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[2] O'Neill LA. Therapeutic targeting of Toll-like receptors for inflammatory and infectious diseases. Curr Opin Pharmacol, 2003, 3: 396-403.
[3] Bochud PY, Hawn TR, Aderem A. Cutting edge: a Toll-like receptor2 polymorphism that is associated with lepromatous leprosy is unable to mediate mycobacterial signaling. J Immunol, 2003, 170:3451-3454.
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[11] Deva R, Shankaranarayanan P, Ciccoli R, et al. Candida albicans induces selectively transcriptional activation of cyclooxygenase-2 in HeLa cells: pivotal roles of Toll-like receptors, p38 mitogen-activated protein kinase, and NF-kappa B. J Immunol, 2003, 171:3047-3055.
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[17] Kim J, Ochoa MT, Krutzik SR, et al. Activation of toll-like receptor2 in acne triggers inflammatory cytokine responses. J Immunol, 2002,169:1535-1541.
[18] Koreck A, Pivarcsi A, Dobozy A, et al. The role of innate immunity in the pathogenesis of acne. Dermatology, 2003, 206:96-105.
[19] Dubertret L. Which steroids for the treatment of skin disorders on the face? J Eur Acad Dermatol Venereol, 2002, 16: 121.
[20] Rui L, Vinuesa CG, Blasioli J,et al. Resistance to CpG DNA-induced autoimmunity through tolerogenic B cell antigen receptor ERK signaling. Nat Immunol, 2003, 4:594-600.
[21] Januchowski R, Prokop J, Jagodzinski PP. Role of epigenetic DNA alterations in the pathogenesis of systemic lupus erythematosus. J Appl Genet, 2004,45:237-248.
[22] Miyata M, Ito O, Kobayashi H, et al. CpG-DNA derived from sera in systemic lupus erythematosus enhances ICAM-1 expression on endothelial cells. Ann Rheum Dis, 2001,60:685-689.
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