Tissue distribution, regulation and intracellular localization of murine CD1 molecules

Mandal, Mihir; Chen, X R; Alegre, Maria Luisa; Chiu, Nancy M.; Chen, Y H; Castaño, A. Raúl; Wang, C R

doi:10.1016/s0161-5890(98)00055-8

Cited by 84 publications

(76 citation statements)

References 48 publications

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“…A large number of CD1d ϩ cells rapidly appear in the hearts of H3-infected BALB/c mice. The nature of these cells in not known, but presumably represent various lymphoid cells infiltrating the heart and may even be the ␥␦ ϩ cells themselves (16,34).…”

Section: Discussionmentioning

confidence: 99%

“…Some reports find that multiple cytokines can up regulate CD1d expression on various tumor cell lines including IFN-␥, IL-4, IL-10, and GM-CSF (31). Other investigators find constitutive expression of CD1d without marked enhancement by these cytokines (34,43,44), although activation of T cells can up-regulate CD1d expression through unknown mechanisms (45). Since infections with H3 virus induce high expression of at least certain cytokines (TNF-␣; Ref.…”

Section: Discussionmentioning

confidence: 99%

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Role of CD1d in Coxsackievirus B3-Induced Myocarditis

Huber

Sartini

Exley

2003

The Journal of Immunology

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The myocarditic (H3) variant of Coxsackievirus B3 (CVB3) causes severe myocarditis in BALB/c mice and BALB/c mice lacking the invariant Jα281 gene, but minimal disease in BALB/c CD1d−/− animals. This indicates that CD1d expression is important in this disease but does not involve the invariant NKT cell often associated with CD1d-restricted immunity. The H3 variant of the virus increases CD1d expression in vitro in neonatal cardiac myocytes whereas a nonmyocarditic (H310A1) variant does not. Vγ4+ T cells show increased activation in both H3-infected BALB/c and Jα281−/− mice compared with CD1d−/− animals. The activated BALB/c Vγ4+ T cells from H3-infected mice kill H3-infected BALB/c myocytes and cytotoxicity is blocked with anti-CD1d but not with anti-MHC class I (Kd/Dd) or class II (IA/IE) mAbs. In contrast, H3 virus-infected CD1d−/− myocytes are not killed. These studies demonstrate that CD1d expression is essential for pathogenicity of CVB3-induced myocarditis, that CD1d expression is increased early after infection in vivo in CD1d+ mice infected with the myocarditic but not with the nonmyocarditic CVB3 variant, and that Vγ4+ T cells, which are known to promote myocarditis susceptibility, appear to recognize CD1d expressed by CVB3-infected myocytes.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Role of CD1d in Coxsackievirus B3-Induced Myocarditis

Huber

Sartini

Exley

2003

The Journal of Immunology

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“…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). Similar in structure to MHC class Ia, CD1d associates with ␤ 2 -microglobulin, has three extracellular domains (␣1, ␣2, and ␣3), a transmembrane region, and a short cytoplasmic tail.…”

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

confidence: 99%

“…Allophycocyanin-CD1d/␣GalCer tetramers were prepared as described by Matsuda et al (47). The CD1d-specific mAb 5C6 (hamster IgG) has been described previously (5). Anti-H2-K b , Y3, was obtained from the American Type Culture Collection (Manassas, VA).…”

Section: Cell Preparation and Flow Cytometrymentioning

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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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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“…9,26 -28 Invariant TCR ϩ CD1d-reactive T cells (invariant NKT cells) represent up to 50% of rodent intrahepatic lymphocytes, 29 which is also consistent with expression of the restricting element CD1d within the mammalian liver. 3,7,30,31 Most rodent invariant NKT cells of appropriate strains express the CD161 (NKR-P1) NK1.1 allele, 9 as do the human orthologues, 12 in addition to a variety of cell surface markers classically associated with NK cells; these include CD56, CD69, CD94, and CD161, and, in some cases (at least in mice), killer inhibitory receptors of the C-type lectin NK locus Ly49-type. 9,10,12,26,32 Classical invariant NKT cells are typically either CD4 ϩ or are CD4 Ϫ /CD8 Ϫ (double negative), although in the human there is an appreciable CD8 ϩ subset.…”

mentioning

confidence: 99%

To be or not to be NKT: Natural killer T cells in the liver

2004

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N KT cells are a diverse group of cells that share features of both classical T cells and natural killer (NK) cells, and have similarly diverse functions. One of the complexities in understanding NKT cells involves sorting through the various terminology that has been applied to them in the emerging literature. 1,2 Functionally, a major subset of these cells are defined by reactivity against CD1d, which is one of five known glycolipid-binding nonpolymorphic major histocompatibility complex class 1-like glycoproteins: CD1a through e. 3 These glycoproteins appear to have evolved to facilitate recognition of nonprotein antigens-specifically glycolipid antigens, including those present in the cell walls of mycobacterial species. CD1d is constitutively expressed on a number of hematopoietic-derived antigenpresenting cell (APC) types-including B cells and myeloid cells-and can be expressed by human T cells as well as healthy hepatocytes. Physiological ligands for CD1d remain poorly defined, although both glycolipids and hydrophobic peptides bind to CD1 family molecules. 4,5 Most antigen studies have used the synthetic glycolipid ␣-galactosylceramide (␣GalCer), which binds to CD1d and activates a specific subset of both murine and human NKT cells in vitro and in vivo. 5,6 CD1d is remarkably conserved across mammalian species, with mouse and human CD1d having greater than 90% sequence homology. 7 Consequently, murine CD1d-reactive T cells recognize human CD1d, and vice versa. 8 After activation, NKT cells are highly versatile and can produce large amounts of interferon gamma (IFN-␥) and interleukin (IL)-4 9,10 as prototypic type 1 and type 2 cytokines, respectively, as well as display NK/lymphokine-activated killing-like FasL-mediated or perforin-dependent CD1d-specific cytotoxicity 11-14 thus potentially contributing to protective and pathogenic responses against multiple infectious agents and tumors.CD1d is expressed by dendritic cells (DCs), and ␣Gal-Cer-loaded DCs mediate activation of invariant NKT cells. [15][16][17][18] Although peripheral NKT cells can recognize and respond to other CD1d ϩ cells, their in vivo activation may be initiated by interactions with DCs and possibly B cells. The interactions between invariant NKT cells and DCs share many features of interactions between conventional CD4 ϩ T cells and DCs. DCs pulsed with ␣GalCer stimulate NKT cells through T cell receptor (TCR) ligation. 2,19,20 NKT cell activation and IFN-␥ production are markedly enhanced by DC-produced IL-12, with an increase in the IL-12 receptor on activated NKT cells. 15,21,22 Conversely, invariant NKT cells also interact with ␣Gal-Cer-loaded DCs to enhance CD4 ϩ and CD8 ϩ T-cell responses 16,17,23,24 and with B cells to provide help for antibody production. 25 However, ␣Galcer is not a physiological antigen, and it is not yet clear whether physiological NKT-DC interactions are mediated by specific CD1d-presented antigens or are antigen independent.The classical CD1d-reactive NKT cell population expresses a highly restricted TCR r...

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Tissue distribution, regulation and intracellular localization of murine CD1 molecules

Cited by 84 publications

References 48 publications

Role of CD1d in Coxsackievirus B3-Induced Myocarditis

Role of CD1d in Coxsackievirus B3-Induced Myocarditis

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

To be or not to be NKT: Natural killer T cells in the liver

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