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Nordin Fredrikson, Gunilla
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Publications (10 of 54) Show all publications
Stanezai, S., Sahlén, E., El-Schich, Z., Fridberg, M., Nordin Fredrikson, G., Anagnostaki, L., . . . Wingren, A. G. (2016). Higher intensity of low molecular weight protein tyrosine phosphatase/ ACP-1 in survivors of patients diagnosed with diffuse large B cell lymphoma (DLBCL) compared to non-survivors (ed.). Austin Biology, 1(2), Article ID 1009.
Open this publication in new window or tab >>Higher intensity of low molecular weight protein tyrosine phosphatase/ ACP-1 in survivors of patients diagnosed with diffuse large B cell lymphoma (DLBCL) compared to non-survivors
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2016 (English)In: Austin Biology, Vol. 1, no 2, article id 1009Article in journal (Refereed) Published
Abstract [en]

Adult diffuse large B cell lymphoma (DLBCL) is a heterogeneous form of hematopoietic cancer and difficult to treat. In order to find a better diagnostic indication for the disease, we analyzed low molecular weight protein tyrosine phosphatase (LMWPTP) that in humans is encoded by the ACP1 gene. LMWPTP is an enzyme shown to counteract protein tyrosine kinases (PTK) and was suggested to be a negative growth factor regulator. However, the 18 kDa PTP can also have a positive effect on cell growth and proliferation, indicating a controversial role in the tumorigenic process. LMWPTP exists in different isoforms which are electrophoretically, kinetically and immunologically distinct. We have studied two subgroups of DLBCL consisting of a germinal center B cell like (GCB) and a non-germinal center B cell like (non-GCB) group. The two subgroups have been defined by gene-expressing profiling and are associated with differential outcome. The expression levels of LMWPTP protein was compared and showed significant differences between the GCB and non-GCB subgroups (p=0.012). Interestingly, when the samples were divided into survivors and non-survivors, and thereafter analyzed for LMWPTP expression, the samples from patients with a higher survival rate showed increased staining intensity, whereas the samples from patients with lower intensity of LMWPTP did not survive the disease (p=0.001). In conclusion, we have shown that DLBCL patients with worse outcome express LMWPTP with a lower intensity, suggesting a tumor suppressor role for this form of the enzyme.

Place, publisher, year, edition, pages
Austin Publishing, 2016
Keywords
ACP1, B-cell, DLBCL, germinal center, LMWPTP, lymphoma, non-germinal center, prognosis
National Category
Medical and Health Sciences
Identifiers
urn:nbn:se:mau:diva-14771 (URN)22058 (Local ID)22058 (Archive number)22058 (OAI)
Available from: 2020-03-30 Created: 2020-03-30 Last updated: 2023-06-16Bibliographically approved
Mantani, P. T., Duner, P., Bengtsson, E., Alm, R., Ljungcrantz, I., Söderberg, I., . . . Nordin Fredrikson, G. (2015). IL-25 Inhibits Atherosclerosis Development in Apolipoprotein E Deficient Mice (ed.). PLOS ONE, 10(1), Article ID e0117255.
Open this publication in new window or tab >>IL-25 Inhibits Atherosclerosis Development in Apolipoprotein E Deficient Mice
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2015 (English)In: PLOS ONE, E-ISSN 1932-6203, Vol. 10, no 1, article id e0117255Article in journal (Refereed)
Abstract [en]

Objective IL-25 has been implicated in the initiation of type 2 immunity and in the protection against autoimmune inflammatory diseases. Recent studies have identified the novel innate lymphoid type 2 cells (ILC2s) as an IL-25 target cell population. The purpose of this study was to evaluate if IL-25 has any influence on atherosclerosis development in mice. Methods and Results Administration of 1 mu g IL-25 per day for one week to atherosclerosis-prone apolipoprotein (apo) E deficient mice, had limited effect on the frequency of T cell populations, but resulted in a large expansion of ILC2s in the spleen. The expansion was accompanied by increased levels of anti-phosphorylcholine (PC) natural IgM antibodies in plasma and elevated levels of IL-5 in plasma and spleen. Transfer of ILC2s to apoE deficient mice elevated the natural antibody-producing B1a cell population in the spleen. Treatment of apoE/Rag-1 deficient mice with IL-25 was also associated with extensive expansion of splenic ILC2s and increased plasma IL-5, suggesting ILC2s to be the source of IL-5. Administration of IL-25 in IL-5 deficient mice resulted in an expanded ILC2 population, but did not stimulate generation of anti-PC IgM, indicating that IL-5 is not required for ILC2 expansion but for the downstream production of natural antibodies. Additionally, administration of 1 mu g IL-25 per day for 4 weeks in apoE deficient mice reduced atherosclerosis in the aorta both during initiation and progression of the disease. Conclusions The present findings demonstrate that IL-25 has a protective role in atherosclerosis mediated by innate responses, including ILC2 expansion, increased IL-5 secretion, B1a expansion and natural anti-PC IgM generation, rather than adaptive Th2 responses.

Place, publisher, year, edition, pages
Public Library of Science, 2015
Keywords
Spleen, Atherosclerosis, Cytokines, Flow cytometry, T-cells, Antibodies, Cell staining, Immune response
National Category
Medical and Health Sciences
Identifiers
urn:nbn:se:mau:diva-4949 (URN)10.1371/journal.pone.0117255 (DOI)000348732100076 ()25629516 (PubMedID)2-s2.0-84922121986 (Scopus ID)19806 (Local ID)19806 (Archive number)19806 (OAI)
Available from: 2020-02-28 Created: 2020-02-28 Last updated: 2024-02-05Bibliographically approved
Mantani, P. T., Ljungcrantz, I., Andersson, L., Alm, R., Hedblad, B., Björkbacka, H., . . . Nordin Fredrikson, G. (2014). Circulating CD40(+) and CD86(+) B Cell Subsets Demonstrate Opposing Associations With Risk of Stroke (ed.). Arteriosclerosis, Thrombosis and Vascular Biology, 34(1), 211-218
Open this publication in new window or tab >>Circulating CD40(+) and CD86(+) B Cell Subsets Demonstrate Opposing Associations With Risk of Stroke
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2014 (English)In: Arteriosclerosis, Thrombosis and Vascular Biology, ISSN 1079-5642, E-ISSN 1524-4636, Vol. 34, no 1, p. 211-218Article in journal (Refereed)
Abstract [en]

Objective-Accumulating evidence shows that immune cells play an important role in atherosclerosis. Most attention has focused on the role of different T cell subsets, whereas the possible involvement of B cells has been less studied. In this study, we assessed the association of 2 different B cell subsets, CD19(+)CD40(+) and CD19(+)CD86(+) B cells, with risk for development of acute cardiovascular events. Approach and Results-The prospective study included 700 subjects randomly selected from the cardiovascular cohort of the Malmo Diet and Cancer study. Mononuclear leukocytes, stored at -140 degrees C at the baseline investigation in 1991-1994, were thawed and B cell subsets analyzed by flow cytometry. Cytokine release from CD3/CD28-stimulated mononuclear leukocytes was measured with multiplex ELISA. Baseline carotid intima-media thickness and stenosis were assessed by ultrasonography, and clinical events were monitored through validated national registers during a median/mean follow-up time of 15 years. The subjects in the highest tertile of CD19(+)CD40(+) B cells had a significantly lower risk of incident stroke after adjustment for other risk factors. In contrast, CD19(+)CD86(+) B cells were associated with higher risk for development of a stroke event and increased release of proinflammatory cytokines from mononuclear leukocytes. Conclusions-These observations provide evidence for an involvement of B cells in the incidence of stroke and suggest that both pathogenic and protective B cell subsets exist.

Place, publisher, year, edition, pages
Lippincott Williams & Wilkins, 2014
Keywords
B-lymphocyte subsets, carotid artery diseases, prospective studies, stroke
National Category
Medical and Health Sciences
Identifiers
urn:nbn:se:mau:diva-5594 (URN)10.1161/ATVBAHA.113.302667 (DOI)000337731100028 ()24202305 (PubMedID)2-s2.0-84891801932 (Scopus ID)27417 (Local ID)27417 (Archive number)27417 (OAI)
Available from: 2020-02-28 Created: 2020-02-28 Last updated: 2024-02-05Bibliographically approved
Pendleton, H., Alm, R., Nordin Fredrikson, G. & Ohlsson, B. (2013). Antibodies Against Gonadotropin-Releasing Hormone in Patients with Posterior Laryngitis (ed.). Drug Target Insights (7), 1-8
Open this publication in new window or tab >>Antibodies Against Gonadotropin-Releasing Hormone in Patients with Posterior Laryngitis
2013 (English)In: Drug Target Insights, E-ISSN 1177-3928, no 7, p. 1-8Article in journal (Refereed) Published
Abstract [en]

Patients with functional gastrointestinal disorders express antibodies against gonadotropin-releasing hormone (GnRH) in serum. One common cause of posterior laryngitis (PL) is extra-esophageal reflux, but a functional etiology has also been suggested. The aim of this study was to scrutinize patients with PL with regard to the presence of GnRH antibodies and to examine the association between antibodies and symptoms and reflux. Consecutive PL patients were included after examination. Serum was analyzed for the presence of antibodies using an enzyme-linked immunosorbent assay (ELISA) method and expressed as relative units (RU). Two age- and gender-matched healthy subjects per case served as controls. The prevalence of IgM GnRH antibodies in patients was 35% compared with 28% in controls (P = 0.06), with higher levels in patients (0.8 (0.3-2.2) RU) than in controls (0.2 (0.1-0.6) RU) (P = 0.007). The corresponding IgG antibody prevalences were 43% and 4%, respectively (P = 0.001), with no difference in levels (P = 0.70). There was no association between antibodies and clinical findings

Place, publisher, year, edition, pages
Libertas Academica, 2013
Keywords
gonadotropin-releasing hormone, posterior laryngitis, functional disorders, acid reflux
National Category
Dentistry
Identifiers
urn:nbn:se:mau:diva-4189 (URN)10.4137/DTI.S10837 (DOI)000215809300001 ()23400339 (PubMedID)17734 (Local ID)17734 (Archive number)17734 (OAI)
Available from: 2020-02-28 Created: 2020-02-28 Last updated: 2024-02-05Bibliographically approved
Kolbus, D., Ljungcrantz, I., Andersson, L., Hedblad, B., Nordin Fredrikson, G., Björkbacka, H. & Nilsson, J. (2013). Association between CD8+ T-cell subsets and cardiovascular disease (ed.). Journal of Internal Medicine, 274(1), 41-51
Open this publication in new window or tab >>Association between CD8+ T-cell subsets and cardiovascular disease
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2013 (English)In: Journal of Internal Medicine, ISSN 0954-6820, E-ISSN 1365-2796, Vol. 274, no 1, p. 41-51Article in journal (Refereed) Published
Abstract [en]

Background The findings of experimental studies suggest that the immune system plays a key role in atherosclerosis, but the clinical importance of different immune cells in cardiovascular disease remains poorly characterized. In this study we investigated the association between CD8+ T cells and carotid disease as well as development of cardiovascular disease events. Methods The study cohort comprised 700 subjects from the cardiovascular arm of the Malmö Diet and Cancer Study. Peripheral blood mononuclear cells, obtained at the 1991–1994 baseline investigation and stored at −140 °C, were thawed and the different CD8+ T-cell populations analysed by flow cytometry. Baseline carotid intima–media thickness and stenosis were assessed by ultrasonography and clinical events were monitored through validated national registers. Results Subjects with a high fraction of CD8+ T cells were characterized by decreased cytokine release from activated leucocytes, metabolic signs of insulin resistance and increased incidence of coronary events; hazard ratios (95% confidence intervals) for the second and third tertiles of CD8+ T cells were 2.57 (1.16, 5.67) and 2.61 (1.19, 5,71), respectively, in a Cox proportional hazards regression model. Correlations were found between the fraction of CD8+CD25+ T cells and the degree of carotid stenosis (r = 0.11, P < 0.01), and between the CD8+CD56−IFN-γ+ T-cell fraction and the degree of stenosis (r = −0.18, P < 0.005). The association between CD8+CD56−IFN-γ+ T cells and carotid stenosis remained significant after controlling for major cardiovascular disease risk factors. Conclusion This study provides prospective clinical evidence for a role of CD8+ T cells in cardiovascular disease and suggests the existence of CD8+ T-cell subsets with different pathological functions.

Place, publisher, year, edition, pages
John Wiley & Sons, 2013
Keywords
carotid intima–media thickness, CD8+ T cell, cytokines, myocardial infarction, stroke
National Category
Medical and Health Sciences
Identifiers
urn:nbn:se:mau:diva-4958 (URN)10.1111/joim.12038 (DOI)000320279000003 ()23356723 (PubMedID)2-s2.0-84879109428 (Scopus ID)17736 (Local ID)17736 (Archive number)17736 (OAI)
Available from: 2020-02-28 Created: 2020-02-28 Last updated: 2024-02-05Bibliographically approved
Berg, K. E., Ljungcrantz, I., Andersson, L., Bryngelsson, C., Hedblad, B., Nordin Fredrikson, G., . . . Björkbacka, H. (2012). Elevated CD14++CD16− Monocytes Predict Cardiovascular Events (ed.). Circulation: Cardiovascular Genetics, 5(1), 122-131
Open this publication in new window or tab >>Elevated CD14++CD16− Monocytes Predict Cardiovascular Events
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2012 (English)In: Circulation: Cardiovascular Genetics, ISSN 1942-325X, E-ISSN 1942-3268, Vol. 5, no 1, p. 122-131Article in journal (Refereed)
Abstract [en]

Background—Although monocytes in peripheral blood are no longer considered to be a homogeneous population, associations between distinct monocyte subsets and cardiovascular disease have not been highlighted in large epidemiological studies. Methods and Results—The study included 700 randomly selected subjects from the cardiovascular arm of the Malmö Diet and Cancer study. Among these, 123 subjects experienced ischemic cardiovascular events during the follow-up until December 2008. Mononuclear leukocytes frozen at the baseline investigation in 1991 to 1994 were thawed and analyzed with flow cytometry to enumerate monocyte subsets, based on CD14 and CD16 expression. The percentage and number of classical CD14++CD16− monocytes were increased in the cardiovascular-event group compared with the event-free subjects (median, 69% [interquartile range, 62% to 76%] versus 67% [59% to 72%], P=0.017; 344 [251 to 419] cells/μL versus 297 [212 to 384] cells/μL, P=0.003). The hazard ratio was 1.66 for suffering a cardiovascular event in the highest tertile of the number of CD14++CD16− monocytes compared with the lowest tertile, even after adjustment for common risk factors (HR, 1.66; 95% CI: 1.02 to 2.72). CD14++CD16− monocytes did not, however, associate with the extent of atherosclerosis at baseline. In contrast, the percentage of monocytes expressing CD16 was negatively associated to the extent of carotid atherosclerosis measured as intima-media thickness at baseline. The chemokine receptors CCR2, CX3CR1, and CCR5 were not differentially expressed between cases and controls on any of the monocyte subsets, but CCR5 expression on CD14+CD16++ monocytes was negatively associated to carotid intima-media thickness. Conclusions—This study shows that classical CD14++CD16− monocytes can predict future cardiovascular risk independently of other risk factors in a randomly selected population.

Place, publisher, year, edition, pages
Lippincott Williams & Wilkins, 2012
Keywords
monocytes, leukocytes, cardiovascular disease, myocardial infarction, ischemic stroke
National Category
Medical and Health Sciences
Identifiers
urn:nbn:se:mau:diva-4026 (URN)10.1161/CIRCGENETICS.111.960385 (DOI)000309884100019 ()22238190 (PubMedID)2-s2.0-84860842552 (Scopus ID)15971 (Local ID)15971 (Archive number)15971 (OAI)
Available from: 2020-02-28 Created: 2020-02-28 Last updated: 2024-02-05Bibliographically approved
Sonestedt, E., Wirfält, E., Wallström, P., Gullberg, B., Drake, I., Hlebowicz, J., . . . Orhu-Melander, M. (2012). High disaccharide intake associates with atherogenic lipoprotein profile (ed.). British Journal of Nutrition, 107(7), 1062-1069
Open this publication in new window or tab >>High disaccharide intake associates with atherogenic lipoprotein profile
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2012 (English)In: British Journal of Nutrition, ISSN 0007-1145, E-ISSN 1475-2662, Vol. 107, no 7, p. 1062-1069Article in journal (Refereed)
Abstract [en]

Increased plasma concentrations of small LDL particles denote an atherogenic lipoprotein phenotype (ALP) that is correlated with increased circulating TAG and reduced HDL-cholesterol. Principal component analyses of subfraction concentrations have previously been used in the Swedish population-based Malmö Diet and Cancer (MDC) cohort to identify three independent components, one pattern representing the ALP. The aim of the present study was to examine the associations between macronutrient intakes and the principal component representing the ALP. We examined 4301 healthy subjects (46–68 years old, 60 % women) at baseline in the MDC cohort. Dietary data were collected using a modified diet history method. Plasma lipoprotein subfractions were measured using a high-resolution ion mobility method. The principal component corresponding to the ALP was significantly associated with a higher intake of disaccharides, and inversely related to protein and alcohol consumption (P < 0·001 for all). The present findings indicate that the ALP may be improved by a low intake of disaccharides, and moderate intakes of protein and alcohol.

Place, publisher, year, edition, pages
Cambridge University Press, 2012
Keywords
Macronutrients, Atherogenic lipoprotein phenotype, Lipoprotein subfractions, Epidemiology
National Category
Medical and Health Sciences
Identifiers
urn:nbn:se:mau:diva-5514 (URN)10.1017/S0007114511003783 (DOI)12829 (Local ID)12829 (Archive number)12829 (OAI)
Available from: 2020-02-28 Created: 2020-02-28 Last updated: 2022-06-27Bibliographically approved
Engelbertsen, D., Anand, D., Nordin Fredrikson, G., Hopkins, D., Corder, R., Shah, P. K., . . . Bengtsson, E. (2012). High levels of IgM against methylglyoxal-modified apolipoprotein B 100 is associated with less coronary artery calcification in patients with type 2 diabetes. (ed.). Journal of Internal Medicine, 271(1), 82-89
Open this publication in new window or tab >>High levels of IgM against methylglyoxal-modified apolipoprotein B 100 is associated with less coronary artery calcification in patients with type 2 diabetes.
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2012 (English)In: Journal of Internal Medicine, ISSN 0954-6820, E-ISSN 1365-2796, Vol. 271, no 1, p. 82-89Article in journal (Refereed) Published
Abstract [en]

Objective: Advanced glycation end products (AGE) have been implicated in diabetic vascular complications through activation of pro‐inflammatory genes. AGE‐modified proteins are also targeted by the immune system resulting in the generation of AGE‐specific autoantibodies, but the association of these immune responses with diabetic vasculopathy remains to be fully elucidated. The aim of this study was to determine whether antibodies against apolipoprotein B100 modified by methylglyoxal (MGO‐apoB100) are associated with coronary atherosclerosis in patients with type 2 diabetes.

Methods: We measured antibodies against MGO‐apoB100 in plasma from 497 type 2 diabetic patients without clinical signs of cardiovascular disease. Severity of coronary disease was assessed as coronary artery calcium (CAC) imaging. Immunoglobulin (Ig)M and IgG levels recognizing MGO‐apoB100 were determined by enzyme‐linked immunosorbent assay.

Results: Anti‐MGO‐apoB100 IgM antibody levels were higher in subjects with a low to moderate CAC score (≤400 Agatston units) than in subjects with a high score (>400 Agatston units; 136.8 ± 4.4 vs. 101.6 ± 7.4 arbitrary units (AU), P < 0.0001) and in subjects demonstrating no progression of CAC during 30 months of follow‐up (136.4 ± 5.7 vs. 113.9 ± 6.2 AU in subjects with progression, P < 0.0001). Subjects with a family history of premature myocardial infarction had lower levels of anti‐MGO‐apoB100 IgM. Female subjects had higher levels of anti‐MGO‐apoB100 antibodies and lower CAC than men. Accordingly, high levels of IgM against MGO‐apoB100 are associated with less severe and a lower risk of progression of coronary disease in subjects with type 2 diabetes.

Conclusions: Although conclusions regarding causal relationships based on epidemiological observations need to be made with caution, our findings suggest the possibility that anti‐MGO‐apoB100 IgM may be protective in diabetic vasculopathy.

Place, publisher, year, edition, pages
John Wiley & Sons, 2012
National Category
Cardiac and Cardiovascular Systems
Identifiers
urn:nbn:se:mau:diva-5328 (URN)10.1111/j.1365-2796.2011.02411.x (DOI)000298582800009 ()21668821 (PubMedID)2-s2.0-83855164160 (Scopus ID)12826 (Local ID)12826 (Archive number)12826 (OAI)
Available from: 2020-02-28 Created: 2020-02-28 Last updated: 2024-02-05Bibliographically approved
Wigren, M., Björkbacka, H., Andersson, L., Ljungcrantz, I., Nordin Fredrikson, G. & Persson, M. (2012). Low Levels of Circulating CD4+FoxP3+ T Cells Are Associated With an Increased Risk for Development of Myocardial Infarction But Not for Stroke (ed.). Arteriosclerosis, Thrombosis and Vascular Biology, 32(8), 2000-2007
Open this publication in new window or tab >>Low Levels of Circulating CD4+FoxP3+ T Cells Are Associated With an Increased Risk for Development of Myocardial Infarction But Not for Stroke
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2012 (English)In: Arteriosclerosis, Thrombosis and Vascular Biology, ISSN 1079-5642, E-ISSN 1524-4636, Vol. 32, no 8, p. 2000-2007Article in journal (Refereed)
Abstract [en]

Objective—Regulatory T cells (Tregs) protect against atherosclerosis in experimental models, but their association with cardiovascular disease in humans remains to be elucidated. The aim of the present study was to determine whether circulating Tregs predict the development of acute cardiovascular events in humans. Methods and Results—The study cohort consisted of a random sample of participants (n=700), aged 68 to 73 years, from the Malmö Diet and Cancer Study. Mononuclear leukocytes, stored at −140○C at the baseline investigation in 1991–1994, were thawed and Tregs, defined by the expression of FoxP3 in CD4+ T cells, were analyzed by flow cytometry. There was no detectable loss of cells during storage, and the viability of thawed leukocytes was 95%. A low fraction of both CD4+FoxP3+ and CD4+CD25+FoxP3+ T cells was associated with a higher release of proinflammatory cytokines from activated mononuclear leukocytes, and this association was strongest for CD4+FoxP3+ cells. Eighty-four coronary events and 66 strokes were registered during follow-up until December 31, 2008. In a Cox proportional hazard regression model adjusting for major risk factors, low levels of baseline CD4+FoxP3+ T cells were associated with an increased risk for the development of acute coronary events but not stroke. There were no associations between CD4+CD25+FoxP3+ T cells and development of an acute coronary event or stroke. Conclusion—This study provides prospective evidence for the role of Tregs in the development of myocardial infarction. The findings are in accordance with previous experimental studies and provide clinical support for a protective role of Tregs in atherosclerosis. The lack of association between Tregs and stroke may reflect the more heterogeneous cause of this disease.

Place, publisher, year, edition, pages
Lippincott Williams & Wilkins, 2012
Keywords
immune system, coronary disease, lymphocytes, carotid arteries
National Category
Dentistry
Identifiers
urn:nbn:se:mau:diva-5517 (URN)10.1161/ATVBAHA.112.251579 (DOI)000306558100040 ()22628434 (PubMedID)2-s2.0-84864282662 (Scopus ID)15972 (Local ID)15972 (Archive number)15972 (OAI)
Available from: 2020-02-28 Created: 2020-02-28 Last updated: 2024-02-05Bibliographically approved
Saxena, A., Björkbacka, H., Ström, Å., Rattik, S., Berg, K. E., Gomez, M. F., . . . Hultgårdh-Nilsson, A. (2012). Mobilization of Regulatory T Cells in Response to Carotid Injury Does Not Influence Subsequent Neointima Formation (ed.). PLOS ONE, 12(7), Article ID e51556.
Open this publication in new window or tab >>Mobilization of Regulatory T Cells in Response to Carotid Injury Does Not Influence Subsequent Neointima Formation
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2012 (English)In: PLOS ONE, E-ISSN 1932-6203, Vol. 12, no 7, article id e51556Article in journal (Refereed)
Abstract [en]

Methods and Results A non-obstructive collar was introduced to inflict carotid artery injury in mice and subsequent activation of immune cells in draining lymph nodes and spleen were studied by flow cytometry. Carotid artery injury of wild type mice was associated with mobilization of both Th1 type CD4+IFNγ+ and regulatory CD4+CD25+FoxP3+ T cells in draining lymph nodes. Studies using FoxP3-green fluorescent protein (GFP) transgenic C57/Bl6 mice demonstrated scattered presence of regulatory T cells in the adventitial tissue of injured arteries as well as a massive emigration of regulatory T cells from the spleen in response to carotid injury. However, deletion of antigen presentation to CD4+ T cells (H20 mice), as well as deletion of regulatory T cells (through treatment with blocking anti-CD25 antibodies), did not affect neointima formation. Also deletion of antigen presentation to CD8+ T cells (Tap10 mice) was without effect on carotid collar-induced neointima formation. Conclusion The results demonstrate that carotid artery injury is associated with mobilization of regulatory T cells. Depletion of regulatory T cells does not, however, influence the subsequent repair processes leading to the formation of a neointima. The results also demonstrate that lack of CD8+ T cells does not influence neointima formation in presence of functional CD4+ T cells and B cells.

Place, publisher, year, edition, pages
Public Library of Science, 2012
National Category
Medical and Health Sciences
Identifiers
urn:nbn:se:mau:diva-5049 (URN)10.1371/journal.pone.0051556 (DOI)000312290800078 ()23240042 (PubMedID)2-s2.0-84871126682 (Scopus ID)15970 (Local ID)15970 (Archive number)15970 (OAI)
Available from: 2020-02-28 Created: 2020-02-28 Last updated: 2024-02-05Bibliographically approved
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