ICOS costimulates invariant NKT cell activation

Kuroda, Hiroshi; Takeda, Kazuyoshi; Ota, Tsuyoshi; Kaduka, Yuki; Akiba, Hisaya; Ikarashi, Yoshinori; Wakasugi, Hiro; Kronenberg, Mitchell; Kinoshita, Katsuyuki; Yagita, Hideo; Okumura, Ko

doi:10.1016/j.bbrc.2004.12.004

Cited by 41 publications

(42 citation statements)

References 23 publications

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“…It has been shown that ICOS is also up-regulated on activated NK cells, and it regulates NK cell functions including cytotoxic activity and IFN-c production [38]. Moreover, we have recently demonstrated that NKT cells express ICOS constitutively, which regulates both IFN-c and IL-4 production by NKT cells [39]. Therefore, the inhibition of NK and/or NKT cell function by the blockade of ICOS/B7RP-1 interaction may lead to the exacerbation of EAE and the amelioration of EAU.…”

Section: Discussionmentioning

confidence: 92%

The role of the ICOS/B7RP‐1 T cell costimulatory pathway in murine experimental autoimmune uveoretinitis

et al. 2006

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ICOS/B7RP-1 is a new member of the CD28/B7 family of costimulatory molecules and plays differential roles in autoimmune diseases. In this study, we examined the role of ICOS/B7RP-1 pathway in the pathogenesis of mouse experimental autoimmune uveoretinitis (EAU), an animal model of human autoimmune uveitis. ICOS expression was found on infiltrating CD4 + T cells in the region of the retina in EAU-induced mice. The anti-B7RP-1 monoclonal antibody (mAb)-treated or ICOS-deficient mice showed a substantial reduction of disease scores. Blockade of ICOS/B7RP-1 interaction during the effector phase ameliorated the disease, whereas its blockade during the induction phase exhibited no significant effect. Moreover, administration of anti-B7RP-1 mAb effectively ameliorated the disease induced by adoptive transfer of pathogenic T cells. The anti-B7RP-1 mAb treatment inhibited the expansion and/or effector function of pathogenic T cells, given that proliferative response and IFN-c production by lymph node cells were reduced upon restimulation with the antigen peptide in vitro. These results suggest that the ICOS/B7RP-1 interaction plays a critical role in the pathogenesis of uveitis. We also indicated that ICOS-mediated costimulation plays differential roles in EAU and experimental autoimmune encephalomyelitis, which is also a Th1 disease induced in the same manner as EAU.

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Section: Discussionmentioning

confidence: 92%

The role of the ICOS/B7RP‐1 T cell costimulatory pathway in murine experimental autoimmune uveoretinitis

et al. 2006

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“…The particular costimulatory molecules that could account for this difference and might be lacking from Schwann cells have not yet been determined. However, studies of murine iNKT cells have established that costimulation through CD28 and ICOS are required for maximal responses of these cells, suggesting that the ligands for these costimulatory receptors may be lacking on the Schwann cells that we have studied (44,45).…”

Section: Discussionmentioning

confidence: 99%

Expression of CD1d Molecules by Human Schwann Cells and Potential Interactions with Immunoregulatory Invariant NK T Cells

Im¹,

Tapinos

Chae³

et al. 2006

The Journal of Immunology

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CD1d-restricted NKT cells expressing invariant TCR α-chains (iNKT cells) produce both proinflammatory and anti-inflammatory cytokines rapidly upon activation, and are believed to play an important role in both host defense and immunoregulation. To address the potential implications of iNKT cell responses for infectious or inflammatory diseases of the nervous system, we investigated the expression of CD1d in human peripheral nerve. We found that CD1d was expressed on the surface of Schwann cells in situ and on primary or immortalized Schwann cell lines in culture. Schwann cells activated iNKT cells in a CD1d-dependent manner in the presence of α-galactosylceramide. Surprisingly, the cytokine production of iNKT cells stimulated by α-galactosylceramide presented by CD1d+ Schwann cells showed a predominance of Th2-associated cytokines such as IL-5 and IL-13 with a marked deficiency of proinflammatory Th1 cytokines such as IFN-γ or TNF-α. Our findings suggest a mechanism by which iNKT cells may restrain inflammatory responses in peripheral nerves, and raise the possibility that the expression of CD1d by Schwann cells could be relevant in the pathogenesis of infectious and inflammatory diseases of the peripheral nervous system.

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“…Moreover, MZ B cells have been shown to continuously shuttle between MZ and white pulp, which allows them to transport antigens into the follicles [3]. Remarkably, when compared to other mouse APCs, MZ B cells were found to express high levels of CD1d, the non-classical MHC I molecule responsible for presentation of lipid or glycolipid antigens to NKT cells [4][5][6][7].The major subset of CD1d-restricted murine NKT cells (invariant or type I) expresses a semi-conservative T-cell receptor (TCR) consisting of Va14-Ja18 in conjunction with Vb8.2, Vb7 or Vb2 (7,8,16). This population is able to recognize the glycolipid ligand a-galactosylceramide (aGalCer) bound to CD1d.…”

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“…This population is able to recognize the glycolipid ligand a-galactosylceramide (aGalCer) bound to CD1d. Yet, existence of a smaller, so-called variant (or type II), CD1d-restriced NKT-cell population was also shown [8,9] This population expresses a diverse repertoire of TCRab and is unable to recognize aGalCer.Ã These authors contributed equally to this work. …”

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confidence: 99%

“…However, it is more likely that particular activation situations, i.e. particular co-stimulators, promote differential NKT-cell reactions.NKT cells constitutively express receptors like CD28, CD40L, ICOS and glucocorticoid-induced TNF receptor (GITR) [8,[14][15][16][17][18][19][20]. It has been suggested that engagement of CD40L or CD28 provides important co-stimulatory signals to NKT cells, thus modulating production of cytokines in vitro as well as in vivo [19,21,22].…”

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ICOS‐dependent stimulation of NKT cells by marginal zone B cells

et al. 2011

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Marginal zone (MZ) B cells express high levels of CD1d molecules. In accordance, MZ B cells, like splenic conventional DCs (cDCs), efficiently trigger NKT-cell proliferation. Importantly, MZ B cells exclusively induced production of IL-4 and IL-13 by such cells whereas cDCs induced robust production of mainly IFN-c. NKT-cell proliferation, IL-4 and IL-13 production induced by MZ B cells were dependent on ICOS/ICOS ligand interaction while IFN-c and IL-17 induction by cDCs required glucocorticoid-induced TNF receptor/ glucocorticoid-induced TNF receptor ligand interplay. Our data illustrate that both MZ B cells and cDCs act as efficient APCs for NKT cells and might differentially influence the quality of the subsequent immune response. IntroductionThe marginal zone (MZ) represents a unique structure in spleen that surrounds the primary follicles. It consists of a mixture of different types of cells that include macrophages, DCs, NKT cells as well as so-called MZ B cells. MZ B cells are enriched in germline-encoded specificities with low level of self-reactivity [1]. Therefore, they are maintained in a pre-activated state, which allows them to respond rapidly and T-cell independently to pathogens by antibody production. In addition, MZ B cells express high levels of the complement receptor CD21, which may enhance their response to complement coated antigens. This results in short-lived antibody responses to antigenic determinants expressed on invading viral and encapsulated bacterial species [2]. Due to their strategic location, MZ B cells, in concert with other innate cells, serve as a first line of defense against blood-borne antigens that reach the spleen [1,2]. Beyond their fast and efficient protective antibody response, MZ B cells exhibit additional important functions. They were shown to directly activate T cells and interact with APCs [1]. Moreover, MZ B cells have been shown to continuously shuttle between MZ and white pulp, which allows them to transport antigens into the follicles [3]. Remarkably, when compared to other mouse APCs, MZ B cells were found to express high levels of CD1d, the non-classical MHC I molecule responsible for presentation of lipid or glycolipid antigens to NKT cells [4][5][6][7].The major subset of CD1d-restricted murine NKT cells (invariant or type I) expresses a semi-conservative T-cell receptor (TCR) consisting of Va14-Ja18 in conjunction with Vb8.2, Vb7 or Vb2 (7,8,16). This population is able to recognize the glycolipid ligand a-galactosylceramide (aGalCer) bound to CD1d. Yet, existence of a smaller, so-called variant (or type II), CD1d-restriced NKT-cell population was also shown [8,9] This population expresses a diverse repertoire of TCRab and is unable to recognize aGalCer.Ã These authors contributed equally to this work. 3125The biological function of NKT cells seems paradoxical. They are able to rapidly produce large amounts of either T H 1 or T H 2 as well as T H 17 cytokines [10,11] and might promote immune responses in some settings but suppress cell-mediated immun...

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ICOS costimulates invariant NKT cell activation

Cited by 41 publications

References 23 publications

The role of the ICOS/B7RP‐1 T cell costimulatory pathway in murine experimental autoimmune uveoretinitis

The role of the ICOS/B7RP‐1 T cell costimulatory pathway in murine experimental autoimmune uveoretinitis

Expression of CD1d Molecules by Human Schwann Cells and Potential Interactions with Immunoregulatory Invariant NK T Cells

ICOS‐dependent stimulation of NKT cells by marginal zone B cells

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