A. Huber

Publications58
h-index22
Citations2,044
Highly Influential Citations88
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Neutrophil-related factors as biomarkers in EAE and MS
TLDR
It is shown that neutrophils expand in the bone marrow and accumulate in the circulation before clinical onset of disease, and systemic expression of neutrophil-related mediators correlates with new lesion formation, lesion burden, and clinical disability in patients with MS.
Joint genetic susceptibility to type 1 diabetes and autoimmune thyroiditis: from epidemiology to mechanisms.
TLDR
All the joint genes for T1D and AITD identified so far are involved in immune regulation, specifically in the presentation of antigenic peptides to T cells, and gene-gene and genetic-epigenetic interactions most likely play a role in the shared genetic susceptibility.
The etiology of autoimmune thyroid disease: a story of genes and environment.
The HLA gene complex in thyroid autoimmunity: from epidemiology to etiology.
Site-Specific Chemokine Expression Regulates Central Nervous System Inflammation and Determines Clinical Phenotype in Autoimmune Encephalomyelitis
TLDR
It is shown that atypical EAE correlates with preferential upregulation of CXCL2 in the brainstem, and is driven by CXCR2-dependent recruitment of neutrophils, in contrast to conventional EAE, which is associated with up regulation of CCL1 in the spinal cord, and was driven by recruitment of monocytes via a partially CCR1-dependent pathway.
Autoimmune thyroiditis and diabetes: dissecting the joint genetic susceptibility in a large cohort of multiplex families.
TLDR
The results demonstrate a strong shared genetic susceptibility to T1D and AITD, with most shared genes involved in immune regulation, suggesting that immune dysregulation plays an important role in the joint susceptibility.
Hyperthyroid-associated osteoporosis is exacerbated by the loss of TSH signaling.
TLDR
It is found thathyperthyroid mice lacking TSHR had greater bone loss and resorption than hyperthyroid wild-type mice, thereby demonstrating that the absence of TSH signaling contributes to bone loss.
A CD40 Kozak sequence polymorphism and susceptibility to antibody-mediated autoimmune conditions: the role of CD40 tissue-specific expression
TLDR
The genetic and tissue expression data suggest that the CD40 Kozak SNP is specific for thyroid antibody production involved in the etiology of GD, and increased thyroidal expression of CD40 driven by the SNP may contribute to this disease specificity.
Novel Variant of Thyroglobulin Promoter Triggers Thyroid Autoimmunity through an Epigenetic Interferon α-modulated Mechanism*
TLDR
A genetic/epigenetic mechanism by which a newly identified TG promoter single-nucleotide polymorphism (SNP) variant predisposes to AITD is described, revealing a new mechanism of interaction between environmental and genetic factors to trigger autoimmune thyroid diseases.
Regulation of heterotopic ossification by monocytes in a mouse model of aberrant wound healing
TLDR
It is shown, using a mouse burn/trauma model, that TGFβ-producing monocytes/macrophages at the injury site contribute to HO induction, while CD47 activation helps antagonize this process.
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