HLA-DRB1*11and variants of the MHC class II locus are strong risk factors for systemic juvenile idiopathic arthritis

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Intracellular MHC class II molecules promote TLR-triggered innate immune responses by maintaining activation of the kinase Btk

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Juvenile idiopathic arthritis and HLA Class I and Class II interactions and age-at-onset effects

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MHC class II molecules activate NFAT and the ERK group of MAPK through distinct signaling pathways in B cells

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The pattern of response to anti–interleukin-1 treatment distinguishes two subsets of patients with systemic-onset juvenile idiopathic arthritis

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