Amanda K Huber

Summary

Affiliation: Mount Sinai School of Medicine
Country: USA

Publications

  1. pmc Analysis of immune regulatory genes' copy number variants in Graves' disease
    Amanda K Huber
    Division of Endocrinology, Department of Medicine, Mount Sinai School of Medicine, New York, New York 10029, USA
    Thyroid 21:69-74. 2011
  2. pmc Genetically driven target tissue overexpression of CD40: a novel mechanism in autoimmune disease
    Amanda K Huber
    Division of Endocrinology, Mount Sinai School of Medicine, New York, NY 10029, USA
    J Immunol 189:3043-53. 2012
  3. pmc IFN-α mediates the development of autoimmunity both by direct tissue toxicity and through immune cell recruitment mechanisms
    Nagako Akeno
    Division of Endocrinology, University of Cincinnati College of Medicine, Cincinnati, OH 45267, USA
    J Immunol 186:4693-706. 2011
  4. pmc Novel variant of thyroglobulin promoter triggers thyroid autoimmunity through an epigenetic interferon alpha-modulated mechanism
    Mihaela Stefan
    Division of Endocrinology, Department of Medicine, Mount Sinai Medical Center, New York, New York 10029, USA
    J Biol Chem 286:31168-79. 2011
  5. pmc Autoimmune thyroiditis and diabetes: dissecting the joint genetic susceptibility in a large cohort of multiplex families
    Maria Justina B Villano
    Department of Internal Medicine, Division of Endocrinology, University of Cincinnati College of Medicine, Cincinnati, Ohio 45267, USA
    J Clin Endocrinol Metab 94:1458-66. 2009
  6. pmc Interleukin (IL)-23 receptor is a major susceptibility gene for Graves' ophthalmopathy: the IL-23/T-helper 17 axis extends to thyroid autoimmunity
    Amanda K Huber
    Division of Endocrinology, The Vontz Center, ML 0547, University of Cincinnati College of Medicine, 3125 Eden Avenue, Cincinnati, Ohio 45267, USA
    J Clin Endocrinol Metab 93:1077-81. 2008
  7. pmc Hyperthyroid-associated osteoporosis is exacerbated by the loss of TSH signaling
    Ramkumarie Baliram
    Thyroid Research Unit and The Mount Sinai Bone Program, Department of Medicine, Mount Sinai School of Medicine, and James J Peters VA Medical Center, New York, New York 10029, USA
    J Clin Invest 122:3737-41. 2012

Collaborators

Detail Information

Publications7

  1. pmc Analysis of immune regulatory genes' copy number variants in Graves' disease
    Amanda K Huber
    Division of Endocrinology, Department of Medicine, Mount Sinai School of Medicine, New York, New York 10029, USA
    Thyroid 21:69-74. 2011
    ..Moreover, loci involved in immunity are enriched in CNVs. Therefore, we hypothesized that CNVs in immune genes associated with Graves' disease (GD) may contribute to the etiology of disease...
  2. pmc Genetically driven target tissue overexpression of CD40: a novel mechanism in autoimmune disease
    Amanda K Huber
    Division of Endocrinology, Mount Sinai School of Medicine, New York, NY 10029, USA
    J Immunol 189:3043-53. 2012
    ..We conclude that target tissue overexpression of CD40 plays a key role in the etiology of organ-specific autoimmune disease...
  3. pmc IFN-α mediates the development of autoimmunity both by direct tissue toxicity and through immune cell recruitment mechanisms
    Nagako Akeno
    Division of Endocrinology, University of Cincinnati College of Medicine, Cincinnati, OH 45267, USA
    J Immunol 186:4693-706. 2011
    ..Taken together, our data demonstrate that the induction of tissue inflammation and autoimmunity by IFN-α involves direct tissue toxic effects as well as provocation of destructive bystander immune responses...
  4. pmc Novel variant of thyroglobulin promoter triggers thyroid autoimmunity through an epigenetic interferon alpha-modulated mechanism
    Mihaela Stefan
    Division of Endocrinology, Department of Medicine, Mount Sinai Medical Center, New York, New York 10029, USA
    J Biol Chem 286:31168-79. 2011
    ..These results reveal a new mechanism of interaction between environmental (IFNα) and genetic (TG) factors to trigger AITD...
  5. pmc Autoimmune thyroiditis and diabetes: dissecting the joint genetic susceptibility in a large cohort of multiplex families
    Maria Justina B Villano
    Department of Internal Medicine, Division of Endocrinology, University of Cincinnati College of Medicine, Cincinnati, Ohio 45267, USA
    J Clin Endocrinol Metab 94:1458-66. 2009
    ..Both diseases frequently occur within the same family and in the same individual. Patients developing both T1D and AITD are considered to have an autoimmune polyglandular syndrome type 3 variant (APS3v)...
  6. pmc Interleukin (IL)-23 receptor is a major susceptibility gene for Graves' ophthalmopathy: the IL-23/T-helper 17 axis extends to thyroid autoimmunity
    Amanda K Huber
    Division of Endocrinology, The Vontz Center, ML 0547, University of Cincinnati College of Medicine, 3125 Eden Avenue, Cincinnati, Ohio 45267, USA
    J Clin Endocrinol Metab 93:1077-81. 2008
    ..IL-23 and its receptor (IL-23R) guide T cells toward the T-helper 17 phenotype. IL-23R single nucleotide polymorphisms (SNPs) have been associated with several autoimmune diseases, including Crohn's disease and rheumatoid arthritis...
  7. pmc Hyperthyroid-associated osteoporosis is exacerbated by the loss of TSH signaling
    Ramkumarie Baliram
    Thyroid Research Unit and The Mount Sinai Bone Program, Department of Medicine, Mount Sinai School of Medicine, and James J Peters VA Medical Center, New York, New York 10029, USA
    J Clin Invest 122:3737-41. 2012
    ..Further, we identified a TSH-like factor that may confer osteoprotection. These studies suggest that therapeutic suppression of TSH to very low levels may contribute to bone loss in people...