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Lucas A. C. Brandão, BSc; Rafael L. Guimarães, BSc; Matilde Carrera, MD; Michele Milanese, BSc; Ludovica Segat, BSc; José Luiz de Lima-Filho, MD; Luiz Claudio Arraes, MD; Sergio Crovella, PhD

Arch Dermatol. 2008;144(3):412-413.

	Since this article does not have an abstract, we have provided the first 150 words of the full text and any section headings.

Atopic dermatitis (AD) is a chronic inflammatory skin disease. Patients with AD have a cutaneous immune defect, and innate immunity has been suggested to play a possible role in the cause of AD.¹

Mannose-binding lectin (MBL) is an important molecule of the immune system able to activate the complement system and induce phagocytosis. Deficiencies of MBL have been associated with increased susceptibility to infections, autoimmunity, and other diseases.²

In the present article, we analyze functional allelic variants in the MBL2 gene (GenBank 4153) (namely, allele A/0 in exon 1 and H/L and X/Y in the promoter) in 165 Brazilian children with AD and adult controls. Our aim was to investigate an association between MBL defective-producer genotypes and susceptibility to . . . [Full Text of this Article]

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