-207Article in journal (Refereed) Published
Abstract [en]

BACKGROUND: Innate lymphoid cells (ILCs) are the most recently identified leukocytes of the immune system and these cells are increasingly acknowledged to play important roles in host defence and tissue repair. ILCs are also contributors of inflammatory diseases such as asthma and colitis. We analyzed the presence and relative proportions of the different ILC subsets (ILC1, ILC2 and ILC3) in gingivitis and periodontitis. Further, we investigated if ILCs express receptor activator of nuclear factor kappa-B ligand (RANKL), a cytokine crucial for osteoclast differentiation and bone resorption.

METHODS: We collected gingivitis and periodontitis soft tissue and characterized ILC subsets including RANKL expression in single-cell suspensions using flow cytometry.

RESULTS: ILCs were detected both in gingivitis and periodontitis. The majority of ILCs, in both conditions, were ILC1s. Furthermore, RANKL expression was detected on a fraction of the ILC1s.

CONCLUSIONS: Our discovery of the presence of ILCs both in gingivitis and periodontitis and concomitant expression of RANKL on a fraction of the ILC1 population suggest that these cells may be of importance in periodontal disease. In addition, our findings provide a new insight into the field of oral immunology.

Place, publisher, year, edition, pages
Wiley-Blackwell, 2019
Keywords
RANK ligand, gingivitis, innate immunity, periodontitis
National Category
Medical and Health Sciences Immunology Dentistry
Identifiers
urn:nbn:se:umu:diva-151758 (URN)10.1002/JPER.17-0750 (DOI)000457129200011 ()30070705 (PubMedID)
Funder
Swedish Rheumatism AssociationVästerbotten County Council
Available from: 2018-09-13 Created: 2018-09-13 Last updated: 2019-02-12Bibliographically approved
Wahlin, B., Fasth, A. E., Karp, K., Lejon, K., Södergren, A. & Wållberg-Jonsson, S. (2017). Cd8+cd28- t-lymphocytes are associated with subclinical atherosclerosis in patients with rheumatoid arthritis. Paper presented at Annual European Congress of Rheumatology, JUN 14-17, 2017, Madrid, SPAIN. Annals of the Rheumatic Diseases, 76, 250-250
Open this publication in new window or tab >>Cd8+cd28- t-lymphocytes are associated with subclinical atherosclerosis in patients with rheumatoid arthritis
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2017 (English)In: Annals of the Rheumatic Diseases, ISSN 0003-4967, E-ISSN 1468-2060, Vol. 76, p. 250-250Article in journal, Meeting abstract (Other academic) Published
Place, publisher, year, edition, pages
BMJ PUBLISHING GROUP, 2017
National Category
Rheumatology and Autoimmunity
Identifiers
urn:nbn:se:umu:diva-142290 (URN)10.1136/annrheumdis-2017-eular.4364 (DOI)000413181400665 ()
Conference
Annual European Congress of Rheumatology, JUN 14-17, 2017, Madrid, SPAIN
Available from: 2017-11-29 Created: 2017-11-29 Last updated: 2018-06-09Bibliographically approved
Banday, V. S., Thyagarajan, R. & Lejon, K. (2017). Contribution of both B cell intrinsic alterations as well as non-hematopoietic derived factors in the enhanced immune response of the NOD mouse. Paper presented at 44th Annual Meeting of the Scandinavian-Society-for-Immunology (SSI), OCT 17-20, 2017, Stockholm, SWEDEN. Scandinavian Journal of Immunology, 86(4), 252-252
Open this publication in new window or tab >>Contribution of both B cell intrinsic alterations as well as non-hematopoietic derived factors in the enhanced immune response of the NOD mouse
2017 (English)In: Scandinavian Journal of Immunology, ISSN 0300-9475, E-ISSN 1365-3083, Vol. 86, no 4, p. 252-252Article in journal, Meeting abstract (Other academic) Published
Place, publisher, year, edition, pages
WILEY, 2017
National Category
Immunology
Identifiers
urn:nbn:se:umu:diva-140890 (URN)10.1111/sji.12587 (DOI)000411865200015 ()
Conference
44th Annual Meeting of the Scandinavian-Society-for-Immunology (SSI), OCT 17-20, 2017, Stockholm, SWEDEN
Note

Meeting Abstract: A-31163

Available from: 2017-11-21 Created: 2017-11-21 Last updated: 2018-06-09Bibliographically approved
Banday, V. S., Thyagarajan, R. & Lejon, K. (2017). Contribution of both B-cell intrinsic alterations as well as non-hematopoietic-derived factors in the enhanced immune response of the NOD mouse. Autoimmunity, 50(6), 363-369
Open this publication in new window or tab >>Contribution of both B-cell intrinsic alterations as well as non-hematopoietic-derived factors in the enhanced immune response of the NOD mouse
2017 (English)In: Autoimmunity, ISSN 0891-6934, E-ISSN 1607-842X, Vol. 50, no 6, p. 363-369Article in journal (Refereed) Published
Abstract [en]

The underlying cellular and molecular mechanism for the development of Type 1 diabetes is still to be fully revealed. We have previously demonstrated that the NOD mouse, a model for Type 1 diabetes, display a prolonged and enhanced immune response to both self and non-self-antigens. The molecular explanation for this defect however, has not been determined. In this study we immunized NOD and C57BL/6 (B6) with the conventional antigen i.e. hen egg lysozyme (HEL) and analyzed B cell activation, germinal center reaction and antibody clearance. Corroborating our previous observations NOD mice responded robustly to a single immunization of HEL. Immunofluorescence analysis of the spleen revealed an increased number of germinal centers in unimmunized NOD compared to B6. However, post immunization germinal center numbers were similar in NOD and B6. NOD mice showed lower response to BCR stimulation with anti-IgM, in particular at lower concentrations of anti-IgM. Antibody clearance in vivo did not differ between the strains. To determine the cell type that is responsible for the prolonged and enhance immune response, we reconstituted NOD-RAGs with cells from primed donors in different combinations. NOD B cells were required to reproduce the phenotype; however the non-lymphoid compartment of NOD origin also played a role. Based on our results we propose that preexisting GCs in the NOD promote the robust response and alteration in the BCR signaling could promote survival of stimulated cells. Overall, this mechanism could in turn also contribute to the activation and maintenance of autoreactive B cells in the NOD mouse.

Place, publisher, year, edition, pages
TAYLOR & FRANCIS LTD, 2017
Keywords
Type 1 diabetes, immune response, NOD mouse, B lymphocytes, hen egg lysozyme
National Category
Immunology in the medical area
Identifiers
urn:nbn:se:umu:diva-140061 (URN)10.1080/08916934.2017.1344977 (DOI)000410935800004 ()28686488 (PubMedID)
Available from: 2017-09-29 Created: 2017-09-29 Last updated: 2018-06-09Bibliographically approved
Banday, V. S. & Lejon, K. (2017). Elevated Systemic Glutamic Acid Level in the Non-Obese Diabetic Mouse is Idd Linked and Induces Beta Cell Apoptosis. Immunology, 150(2), 162-171
Open this publication in new window or tab >>Elevated Systemic Glutamic Acid Level in the Non-Obese Diabetic Mouse is Idd Linked and Induces Beta Cell Apoptosis
2017 (English)In: Immunology, ISSN 0019-2805, E-ISSN 1365-2567, Vol. 150, no 2, p. 162-171Article in journal (Refereed) Published
Abstract [en]

Although type 1 diabetes (T1D) is a T-cell-mediated disease in the effector stage, the mechanism behind the initial beta cell assault is less understood. Metabolomic differences, including elevated levels of glutamic acid, have been observed in patients with T1D before disease onset, as well as in pre-diabetic non-obese diabetic (NOD) mice. Increased levels of glutamic acid damage both neurons and beta cells, implying that this could contribute to the initial events of T1D pathogenesis. We investigated the underlying genetic factors and consequences of the increased levels of glutamic acid in NOD mice. Serum glutamic acid levels from a (NODxB6) F-2 cohort (n = 182) were measured. By genome-wide and Idd region targeted microsatellite mapping, genetic association was detected for six regions including Idd2, Idd4 and Idd22. In silico analysis of potential enzymes and transporters located in and around the mapped regions that are involved in glutamic acid metabolism consisted of alanine aminotransferase, glutamic-oxaloacetic transaminase, aldehyde dehydrogenase 18 family, alutamyl-prolyl-tRNA synthetase, glutamic acid transporters GLAST and EAAC1. Increased EAAC1 protein expression was observed in lysates from livers of NOD mice compared with B6 mice. Functional consequence of the elevated glutamic acid level in NOD mice was tested by culturing NOD. Rag2(-/-) Langerhans' islets with glutamic acid. Induction of apoptosis of the islets was detected upon glutamic acid challenge using TUNEL assay. Our results support the notion that a dysregulated metabolome could contribute to the initiation of T1D. We suggest that targeting of the increased glutamic acid in pre-diabetic patients could be used as a potential therapy.

Keywords
beta cell apoptosis, genetics, glutamic acid, Idd, non-obese diabetic mice
National Category
Microbiology in the medical area
Identifiers
urn:nbn:se:umu:diva-119451 (URN)10.1111/imm.12674 (DOI)000394790400005 ()27649685 (PubMedID)
Available from: 2016-04-19 Created: 2016-04-19 Last updated: 2018-06-07Bibliographically approved
Lejon, K. (2017). Immunsystemets fina balansgång. Barndiabetesfondens tidskrift "Sticket", 3(3), 4-4
Open this publication in new window or tab >>Immunsystemets fina balansgång
2017 (Swedish)In: Barndiabetesfondens tidskrift "Sticket", ISSN 1400-8505, Vol. 3, no 3, p. 4-4Article, review/survey (Other (popular science, discussion, etc.)) Published
Place, publisher, year, edition, pages
Linköping: , 2017
Keywords
Barndiabetes, immunologi
National Category
Medical and Health Sciences
Research subject
Immunology
Identifiers
urn:nbn:se:umu:diva-141613 (URN)
Funder
Swedish Child Diabetes Foundation
Available from: 2017-11-09 Created: 2017-11-09 Last updated: 2018-06-09
Rasmuson, J., Pourazar, J., Mohamed, N., Lejon, K., Evander, M., Blomberg, A. & Ahlm, C. (2016). Cytotoxic immune responses in the lungs correlate to disease severity in patients with hantavirus infection. European Journal of Clinical Microbiology and Infectious Diseases, 35(4), 713-721
Open this publication in new window or tab >>Cytotoxic immune responses in the lungs correlate to disease severity in patients with hantavirus infection
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2016 (English)In: European Journal of Clinical Microbiology and Infectious Diseases, ISSN 0934-9723, E-ISSN 1435-4373, Vol. 35, no 4, p. 713-721Article in journal (Refereed) Published
Abstract [en]

Hantavirus infections may cause severe and sometime life-threatening lung failure. The pathogenesis is not fully known and there is an urgent need for effective treatment. We aimed to investigate the association between pulmonary viral load and immune responses, and their relation to disease severity. Bronchoscopy with sampling of bronchoalveolar lavage (BAL) fluid was performed in 17 patients with acute Puumala hantavirus infection and 16 healthy volunteers acting as controls. Lymphocyte subsets, granzyme concentrations, and viral load were determined by flow cytometry, enzyme-linked immunosorbent assay (ELISA), and quantitative reverse transcription polymerase chain reaction (RT-PCR), respectively. Analyses of BAL fluid revealed significantly higher numbers of activated CD8+ T cells and natural killer (NK) cells, as well as higher concentrations of the cytotoxins granzymes A and B in hantavirus-infected patients, compared to controls. In patients, Puumala hantavirus RNA was detected in 88 % of BAL cell samples and correlated inversely to the T cell response. The magnitude of the pulmonary cytotoxic lymphocyte response correlated to the severity of disease and systemic organ dysfunction, in terms of need for supplemental oxygen treatment, hypotension, and laboratory data indicating renal failure, cardiac dysfunction, vascular leakage, and cell damage. Regulatory T cell numbers were significantly lower in patients compared to controls, and may reflect inadequate immune regulation during hantavirus infection. Hantavirus infection elicits a pronounced cytotoxic lymphocyte response in the lungs. The magnitude of the immune response was associated with disease severity. These results give insights into the pathogenesis and possibilities for new treatments.

Keywords
hantavirus, hemorrhagic fever with renal syndrome, bronchoalveolar lavage, granzymes, viral load, cytotoxic T-lymphocytes, regulatory T-cells
National Category
Infectious Medicine
Research subject
Infectious Diseases
Identifiers
urn:nbn:se:umu:diva-99100 (URN)10.1007/s10096-016-2592-1 (DOI)000373300000023 ()26873376 (PubMedID)
Note

Originally included in thesis in manuscript form

Available from: 2015-02-04 Created: 2015-02-04 Last updated: 2018-09-17Bibliographically approved
Banday, V. S., Thyagarajan, R., Sundström, M. & Lejon, K. (2016). Increased expression of TACI on NOD B cells results in germinal centre reaction anomalies, enhanced plasma cell differentiation and immunoglobulin production. Immunology, 149(3), 297-305
Open this publication in new window or tab >>Increased expression of TACI on NOD B cells results in germinal centre reaction anomalies, enhanced plasma cell differentiation and immunoglobulin production
2016 (English)In: Immunology, ISSN 0019-2805, E-ISSN 1365-2567, Vol. 149, no 3, p. 297-305Article in journal (Refereed) Published
Abstract [en]

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 TACIhigh-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.

Keywords
affinity maturation, B cells, B-cell activating factor, non-obese diabetic mouse, transmembrane activat or, calcium modulator and cyclophilin ligand interactor
National Category
Microbiology in the medical area
Identifiers
urn:nbn:se:umu:diva-119452 (URN)10.1111/imm.12651 (DOI)000387360300005 ()27444337 (PubMedID)
Note

Originally published in thesis in manuscript form with the title: Increased expression of TACI in the NOD mouse results in enhanced plasma cell differentiation and immunoglobulin production

Available from: 2016-04-19 Created: 2016-04-19 Last updated: 2018-06-07Bibliographically approved
Thyagarajan, R., Banday, V., Ding, Z. & Lejon, K. (2015). Contribution of autoallergy to the pathogenesis in the NOD mice. Autoimmunity, 48(5), 298-304
Open this publication in new window or tab >>Contribution of autoallergy to the pathogenesis in the NOD mice
2015 (English)In: Autoimmunity, ISSN 0891-6934, E-ISSN 1607-842X, Vol. 48, no 5, p. 298-304Article in journal (Refereed) Published
Abstract [en]

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.

Keywords
Autoallergy, B lymphocytes, IgE, NOD mouse, Type 1 diabetes
National Category
Immunology in the medical area
Identifiers
urn:nbn:se:umu:diva-102419 (URN)10.3109/08916934.2015.1016220 (DOI)000359797600004 ()25707684 (PubMedID)
Available from: 2015-04-24 Created: 2015-04-24 Last updated: 2018-06-07Bibliographically approved
Kolan, S., Boman, A., Matozaki, T., Lejon, K. & Oldenborg, P.-A. (2015). Lack of non-hematopoietic SIRPα signaling disturbs the splenic marginal zone architecture resulting in accumulation and displacement of marginal zone B cells. Biochemical and Biophysical Research Communications - BBRC, 460(3), 645-650
Open this publication in new window or tab >>Lack of non-hematopoietic SIRPα signaling disturbs the splenic marginal zone architecture resulting in accumulation and displacement of marginal zone B cells
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2015 (English)In: Biochemical and Biophysical Research Communications - BBRC, ISSN 0006-291X, E-ISSN 1090-2104, Vol. 460, no 3, p. 645-650Article in journal (Refereed) Published
Abstract [en]

Signal regulatory protein α (SIRPα) is an immunoglobulin super family protein predominantly expressed by myeloid but not lymphoid cells, and its role in lymphocyte homeostasis and function is still to be revealed. We demonstrate that mice bearing a mutant SIRPα lacking the cytoplasmic signaling domain (SIRPα MT) had an increased amount of splenic marginal zone (MZ) B cells compared to wild-type controls. Immunohistochemical analysis revealed an increased localization of MZB cells into B cell follicular areas of the white pulp in SIRPα MT spleens. However, we found no signs of an increased MZB cell activation level in MT mice. The immune response to T-independent antigens in vivo was slightly increased in SIRPα MT mice while sorted MZB from these mice responded normally to LPS in vitro. Bone marrow reconstitution experiments demonstrated that the MZB cell phenotype of SIRPα MT mice was due to lack of SIRPα signaling in non-hematopoietic cells. In contrast, MZ retention of MZ macrophages required hematopoietic SIRPα, while normal distribution of metallophilic macrophages required non-hematopoietic SIRPα signaling. In summary, these data identified SIRPα signaling in non-hematopoietic cells to play an important role in regulating the numbers and positioning MZB cell in the spleen.

Keywords
Marginal zone B cells, Signal regulatory protein alpha, Marginal zone macrophages
National Category
Immunology in the medical area
Research subject
Immunology
Identifiers
urn:nbn:se:umu:diva-107627 (URN)10.1016/j.bbrc.2015.03.084 (DOI)000359885300026 ()
Available from: 2015-08-25 Created: 2015-08-25 Last updated: 2018-06-07Bibliographically approved
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