alopecia areata/tyrosine

BACKGROUND There is strong evidence to suggest that alopecia areata (AA) is a tissue-specific, T cell-mediated autoimmune disease, which is usually characterized by patchy areas of hair loss on the scalp. Tyrosine hydroxylase (TH) is a known B-cell autoantigen in patients with autoimmune

BACKGROUND We previously detected antibodies against tyrosine hydroxylase (TH) in 23% of patients with nonsegmental vitiligo and in 19% of patients with alopecia areata (AA). OBJECTIVE To identify TH epitopes recognized by TH antibodies in patients with vitiligo and AA. METHODS Recombinant plasmids

Alopecia areata (AA) is hypothesized to be an organ-specific autoimmune disease mediated by T cells to the hair follicles. Despite the fact that most cases of AA are sporadic, there is an accumulation of evidence that AA is a complex multigenetic trait with components of inherited predisposition. In

BACKGROUND The functional R620W (c.1858C>T) variant of the protein tyrosine phosphatase nonreceptor 22 gene (PTPN22) has been associated with a variety of autoimmune disorders. A recent study has suggested that R620W also contributes to the severe form of alopecia areata (AA). OBJECTIVE We sought to

Alopecia areata (AA) is a genetically determined autoimmune hair loss disorder. A polymorphism in protein tyrosine phosphatase N22 (PTPN22), which normally suppresses T-cell proliferation, has been associated with human autoimmune disease, including AA in European populations. PTPN22 genotype

Alopecia areata (AA) is a skin condition in which hair is lost from certain or all areas of the body. This condition has been described as an immune-mediated complex genetic disease, characterized by the presence of lymphocytes that are directed to the hair follicles in the anagen phase. The gene

Patients with the autosomal recessively inherited autoimmune polyendocrine syndrome type I (APS I) have autoantibodies directed against several endocrine and nonendocrine organs. In this study a new autoantigen related to this syndrome, tyrosine hydroxylase, was identified in sera from patients with

Alopecia areata is an acquired hair loss disorder resulting from an immunologically- mediated attack on hair follicles and autoimmunity may play a part in its pathogenesis. The non-synonymous C1858T substitution in the PTPN22 gene, which encodes lymphoid protein tyrosine phosphatase, has been shown

Tyrosine kinases relay signals from diverse leukocyte antigen receptors, innate immune receptors, and cytokine receptors, and therefore mediate the recruitment and activation of various leukocyte populations. Non-receptor tyrosine kinases of the Jak, Src, Syk, and Btk families play major roles in

Tyrosine kinase enzymes are an attractive target for anticancer therapies. Tyrosine kinase inhibitors (TKI) are well tolerated; somehow severe systemic side effects are rarely seen during treatment. Toxicities of skin and appendages may lead to poor compliance, psychosocial inconvenience, and drug

Alopecia areata (AA) is a common autoimmune disease resulting from damage of the hair follicle by T cells. The immune pathways required for autoreactive T cell activation in AA are not defined limiting clinical development of rational targeted therapies. Genome-wide association studies (GWAS)

The therapeutic revolution in the management of inflammatory dermatoses is under way. The therapeutic arsenal is expanding in the field of psoriasis, including biologics (TNF blockers, anti-IL12/IL23, anti-IL17, and anti-IL23 antibodies), new small molecules (tyrosine kinase inhibitor), and a new

Interleukin (IL)-1 has been shown to be a potent inhibitor of hair growth in vitro. We hypothesized that this cytokine might be a decisive factor causing hair loss during the lymphocytic attack in alopecia areata. Neither the intracellular pathways involved in hair growth inhibition mediated by