Mouse CD1 is distinct from and co-exists with TL in the same thymus.

Bradbury, Andrew; Belt, Katharina; Néri, Tui; Milstein, C.; Calabi, Franco

doi:10.1002/j.1460-2075.1988.tb03173.x

Cited by 134 publications

(79 citation statements)

References 30 publications

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“…Wang., unpublished results). Additionally, CD1d genes are located outside of the MHC in both mice and humans (3,57). The segregation of these two gene complexes during evolution may facilitate the development of different regulatory mechanisms to control the expression of these Ag-presenting molecules.…”

Section: Discussionmentioning

confidence: 99%

“…In this study, we show that cell type-specific expression levels of CD1d establish a narrow window between positive and negative selection, suggesting that the distinct CD1d expression pattern may be selected evolutionarily to ensure optimal output of NKT cells. T he CD1 molecules are MHC-unlinked class Ib molecules that have been conserved throughout mammalian evolution (1)(2)(3). The mouse CD1d is relatively nonpolymorphic and widely expressed on cells of multiple hemopoietic lineages, including B and T cells, macrophages, and dendritic cells (DCs) 5 (4 -6).…”

Section: Expression Of Cd1d Under the Control Of A Mhc Class Iamentioning

confidence: 99%

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Expression of CD1d Under the Control of a MHC Class Ia Promoter Skews the Development of NKT Cells, But Not CD8+ T Cells

Chun

Colmone

et al. 2003

The Journal of Immunology

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Although CD1d and MHC class Ia share similar overall structure, they have distinct levels and patterns of surface expression. While the expression of CD1d1 is known to be essential for the development of NKT cells, the contribution of CD1d1 to the development of CD8+ T cells appears to be inconsequential. To investigate whether CD1d tissue distribution and expression levels confer differential capacity in selecting these two T cell subsets, we analyzed CD8 and NKT cell compartments in Kb-CD1d-transgenic mice that lack endogenous MHC class Ia and CD1d, respectively. We found that MHC class Ia-like expression pattern and tissue distribution are not sufficient for CD1d to rescue the development of CD8+ T cells, suggesting that unique structural features of CD1d preclude its active participation in selection of CD8+ T cells. Conversely, cell type-specific CD1d surface density is important for the selection of NKT cells, as the NKT cell compartment was only partially rescued by the Kb-CD1d transgene. We have previously demonstrated that increased CD1d expression on dendritic cells enhanced negative selection of NKT cells. In this study, we show that cell type-specific expression levels of CD1d establish a narrow window between positive and negative selection, suggesting that the distinct CD1d expression pattern may be selected evolutionarily to ensure optimal output of NKT cells.

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Section: Discussionmentioning

confidence: 99%

Section: Expression Of Cd1d Under the Control Of A Mhc Class Iamentioning

confidence: 99%

Expression of CD1d Under the Control of a MHC Class Ia Promoter Skews the Development of NKT Cells, But Not CD8+ T Cells

Chun

Colmone

et al. 2003

The Journal of Immunology

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“…There is a variation in the number of CD1 genes present in different mammalian genomes. Rodents have only two, but rabbits may well contain eight or more CD1 genes (Bradbury et al, 1988;Calabi et al, 1989a). The human R3 (CDID) gene is more homologous to the mouse CD1 than to the other four (classic) human CDl genes in the leader, et1 and cx2 exons, and further sequence analysis with two rabbit CD1 genes has allowed categorization of CD1 genes into two classes, separating the R3 (CDID) from the CDIA, -B, -C classic genes.…”

Section: Introductionmentioning

confidence: 99%

A physical map linking the five CD1 human thymocyte differentiation antigen genes.

Milstein

1989

The EMBO Journal

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Human CD1 is a family of thymocyte differentiation antigens which consist of heavy chains with mol. wts between 43 and 49 kd binding to beta 2 microglobulin. They are distant relatives of the major histocompatibility complex (MHC) class I and II products. Five human CD1 genes have been described. Three (CD1A, ‐B and ‐C) code for the serologically defined CD1a, ‐b and ‐c antigens. The protein products of the other two genes, CD1D and CD1E, remain unknown. All CD1 genes are located on chromosome 1 and hence are independent of the MHC locus. In this paper, the tight linkage of the CD1 genes has been established by pulse field gel electrophoresis, cosmid cloning and walking techniques. The 190 kb of DNA linking all five CD1 genes has been spanned by 14 overlapping cosmids. The order of the genes in the CD1 complex is CD1D‐CD1A‐CD1C‐CD1B‐CD1E, and, with the exception of CD1B, they are arranged in the same transcriptional orientation. The genes are evenly spaced in the complex except for the distance between CD1D and CD1A, which is two to three times greater than the average.

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“…iNKT cells also partially inhibit autoreactive B cells in a CD1d-dependent manner [24]. Despite two highly homologous CD1d genes in mice, CD1d1 and CD1d2 [25], the expression of the latter is not sufficient for the development and function of iNKT cells [26]. Interestingly, recent studies have shown that patients with SLE display reduced peripheral iNKT cell frequencies, and lipid-antigen presentation by CD1d + B cells is essential for the homeostasis of iNKT cells [27].…”

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confidence: 99%

TLR9‐induced miR‐155 and Ets‐1 decrease expression of CD1d on B cells in SLE

et al. 2015

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B cells present lipid antigens to CD1d-restricted invariant natural killer T (iNKT) cells to maintain autoimmune tolerance, and this process is disrupted in systemic lupus erythematosus (SLE). Inflammation may inhibit CD1d expression to exacerbate the pathology of lupus. However, how inflammation regulates CD1d expression on B cells is unclear in SLE.In the present study, we showed that the surface expression of CD1d on B cells from SLE mice was decreased and that stimulation of inflammatory responses through TLR9 decreased the membrane and total CD1d levels of CD1d on B cells. Moreover, inflammation-related microRNA-155 (miR-155) negatively correlated with the expression of CD1d in B cells. miR-155 directly targeted the 3 -untranslated region (3 -UTR) of CD1d upon TLR9 activation in both humans and mice. The inhibitory effects of miR-155 on CD1d expression in B cells impaired their antigen-presenting capacity to iNKT cells. In addition, Ets-1, a susceptibility gene of SLE, also directly regulated the expression of the CD1d gene at the transcriptional level. These findings provide new insight into the mechanism underlying decreased CD1d expression on B cells in SLE, suggesting that inhibition of inflammation may increase CD1d expression in B cells to ameliorate SLE via modulating iNKT cells.Keywords: B cells r CD1d r Ets-1 r miR-155 r SLE Additional supporting information may be found in the online version of this article at the publisher's web-site IntroductionSystemic lupus erythematosus (SLE) is a complex and chronic autoimmune disease with an unclear etiology [1]. B cells play a central role in the pathogenesis of SLE [2], and patients with SLE exhibit abnormal B-cell activation and increased sensitivity and proliferation of B cells [3]. Moreover, the Correspondence: Dr. Yayi Hou e-mail: yayihou@nju.edu.cn clinical success of B-cell depletion therapy further proves the important role of B cells in SLE pathogenesis [4,5]. B cells not only produce antibodies and release cytokines and chemokines but also present both peptide and lipid antigens [6].CD1 family molecules are nonclassical MHC proteins related to the class I MHC proteins and are involved in the presentation of lipid antigens to T cells. Several studies have suggested that CD1d may play an immunoregulatory role in the development of lupus, and CD1d deficiency exacerbates lupus nephritis in the pristineinduced model [7] and inflammatory dermatitis in MRL-lpr/lpr C 2015 WILEY-VCH Verlag GmbH & Co. KGaA, Weinheim www.eji-journal.eu Eur. J. Immunol. 2015. 45: 1934-1945 Cellular immune response 1935 mice [8]. Importantly, endogenous DNA stimulates inflammatory responses through TLR9 and exacerbates lupus disease pathology [9,10]. Viral infection could downregulate the expression of CD1d in APCs, such as B cells [11,12], DCs, and macrophages [13]. A number of exogenous viruses, especially Epstein-Barr virus (EBV) [14,15], also have been linked to the pathogenesis of SLE [16]. Our previous studies have indicated that ligands for both TLR9 and TLR7 lead to B...

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Mouse CD1 is distinct from and co-exists with TL in the same thymus.

Cited by 134 publications

References 30 publications

Expression of CD1d Under the Control of a MHC Class Ia Promoter Skews the Development of NKT Cells, But Not CD8+ T Cells

Expression of CD1d Under the Control of a MHC Class Ia Promoter Skews the Development of NKT Cells, But Not CD8+ T Cells

A physical map linking the five CD1 human thymocyte differentiation antigen genes.

TLR9‐induced miR‐155 and Ets‐1 decrease expression of CD1d on B cells in SLE

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