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Sialic acid cyclization of human Th homing receptor glycan associated with recurrent exacerbations of atopic dermatitis.

Abstract：

BACKGROUND:The molecular pathogenesis underlying recurrent exacerbations of atopic dermatitis (AD) is unclear. Some peripheral CCR4(+) and CCR7(+) helper memory T cells express the specific homing receptor, sialyl 6-sulfo Lewis X (G152 glycan). This glycan loses receptor activity via cyclization of its sialic acid moiety, thus becoming cyclic sialyl 6-sulfo Lewis X (G159 glycan). These findings suggest that the disordered expression of G152 and G159 glycans may be associated with recurrent exacerbations of AD. OBJECTIVE:To assess the possible association of G152 and G159 glycans, which are expressed on peripheral helper T (Th) cells, with frequency of exacerbations. METHODS:The percentage of glycan-expressing cells among peripheral blood CD4(+)CD45RO(+) lymphocytes was determined by flow cytometry. The association of glycans with the frequency of exacerbations determined by recurrence scores as well as with current disease activity was statistically tested. RESULTS:Current disease activity was significantly associated with CCR4(+)CCR7(-) memory Th cells expressing CSLEX-1 glycan, the conventional skin-trafficking receptor without sialic-acid-cyclization activity. In contrast, the frequency of exacerbations was positively and negatively associated with CCR4(+)CCR7(+) memory Th cells expressing G152 and G159 glycans, respectively. Receiver operating characteristics analyses indicated that the ratio of the G152(+)/G159(+) cell percentages discriminated patients with highly recurrent AD with the best accuracy. CONCLUSION:Flow cytometric determination of G159 and G152 glycans on peripheral helper memory T cells may be clinically useful for identifying patients with highly recurrent AD. Disordered sialic acid cyclization of G152 glycan may underlie highly recurrent AD, which may provide a novel therapeutic approach.

journal_name

J Dermatol Sci

journal_title

Journal of dermatological science

authors

Sakuma K,Furuhashi T,Kondo S,Yabe U,Ohmori K,Ito H,Aoki M,Morita A,Kannagi R

doi

10.1016/j.jdermsci.2012.09.015

subject

Has Abstract

pub_date

2012-12-01 00:00:00

pages

187-93

issue

3

eissn

0923-1811

issn

1873-569X

pii

S0923-1811(12)00294-0

journal_volume

68

pub_type

杂志文章

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