Family studies of type 1 diabetes reveal additive and epistatic effects between MGAT1 and three other polymorphisms

Hypomorphic MGAT5 polymorphisms promote multiple sclerosis cooperatively with MGAT1 and interleukin-2 and 7 receptor variants

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Interleukin-2, Interleukin-7, T cell-mediated autoimmunity, and N-glycosylation

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Pathogenesis of multiple sclerosis via environmental and genetic dysregulation of N-glycosylation

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N-Acetylglucosamine Inhibits T-helper 1 (Th1)/T-helper 17 (Th17) Cell Responses and Treats Experimental Autoimmune Encephalomyelitis

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Pseudosibship methods in the case-parents design

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Genetics and the environment converge to dysregulate N-glycosylation in multiple sclerosis

(2011) Haik Mkhikian et al.   Nature Communications

Pervasive Sharing of Genetic Effects in Autoimmune Disease

(2011) Chris Cotsapas et al.   PLoS Genetics

Genetics of Type 1 Diabetes: What's Next?

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Etiology of Type 1 Diabetes

(2010) John A. Todd   IMMUNITY

FAM-MDR: A Flexible Family-Based Multifactor Dimensionality Reduction Technique to Detect Epistasis Using Related Individuals

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Finding the missing heritability of complex diseases

(2009) Teri A. Manolio et al.   NATURE

Autoimmune Disease Classification by Inverse Association with SNP Alleles

(2009) Marina Sirota et al.   PLoS Genetics

IL2RA Genetic Heterogeneity in Multiple Sclerosis and Type 1 Diabetes Susceptibility and Soluble Interleukin-2 Receptor Production

(2009) Lisa M. Maier et al.   PLoS Genetics

Study of the association between the CAPSL-IL7R locus and type 1 diabetes

(2008) J. L. Santiago et al.   DIABETOLOGIA

Detecting shared pathogenesis from the shared genetics of immune-related diseases

(2008) Alexandra Zhernakova et al.   NATURE REVIEWS GENETICS

Shared and Distinct Genetic Variants in Type 1 Diabetes and Celiac Disease

(2008) Deborah J. Smyth et al.   NEW ENGLAND JOURNAL OF MEDICINE