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In healthy PBMCs, SoJIA patient serum induced transcription 586 HESSNER et al of numerous genes related to innate immunity, including several members of the IL-1 cytokine/cytokine receptor family (IL-1b, IL-1R1, and IL-1R2), and chemokines involved in the chemotaxis of neutrophils (CXCL1, CXCL3, CXCL5, CXCL6). When directly comparing the expression profiles of SoJIA patient PBMCs versus healthy controls, many of the transcripts that were induced by SoJIA sera were present in SoJIA PBMCs, including IL-1b and the IL-1 decoy receptor (IL-1R2), CXCL1, and CCR1.

54] Hessner MJ, Wang X, Meyer L, et al. Involvement of eotaxin, eosinophils, and pancreatic predisposition in development of type 1 diabetes mellitus in the BioBreeding rat. J Immunol 2004;173(11):6993–7002. [55] Benoist C, Mathis D. Mast cells in autoimmune disease. Nature 2002;420(6917):875–8. [56] Seeldrayers PA, Yasui D, Weiner HL, et al. Treatment of experimental allergic neuritis with nedocromil sodium. J Neuroimmunol 1989;25(2–3):221–6. [57] Lock C, Hermans G, Pedotti R, et al. Gene–microarray analysis of multiple sclerosis lesions yields new targets validated in autoimmune encephalomyelitis.

05 for the comparison with combination A/A, and the daggers P ! 05 for the comparison with combination A/B. The T bars represent standard errors. (From Rieder MJ, Reiner AP, Gage BF, et al. Effect of VKORC1 haplotype on transcriptional regulation and warfarin dose. ) 602 HINES & MCCARVER observed in response to corticosteroid therapy, including instances of frank resistance [56,61], is consistent with genetic variation contributing to differences in response. Acknowledging the complexity of the pathways involved in effecting corticosteroid therapy, Tantisira and colleagues [62] selected 14 candidate genes involved in glucocorticoid synthesis, binding, signaling, and metabolism most likely to influence therapeutic response.

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