Identification of cutaneous lymphocyte-associated antigen as sialyl 6-sulfo Lewis X, a selectin ligand expressed on a subset of skin-homing helper memory T cells

Ohmori, Katsuyuki; Fukui, Fumiyo; Kiso, Makoto; Imai, Toshio; Yoshie, Osamu; Hasegawa, Hitoshi; Matsushima, Kouji; Kannagi, Reiji

doi:10.1182/blood-2005-05-2185

Cited by 55 publications

(54 citation statements)

References 49 publications

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“…The binding between sLe x and selectins has been known to be important for regulation of leukocyte migration into inflamed tissues [28 -30]. Recently, it had been reported that the CLA, recognized by the HECA-452 antibody against sialyl 6-sulfo Lewis x antigen, was expressed on a subset of memory CD4 ϩ T cells [18]. In addition, it has been indicated that the HECA-452-defining CLA, binding with E-, P-, and L-selectins, was closely related with skin homing of memory Th cells [19].…”

Section: Discussionmentioning

confidence: 99%

“…One of the most important oligosaccharides is a fucose-containing tetrasaccharide, serving sialyl Lewis x (sLe x ) as a ligand for the adhesion molecules such as E-selectin and P-selectin on endothelial cells [16,17]. It had been reported that the cutaneous lymphocyte-associated antigen (CLA), recognized by HECA-452 antibody against sialyl 6-sulfo Lewis x antigen, was expressed on a subset of memory CD4 ϩ T cells [18]. In addition, it has been revealed that the HECA-452 defining CLA, binding with E-, P-, and L-selectins, was closely related with skin homing of memory Th cells [19].…”

Section: Introductionmentioning

confidence: 99%

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Sialyl lewisx antigen-expressing human CD4+ T and CD8+ T cells as initial immune responders in memory phenotype subsets

Zhang

Ohkuri

Wakita

et al. 2008

Journal of Leukocyte Biology

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Sialyl lewisx antigen-expressing human CD4+ T and CD8+ T cells as initial immune responders in memory phenotype subsets

Zhang

Ohkuri

Wakita

et al. 2008

Journal of Leukocyte Biology

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“…Sialyl Lewis X determinant, the specific carbohydrate ligand for selectins, is constitutively expressed on granulocytes and monocytes and mediates inflammatory extravasation of these cells (4)(5)(6). Most resting peripheral T and B lymphocytes, on the other hand, lack its expression, and are induced to strongly express sialyl Lewis X upon activation (7,8). Among T lymphocytes, the sialyl Lewis X determinant is known to be preferentially expressed on activated Th1 cells but not on Th2 cells (9).…”

mentioning

confidence: 99%

“…The induction of sialyl Lewis X on lymphocytes accompanies transcriptional activation of fucosyltransferase VII gene (FUT7), which is involved in the last step of sialyl Lewis X synthesis (8,(10)(11)(12)(13)(14)(15). Previously, we have shown that the human FUT7 promoter is equipped with binding sites for the cAMP response element (CRE)-binding protein (CREB)͞activating transcription factor (ATF) family, myeloid zinc finger protein 1 (MZF-1) and Sp1 (16,17), and also GATA and T-bet (3).…”

mentioning

confidence: 99%

Interaction of GATA-3/T-bet transcription factors regulates expression of sialyl Lewis X homing receptors on Th1/Th2 lymphocytes

Chen

Osada

Santamaria‐Babí

et al. 2006

Proc. Natl. Acad. Sci. U.S.A.

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Selectin-dependent cell adhesion mediates inflammatory extravasation and routine homing of lymphocytes. Most resting peripheral T lymphocytes lack expression of sialyl Lewis X, the carbohydrate ligand for selectins, and are induced to strongly express it upon activation. T helper 1 (Th1) cells are known to more preferentially express sialyl Lewis X as compared with T helper 2 (Th2) cells upon activation. The molecular basis for this preferential expression, however, has not been elucidated to date. Here we show that the gene for fucosyltransferase VII (FUT7), the rate-limiting enzyme for sialyl Lewis X synthesis, is a unique example of the human genes with binding sites for both GATA-3 and T-bet, two opposing factors for Th1 and Th2 development, and is regulated transcriptionally by a balance of the two interacting transcription factors. T-bet promotes and GATA-3 represses FUT7 transcription. Our results indicated that T-bet interferes with the binding of GATA-3 to its target DNA, and also that GATA-3 significantly interferes with the binding of T-bet to the FUT7 promoter. T-bet has a binding ability to GATA-3, CBP͞P300, and Sp1 to form a transcription factor complex, and GATA-3 regulates FUT7 transcription by phosphorylationdependently recruiting histone deacetylase (HDAC)-3͞HDAC-5 and by competing with CBP͞P300 in binding to the N terminus of T-bet. Suppression of GATA-3 activity by dominant-negative GATA-3 or repressor of GATA (ROG) was necessary to attain a maximum expression of FUT7 and sialyl Lewis X in human T lymphoid cells. These results indicate that the GATA-3͞T-bet transcription factor complex regulates the cell-lineage-specific expression of the lymphocyte homing receptors.fucosyltransferase ͉ helper memory T cells ͉ lymphocyte homing ͉ selectin ͉ GATA-3͞HDAC-3 interaction

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“…Human T cells express cutaneous lymphocyte Ag (CLA), a ligand for E-selectin (15), and they upregulate CLA after activation in vitro (16,17). In skin biopsies of patients with atopic dermatitis and psoriasis, 80-90% of CD4 and CD8 T cells express CLA (10,18).…”

mentioning

confidence: 99%

Differing Requirements for CCR4, E-Selectin, and α4β1 for the Migration of Memory CD4 and Activated T Cells to Dermal Inflammation

Gehad

Al-Banna

Vaci

et al. 2012

The Journal of Immunology

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CCR4 on T cells is suggested to mediate skin homing in mice. Our objective was to determine the interaction of CCR4, E-selectin ligand (ESL), and α4β1 on memory and activated T cells in recruitment to dermal inflammation. mAbs to rat CCR4 were developed. CCR4 was on 5–21% of memory CD4 cells, and 20% were also ESL+. Anti–TCR-activated CD4 and CD8 cells were 40–55% CCR4+, and ∼75% of both CCR4+ and CCR4− cells were ESL+. CCR4+ memory CD4 cells migrated 4- to 7-fold more to dermal inflammation induced by IFN-γ, TNF, TLR agonists, and delayed-type hypersensitivity than CCR4− cells. CCR4+ activated CD4 cells migrated only 5–50% more than CCR4− cells to these sites. E-selectin blockade inhibited ∼60% of CCR4+ activated CD4 cell migration but was less effective on memory cells where α4β1 was more important. Anti-α4β1 also inhibited CCR4− activated CD4 cells more than CCR4+ cells. Anti–E-selectin reduced activated CD8 more than CD4 cell migration. These findings modify our understanding of CCR4, ESL, α4β1, and dermal tropism. There is no strict relationship between CCR4 and ESL for skin homing of CD4 cells, because the activation state and inflammatory stimulus are critical determinants. Dermal homing memory CD4 cells express CCR4 and depend more on α4β1 than ESL. Activated CD4 cells do not require CCR4, but CCR4+ cells are more dependent on ESL than on α4β1, and CCR4− cells preferentially use α4β1. The differentiation from activated to memory CD4 cells increases the dependence on CCR4 for skin homing and decreases the requirement for ESL.

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Identification of cutaneous lymphocyte-associated antigen as sialyl 6-sulfo Lewis X, a selectin ligand expressed on a subset of skin-homing helper memory T cells

Abstract: We previously identified the carbohydrate determinant sialyl 6-sulfo Lewis X (Le x ) as the major L-selectin ligand on high endothelial venules of peripheral lymph nodes. In this study, we examined the distribution of the sialyl 6-sulfo Le x determinant among peripheral lymphocytes.

Cited by 55 publications

References 49 publications

Sialyl lewisx antigen-expressing human CD4+ T and CD8+ T cells as initial immune responders in memory phenotype subsets

Sialyl lewisx antigen-expressing human CD4+ T and CD8+ T cells as initial immune responders in memory phenotype subsets

Interaction of GATA-3/T-bet transcription factors regulates expression of sialyl Lewis X homing receptors on Th1/Th2 lymphocytes

Differing Requirements for CCR4, E-Selectin, and α4β1 for the Migration of Memory CD4 and Activated T Cells to Dermal Inflammation

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