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  • 1
    Online Resource
    Online Resource
    B cells from periodontal disease patients express surface Toll-like receptor 4
    Oxford University Press (OUP) ; 2009
    In:  Journal of Leukocyte Biology Vol. 85, No. 4 ( 2009-04-01), p. 648-655
    Details
    In: Journal of Leukocyte Biology, Oxford University Press (OUP), Vol. 85, No. 4 ( 2009-04-01), p. 648-655
    Abstract: Chronic systemic inflammation links periodontal disease (PD) to increased incidence of cardiovascular disease. Activation of TLRs, particularly TLR4, promotes chronic inflammation in PD by stimulating myeloid cells. B cells from healthy individuals are generally refractory to TLR4 agonists as a result of low surface TLR4 expression. Unexpectedly, a significantly increased percentage of gingival and peripheral blood B cells from patients with PD expressed surface TLR4. Surface expression correlated with an active TLR4 promoter that mimicked the TLR4 promoter in neutrophils. B cells from PD patients were surface myeloid differentiation protein 2-positive and also packaged the enhancer of a proinflammatory cytokine, IL-1β, into an active structure, demonstrating that these cells harbor key characteristics of proinflammatory cell types. Furthermore, B cells lacked activating signatures of a natural IL-1β inhibitor, IL-1 receptor antagonist. Surprisingly, despite multiple signatures of proinflammatory cells, freshly isolated B cells from PD patients had decreased expression of TLR pathway genes compared with B cells from healthy individuals. Decreases in inflammatory gene expression were even more dramatic in B cells stimulated with a TLR4 ligand from a periodontal pathogen, Porphyromonas gingivalis LPS 1690. In contrast, B cell TLR4 was not activated by the prototypic TLR4 ligand Escherichia coli LPS. These findings raise the unexpected possibility that TLR4 engagement modulates B cell activation in PD patients.
    Type of Medium: Online Resource
    ISSN: 0741-5400 , 1938-3673
    URL: Article
    DOI: 10.1189/jlb.0708428
    RVK:
    XA 10000
    Language: English
    Publisher: Oxford University Press (OUP)
    Publication Date: 2009
    detail.hit.zdb_id: 2026833-6
    SSG: 12
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  • 2
    Online Resource
    Online Resource
    Differential regulation of TLR4 expression in human B cells and monocytes
    Elsevier BV ; 2010
    In:  Molecular Immunology Vol. 48, No. 1-3 ( 2010-11), p. 82-88
    Details
    In: Molecular Immunology, Elsevier BV, Vol. 48, No. 1-3 ( 2010-11), p. 82-88
    Type of Medium: Online Resource
    ISSN: 0161-5890
    URL: Article
    DOI: 10.1016/j.molimm.2010.09.008
    Language: English
    Publisher: Elsevier BV
    Publication Date: 2010
    detail.hit.zdb_id: 2013448-4
    SSG: 12
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  • 3
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    Th17 cytokines differentiate obesity from obesity‐associated type 2 diabetes and promote TNF α production
    Wiley ; 2016
    In:  Obesity Vol. 24, No. 1 ( 2016-01), p. 102-112
    Details
    In: Obesity, Wiley, Vol. 24, No. 1 ( 2016-01), p. 102-112
    Abstract: T cell inflammation plays pivotal roles in obesity‐associated type 2 diabetes (T2DM). The identification of dominant sources of T cell inflammation in humans remains a significant gap in understanding disease pathogenesis. It was hypothesized that cytokine profiles from circulating T cells identify T cell subsets and T cell cytokines that define T2DM‐associated inflammation. Methods Multiplex analyses were used to quantify T cell‐associated cytokines in αCD3/αCD28‐stimulated PBMCs, or B cell‐depleted PBMCs, from subjects with T2DM or BMI‐matched controls. Cytokine measurements were subjected to multivariate (principal component and partial least squares) analyses. Flow cytometry detected intracellular TNFα in multiple immune cell subsets in the presence/absence of antibodies that neutralize T cell cytokines. Results T cell cytokines were generally higher in T2DM samples, but Th17 cytokines are specifically important for classifying individuals correctly as T2DM. Multivariate analyses indicated that B cells support Th17 inflammation in T2DM but not control samples, while monocytes supported Th17 inflammation regardless of T2DM status. Partial least squares regression analysis indicated that both Th17 and Th1 cytokines impact %HbA1c. Conclusions Among various T cell subsets, Th17 cells are major contributors to inflammation and hyperglycemia and are uniquely supported by B cells in obesity‐associated T2DM.
    Type of Medium: Online Resource
    ISSN: 1930-7381 , 1930-739X
    URL: Issue
    URL: Article
    DOI: 10.1002/oby.v24.1
    DOI: 10.1002/oby.21243
    Language: English
    Publisher: Wiley
    Publication Date: 2016
    detail.hit.zdb_id: 2027211-X
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  • 4
    Online Resource
    Online Resource
    TLR Cross-Talk Specifically Regulates Cytokine Production by B Cells from Chronic Inflammatory Disease Patients
    The American Association of Immunologists ; 2009
    In:  The Journal of Immunology Vol. 183, No. 11 ( 2009-12-01), p. 7461-7470
    Details
    In: The Journal of Immunology, The American Association of Immunologists, Vol. 183, No. 11 ( 2009-12-01), p. 7461-7470
    Abstract: Chronic systemic inflammation links periodontal disease and diabetes to increased incidence of serious comorbidities. Activation of TLRs, particularly TLR2 and TLR4, promotes chronic systemic inflammation. Human B cells have been generally thought to lack these TLRs. However, recent work showed that an increased percentage of circulating B cells from inflammatory disease patients express TLR2 and TLR4, and that TLR engagement on B cells resulted in unexpected changes in gene expression. New data show that B cells from inflammatory disease patients secrete multiple cytokines in response to different classes of TLR ligands. Furthermore, the B cell response to combinations of TLR ligands is cytokine- and ligand-specific. Some cytokines (IL-1β and IL-10) are predominantly regulated by TLR4, but others (IL-8 and TNF-α) are predominantly regulated by TLR2, due in part to TLR-dictated changes in transcription factor/promoter association. TLR2 and TLR9 also regulate B cell TLR4 expression, demonstrating that TLR cross-talk controls B cell responses at multiple levels. Parallel examination of B cells from periodontal disease and diabetes patients suggested that outcomes of TLR cross-talk are influenced by disease pathology. We conclude that disease-associated alteration of B cell TLR responses specifically regulates cytokine production and may influence chronic inflammation.
    Type of Medium: Online Resource
    ISSN: 0022-1767 , 1550-6606
    URL: Article
    DOI: 10.4049/jimmunol.0901517
    RVK:
    XA 54100
    RVK:
    XA 10000
    Language: English
    Publisher: The American Association of Immunologists
    Publication Date: 2009
    detail.hit.zdb_id: 1475085-5
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  • 5
    Online Resource
    Online Resource
    Elevated Proinflammatory Cytokine Production by a Skewed T Cell Compartment Requires Monocytes and Promotes Inflammation in Type 2 Diabetes
    The American Association of Immunologists ; 2011
    In:  The Journal of Immunology Vol. 186, No. 2 ( 2011-01-15), p. 1162-1172
    Details
    In: The Journal of Immunology, The American Association of Immunologists, Vol. 186, No. 2 ( 2011-01-15), p. 1162-1172
    Abstract: An appropriate balance between proinflammatory (Th17 and Th1) and anti-inflammatory (regulatory T cells [Tregs] and Th2) subsets of T cells is critical to maintain homeostasis and avoid inflammatory disease. Type 2 diabetes (T2D) is a chronic inflammatory disease promoted by changes in immune cell function. Recent work indicates T cells are important mediators of inflammation in a mouse model of T2D. These studies identified an elevation in the Th17 and Th1 subsets with a decrease in the Treg subset, which culminates in inflammation and insulin resistance. Based on these data, we tested the hypothesis that T cells in T2D patients are skewed toward proinflammatory subsets. Our data show that blood from T2D patients has increased circulating Th17 cells and elevated activation of Th17 signature genes. Importantly, T cells required culture with monocytes to maintain Th17 signatures, and fresh ex vivo T cells from T2D patients appeared to be poised for IL-17 production. T cells from T2D patients also have increased production of IFN-γ, but produce healthy levels of IL-4. In contrast, T2D patients had decreased percentages of CD4+ Tregs. These data indicate that T cells in T2D patients are naturally skewed toward proinflammatory subsets that likely promote chronic inflammation in T2D through elevated cytokine production. Potential therapies targeted toward resetting this balance need to be approached with caution due to the reciprocal relationship between Th17 cells and Tregs. Understanding the unique aspects of T2D T cells is essential to predict outcomes of such treatments.
    Type of Medium: Online Resource
    ISSN: 0022-1767 , 1550-6606
    URL: Article
    DOI: 10.4049/jimmunol.1002615
    RVK:
    XA 54100
    RVK:
    XA 10000
    Language: English
    Publisher: The American Association of Immunologists
    Publication Date: 2011
    detail.hit.zdb_id: 1475085-5
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  • 6
    Online Resource
    Online Resource
    B cells as master regulators of a pro-inflammatory T cell balance in obesity and glucose intolerance (176.17)
    The American Association of Immunologists ; 2012
    In:  The Journal of Immunology Vol. 188, No. 1_Supplement ( 2012-05-01), p. 176.17-176.17
    Details
    In: The Journal of Immunology, The American Association of Immunologists, Vol. 188, No. 1_Supplement ( 2012-05-01), p. 176.17-176.17
    Abstract: Lymphocytes play key roles in the chronic inflammation critical for T2D pathogenesis. T2D patients have an elevated ratio of pro- to anti-inflammatory T cells, and B cells that fail to produce anti-inflammatory IL-10. New data show that B cells from the diet-induced obesity (DIO) mouse model of T2D secrete a pro-inflammatory balance of cytokines, including relatively low IL-10 production, which mirrors our findings in T2D patients. DIO B cells do not secrete auto-antibodies, as evidenced by anti-nuclear antigen staining. Complementary metabolic studies show that B cell-null μMT mice resist the development of glucose intolerance (but not obesity) in response to DIO. Taken together, these data support the conclusion that a pro-inflammatory B cell cytokine balance, rather than antibodies, promotes T2D. To further define roles for B cells in T2D, we immunophenotyped DIO μMT splenocytes. Regulatory T cells (Tregs) expand in DIO μMT, while Tregs fail to expand in WT mice. These data are consistent with new human studies showing B cells from T2D (but not healthy) subjects support pro-inflammatory T cells, and indicate clinical relevance of published studies showing decreased Th1 function in DIO μMT vs. WT mice. We conclude B cells are critical regulators of inflammation in T2D due to 1. Secretion of a pro-inflammatory cytokine balance; and 2. An ability to promote pro-inflammatory T cell function. Thus B cell depletion may represent a valuable tool in the T2D clinic.
    Type of Medium: Online Resource
    ISSN: 0022-1767 , 1550-6606
    URL: Article
    DOI: 10.4049/jimmunol.188.Supp.176.17
    RVK:
    XA 54100
    RVK:
    XA 10000
    Language: English
    Publisher: The American Association of Immunologists
    Publication Date: 2012
    detail.hit.zdb_id: 1475085-5
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  • 7
    Online Resource
    Online Resource
    B cells promote inflammation in obesity and type 2 diabetes through regulation of T-cell function and an inflammatory cytokine profile
    Proceedings of the National Academy of Sciences ; 2013
    In:  Proceedings of the National Academy of Sciences Vol. 110, No. 13 ( 2013-03-26), p. 5133-5138
    Details
    In: Proceedings of the National Academy of Sciences, Proceedings of the National Academy of Sciences, Vol. 110, No. 13 ( 2013-03-26), p. 5133-5138
    Abstract: Patients with type 2 diabetes (T2D) have disease-associated changes in B-cell function, but the role these changes play in disease pathogenesis is not well established. Data herein show B cells from obese mice produce a proinflammatory cytokine profile compared with B cells from lean mice. Complementary in vivo studies show that obese B cell–null mice have decreased systemic inflammation, inflammatory B- and T-cell cytokines, adipose tissue inflammation, and insulin resistance (IR) compared with obese WT mice. Reduced inflammation in obese/insulin resistant B cell–null mice associates with an increased percentage of anti-inflammatory regulatory T cells (Tregs). This increase contrasts with the sharply decreased percentage of Tregs in obese compared with lean WT mice and suggests that B cells may be critical regulators of T-cell functions previously shown to play important roles in IR. We demonstrate that B cells from T2D (but not non-T2D) subjects support proinflammatory T-cell function in obesity/T2D through contact-dependent mechanisms. In contrast, human monocytes increase proinflammatory T-cell cytokines in both T2D and non-T2D analyses. These data support the conclusion that B cells are critical regulators of inflammation in T2D due to their direct ability to promote proinflammatory T-cell function and secrete a proinflammatory cytokine profile. Thus, B cells are potential therapeutic targets for T2D.
    Type of Medium: Online Resource
    ISSN: 0027-8424 , 1091-6490
    URL: Article
    DOI: 10.1073/pnas.1215840110
    RVK:
    TA 1000
    RVK:
    WA 15000
    Language: English
    Publisher: Proceedings of the National Academy of Sciences
    Publication Date: 2013
    detail.hit.zdb_id: 209104-5
    detail.hit.zdb_id: 1461794-8
    SSG: 11
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  • 8
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    Online Resource
    Hematopoiesis
    The Company of Biologists ; 2013
    In:  Development Vol. 140, No. 12 ( 2013-06-15), p. 2463-2467
    Details
    In: Development, The Company of Biologists, Vol. 140, No. 12 ( 2013-06-15), p. 2463-2467
    Abstract: Hematopoiesis – the process by which blood cells are formed – has been studied intensely for over a century using a variety of model systems. There is conservation of the overall hematopoietic process between vertebrates, although some differences do exist. Over the last decade, the zebrafish has come to the forefront as a new model in hematopoiesis research, as it allows the use of large-scale genetics, chemical screens and transgenics. This comparative approach to understanding hematopoiesis has led to fundamental knowledge about the process and to the development of new therapies for disease. Here, we provide a broad overview of vertebrate hematopoiesis. We also highlight the benefits of using zebrafish as a model.
    Type of Medium: Online Resource
    ISSN: 1477-9129 , 0950-1991
    URL: Article
    DOI: 10.1242/dev.083147
    Language: English
    Publisher: The Company of Biologists
    Publication Date: 2013
    detail.hit.zdb_id: 2007916-3
    SSG: 12
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  • 9
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    Online Resource
    B cells support a dominant Th17 cytokine signature in type 2 diabetes (HEM4P.255)
    The American Association of Immunologists ; 2014
    In:  The Journal of Immunology Vol. 192, No. 1_Supplement ( 2014-05-01), p. 117.6-117.6
    Details
    In: The Journal of Immunology, The American Association of Immunologists, Vol. 192, No. 1_Supplement ( 2014-05-01), p. 117.6-117.6
    Abstract: T cell inflammation plays critical roles in the development of obesity-associated type 2 diabetes (T2D). B cells support T cell-mediated inflammation in T2D, but the mechanisms underlying lymphocyte cross-talk and the relative importance of T cell inflammation in human T2D remain untested. Using peripheral blood mononuclear cells (PBMC) and/or purified cells from T2D and non-diabetic (ND) subjects, we show that B cell contact upregulates a pro-inflammatory CD4+ Th17 T cell program in T2D. Neutralization of either B cell CD80/86 or the downstream production of T cell IL-17A/F significantly decreased production of classical diabetogenic cytokines (TNFα, IL-6) in samples from T2D subjects. Although monocytes, B cells and T cells produced TNFα in response to treatment of PBMCs with αCD3/CD28, monocyte TNFα production was independent of IL-17A/F, while IL-17F was critical for maximal TNFα production by both T and B cells. IL-17A/F neutralization also reduced IL-17A and IL-17F production by CD4+ T cells, indicating Th17 function is auto-regulated. We conclude that human B cell co-stimulation broadly supports Th17 cells, which in turn stimulate lymphocytes (but not monocytes) to produce the classical diabetogenic cytokine TNFα.
    Type of Medium: Online Resource
    ISSN: 0022-1767 , 1550-6606
    URL: Article
    DOI: 10.4049/jimmunol.192.Supp.117.6
    RVK:
    XA 54100
    RVK:
    XA 10000
    Language: English
    Publisher: The American Association of Immunologists
    Publication Date: 2014
    detail.hit.zdb_id: 1475085-5
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  • 10
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    Online Resource
    The outliers become a stampede as immunometabolism reaches a tipping point
    Wiley ; 2012
    In:  Immunological Reviews Vol. 249, No. 1 ( 2012-09), p. 253-275
    Details
    In: Immunological Reviews, Wiley, Vol. 249, No. 1 ( 2012-09), p. 253-275
    Abstract: Summary:  Obesity and Type 2 diabetes mellitus (T2D) are characterized by pro‐inflammatory alterations in the immune system including shifts in leukocyte subset differentiation and in cytokine/chemokine balance. The chronic, low‐grade inflammation resulting largely from changes in T‐cell, B‐cell, and myeloid compartments promotes and/or exacerbates insulin resistance (IR) that, together with pancreatic islet failure, defines T2D. Animal model studies show that interruption of immune cell‐mediated inflammation by any one of several methods almost invariably results in the prevention or delay of obesity and/or IR. However, anti‐inflammatory therapies have had a modest impact on established T2D in clinical trials. These seemingly contradictory results indicate that a more comprehensive understanding of human IR/T2D‐associated immune cell function is needed to leverage animal studies into clinical treatments. Important outstanding analyses include identifying potential immunological checkpoints in disease etiology, detailing immune cell/adipose tissue cross‐talk, and defining strengths/weaknesses of model organism studies to determine whether we can harness the promising new field of immunometabolism to curb the global obesity and T2D epidemics.
    Type of Medium: Online Resource
    ISSN: 0105-2896 , 1600-065X
    URL: Issue
    URL: Article
    DOI: 10.1111/imr.2012.249.issue-1
    DOI: 10.1111/j.1600-065X.2012.01142.x
    Language: English
    Publisher: Wiley
    Publication Date: 2012
    detail.hit.zdb_id: 2038276-5
    SSG: 12
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