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Nathan Karin

Researcher at Rappaport Faculty of Medicine

Publications -  46
Citations -  3421

Nathan Karin is an academic researcher from Rappaport Faculty of Medicine. The author has contributed to research in topics: Experimental autoimmune encephalomyelitis & Chemokine. The author has an hindex of 18, co-authored 46 publications receiving 3233 citations.

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Prevention of experimental autoimmune encephalomyelitis by antibodies against alpha 4 beta 1 integrin.

TL;DR: In vitro adhesion assay on tissue sections found that lymphocytes and monocytes bound selectively to inflamed EAE brain vessels, and therapies designed to interfere with α4βl integrin may be useful in treating inflammatory diseases of the central nervous system, such as multiple sclerosis.
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Gain-of-function human STAT1 mutations impair IL-17 immunity and underlie chronic mucocutaneous candidiasis

Luyan Liu, +70 more
TL;DR: Whole-exome sequencing reveals activating STAT1 mutations in some patients with autosomal dominant chronic mucocutaneous candidiasis disease.
Journal Article

Long-Lasting Protective Immunity to Experimental Autoimmune Encephalomyelitis Following Vaccination with Naked DNA Encoding C-C Chemokines

TL;DR: Modulation of EAE with C-C chemokine DNA vaccines is dependent on targeting chemokines that are highly transcribed at the site of inflammation at the onset of disease.
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C-C chemokine–encoding DNA vaccines enhance breakdown of tolerance to their gene products and treat ongoing adjuvant arthritis

TL;DR: Repeated administration of naked DNA vaccines encoding MCP-1, MIP-1 alpha, or RANTES inhibited the development and progression of AA, even when each vaccine was administered only after the onset of disease.
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Tr1 cell–dependent active tolerance blunts the pathogenic effects of determinant spreading

TL;DR: Evidence is brought about showing that Tr1 cells play a pivotal role in the regulation of T cell tolerance during determinant spread and that soluble peptide therapy with the determinant to which the autoimmune response spreads amplifies a de novo regulatory mechanism aimed to reduce the pathological consequences of determinant spreading.