Thymus, innate immunity and autoimmune arthritis: interplay of gene and environment (Q27013062)

Atsushi Tanaka

3

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Yoshinaga Ito

4

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Shinji Maeda

5

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Noriko Sakaguchi

6

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Motomu Hashimoto

7

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language of work or name

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1 December 2011

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585

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PubMed

issue

23

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PubMed

page(s)

3633-9

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Monogenic autoimmune diseases - lessons of self-tolerance

PubMed

cites work

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A role for fungal {beta}-glucans and their receptor Dectin-1 in the induction of autoimmune arthritis in genetically susceptible mice

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Positive and negative selection of T cells

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Graded attenuation of TCR signaling elicits distinct autoimmune diseases by altering thymic T cell selection and regulatory T cell function.

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T cell self-reactivity forms a cytokine milieu for spontaneous development of IL-17+ Th cells that cause autoimmune arthritis.

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A missense single-nucleotide polymorphism in a gene encoding a protein tyrosine phosphatase (PTPN22) is associated with rheumatoid arthritis

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A functional variant of lymphoid tyrosine phosphatase is associated with type I diabetes

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Genetic association of the R620W polymorphism of protein tyrosine phosphatase PTPN22 with human SLE.

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The codon 620 tryptophan allele of the lymphoid tyrosine phosphatase (LYP) gene is a major determinant of Graves' disease

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Identification of substrates of human protein-tyrosine phosphatase PTPN22

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Homeostatic maintenance of natural Foxp3(+) CD25(+) CD4(+) regulatory T cells by interleukin (IL)-2 and induction of autoimmune disease by IL-2 neutralization

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Altered thymic T-cell selection due to a mutation of the ZAP-70 gene causes autoimmune arthritis in mice

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