Literature DB >> 9574570

Enhanced expression of B7.2 (CD86) in patients with atopic dermatitis: a potential role in the modulation of IgE synthesis.

O Jirapongsananuruk1, M F Hofer, A E Trumble, D A Norris, D Y Leung.   

Abstract

Recent studies have suggested that the accessory molecules B7.1 (CD80) and B7.2 (CD86) differ in their capacity to generate Th1 vs Th2 responses. Atopic dermatitis (AD) is a chronic allergic skin disease associated with increased IgE synthesis. To determine the potential role of B7.2 molecules in AD, the present study was conducted to compare the expression of B7.1 vs B7.2 on B cells from patients with AD vs normal subjects or patients with psoriasis. The expression of B7.2 on B cells of AD patients (53.67 +/- 3.10%) was significantly higher than normals (38.02 +/- 4.95%; p = 0.02) and psoriasis patients (40.19 +/- 2.70%; p = 0.006). In contrast, there was no significant difference in B7.1 expression among the three subject groups. Interestingly, total serum IgE from AD patients and normal subjects correlated significantly with B7.2 expression on B cells (r = 0.68; p = 0.004), suggesting a role for B7.2+ B cells in IgE synthesis. Indeed, purified B7.2+ B cells produced significantly more IgE than B7.2- B cells in vitro (p = 0.04). Anti-human B7.2, but not B7.1, mAb significantly (p < 0.05) decreased IgE production by PBMC stimulated with IL-4 and anti-CD40 mAb. Furthermore, B7.2+ B cells had a significantly higher level of IL-4R and CD23 expression than B7.1+ B cells. These data demonstrate the predominant expression of B7.2 in AD, but not psoriasis, and a novel role for this molecule in IgE synthesis.

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Year:  1998        PMID: 9574570

Source DB:  PubMed          Journal:  J Immunol        ISSN: 0022-1767            Impact factor:   5.422


  11 in total

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Authors:  O Jirapongsananuruk; D Y Leung
Journal:  Clin Exp Immunol       Date:  1999-10       Impact factor: 4.330

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Authors:  W Li; R M D Holsinger; C A Kruse; A Flügel; M B Graeber
Journal:  CNS Neurol Disord Drug Targets       Date:  2013-09       Impact factor: 4.388

4.  The cyclic AMP response element modulator {alpha} suppresses CD86 expression and APC function.

Authors:  Martina Ahlmann; Georg Varga; Karsten Sturm; Ralph Lippe; Konrad Benedyk; Dorothee Viemann; Thomas Scholzen; Jan Ehrchen; Frank U Müller; Matthias Seidl; Marek Matus; George C Tsokos; Johannes Roth; Klaus Tenbrock
Journal:  J Immunol       Date:  2009-04-01       Impact factor: 5.422

5.  A functional CD86 polymorphism associated with asthma and related allergic disorders.

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Journal:  J Med Genet       Date:  2007-05-18       Impact factor: 6.318

6.  Cross-linking of CD80 and CD86 Diminishes Expression of CD54 on EBV-transformed B Cells through Inactivation of RhoA and Ras.

Authors:  Ga Bin Park; Yeong Seok Kim; Hyunkeun Song; Seonghan Kim; Dong Man Park; Wang Jae Lee; Dae Young Hur
Journal:  Immune Netw       Date:  2011-12-31       Impact factor: 6.303

7.  Suppressive activity of a macrolide antibiotic, roxithromycin on co-stimulatory molecule expression on mouse splenocytes in vivo.

Authors:  K Kawazu; M Kurokawa; K Asano; A Mita; M Adachi
Journal:  Mediators Inflamm       Date:  2000       Impact factor: 4.711

8.  Suppressive effects of anti-allergic agent suplatast tosilate (IPD-1151T) on the expression of co-stimulatory molecules on mouse splenocytes in vivo.

Authors:  M Kurokawa; K Kawazu; K Asano; K Fumio; A Mita; M Adachi
Journal:  Mediators Inflamm       Date:  2001-12       Impact factor: 4.711

9.  Inhibitory action of a macrolide antibiotic, roxithromycin, on co-stimulatory molecule expressions in vitro and in vivo.

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Review 10.  Molecular Mechanisms of Cutaneous Inflammatory Disorder: Atopic Dermatitis.

Authors:  Jung Eun Kim; Jong Sic Kim; Dae Ho Cho; Hyun Jeong Park
Journal:  Int J Mol Sci       Date:  2016-07-30       Impact factor: 5.923

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