title: Alteration in the production of IL-10 and IL-12 and aberrant expression of CD23, CD83 and CD86 by monocytes or monocyte-derived dendritic cells from atopic dermatitis patients.
abstract: Atopic dermatitis (AD) is characterized by the presence of Th2-type cells in the skin infiltration as well as in the peripheral blood, although a predominant infiltration of interferon-gamma (IFN-gamma)-producing cells is also reported in the chronic skin lesions of AD. Recently it has become clear that the development of Th1 or Th2 is strongly influenced by factors produced by the antigen presenting cells (APCs). To clarify whether APCs from AD patients play a favorable role in the differentiation of Th2 cells, we compared the production of cytokines and the expression of co-stimulatory molecules by monocytes (MOs) and monocyte-derived DCs (MoDCs) after stimulations with various reagents between 13 AD patients and 13 age-matched healthy controls. We examined their production of IL-1 beta, IL-10, IL-12p40, and IL-12p70, and their expression of CD23, CD40, CD54, CD80, CD83, CD86 and HLA-DR. We stimulated them with superantigens, lipopolysaccharide (LPS), agonistic anti-CD40 antibody, phytohemagglutinins (PHA), IL-1beta/TNF-alpha, IL-4, or IFN-gamma. The following results were obtained (1): IL-10 production was significantly enhanced in AD MOs after LPS stimulation. In contrast, IL-12p40 production was significantly lower in AD MOs than in HC MOs after a variety of stimulations (2). IL-12p40 was also significantly lower in AD MoDCs after LPS stimulation (3). The induction of CD23 with IL-4 was significantly higher in AD MOs. and finally (4), AD MoDCs augmented the expression of CD83, CD86, and HLA-DR less significantly than HC MoDCs after anti-CD40 Ab stimulation. These data indicate that AD APCs show some responses different from those observed in HC APCs after several stimulations, such as LPS, IL-1 beta/TNF-alpha, IL-4, or anti-CD40 Ab, and that these responses might play a role in the polarizing process of helper T cells into Th2 cells as recognized in AD patients.
authors.affiliation: Department of Dermatology, Tohoku University School of Medicine, Aobaku, Sendai, Japan. aiba@mail.cc.tohoku.ac.jp
authors.forename: Setsuya
authors.initials: S
authors.lastname: Aiba
authors.forename: Hideaki
authors.initials: H
authors.lastname: Manome
authors.forename: Yumiko
authors.initials: Y
authors.lastname: Yoshino
authors.forename: Hachiro
authors.initials: H
authors.lastname: Tagami
mesh_terms: D000293:Adolescent; D000328:Adult; D015703:Antigens, CD / Q000378:metabolism*; D051940:B7-2 Antigen; D016022:Case-Control Studies; D002460:Cell Line; D003713:Dendritic Cells / Q000378:metabolism*; D003876:Dermatitis, Atopic / Q000378:metabolism*; D005260:Female; D006801:Humans; D007136:Immunoglobulins / Q000378:metabolism; D016753:Interleukin-10 / Q000378:metabolism*; D018664:Interleukin-12 / Q000378:metabolism*; D008297:Male; D008562:Membrane Glycoproteins / Q000378:metabolism; D009000:Monocytes / Q000378:metabolism*; D017455:Receptors, IgE / Q000378:metabolism; D013268:Stimulation, Chemical; D000097802:CD83 Antigen
chemical_list: D015703:Antigens, CD; D051940:B7-2 Antigen; D007136:Immunoglobulins; D016753:Interleukin-10; D018664:Interleukin-12; D008562:Membrane Glycoproteins; D017455:Receptors, IgE; D000097802:CD83 Antigen; C497964:CD86 protein, human