Expression of intercellular adhesion molecule-1 in murine hearts with acute myocarditis caused by coxsackievirus B3.

Seko, Yoshinori; Matsuda, Hiroaki; Kato, Kiminori; Hashimoto, Yuichi; Yagita, Hideo; Okumura, Katsuhiko; Yazaki, Yoshio

doi:10.1172/jci116333

Cited by 109 publications

(60 citation statements)

References 37 publications

(21 reference statements)

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“…Hybridomas producing anti-LFA-1 and anti-ICAM-1 mAbs (KBA and KAT-1, respectively) were described previously (32,33). Hybridomas producing anti-B7-1 and anti-B7-2 mAbs (1G10 and GL1, respectively) were purchased from American Type Culture Collection (ATCC).…”

Section: Materials and Methods Mabs And Reagentsmentioning

confidence: 99%

Requirement for natural killer T (NKT) cells in the induction of allograft tolerance

Seino

Fukao

Muramoto

et al. 2001

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

234

185

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Together, these findings indicate that V␣14͞V␤8.2 is a unique antigen receptor for NKT cells but not for conventional T cells. Because V␣14 NKT cell development was inhibited largely in mice that lack the MHC class I-like molecule CD1d, positive selection of V␣14-expressing immature NKT cells requires CD1d expression (14,15). Recently, it has been shown that glycolipid, ␣-galactosylceramide (␣-GalCer), and glycosylphosphatidylinositol-anchored proteins can be presented by murine CD1d (13, 16). Subsequently, it was demonstrated that NKT cells can recognize cellular lipids or purified phospholipids distinct from ␣-GalCer (17).Although physiological functions of NKT cells remain obscure, some studies have suggested that NKT cells can control autoimmune diseases (18-21) and Th1͞Th2 cell development Here, we have evaluated the role of V␣14 NKT cells in allograft rejection and tolerance by using a murine model of transplantation. We found that V␣14 NKT cells play a critical role in the induction of vascularized cardiac allograft tolerance by blockade of lymphocyte function-associated antigen-1 (LFA-1)͞intercellular adhesion molecule-1 (ICAM-1) or CD28͞B7 interactions. Possible mechanisms for the tolerogenic function of V␣14 NKT cells are examined. Materials and Methods mAbs and Reagents.Hybridomas producing anti-LFA-1 and anti-ICAM-1 mAbs (KBA and KAT-1, respectively) were described previously (32, 33). Hybridomas producing anti-B7-1 and anti-B7-2 mAbs (1G10 and GL1, respectively) were purchased from American Type Culture Collection (ATCC). Hybridoma producing anti-IL-4 mAb (11B11) also was purchased from ATCC. These mAbs were purified from ascites by using protein G column. mAbs against CD1d (1B1) and H-2K b (AF6-88.5, FITC-labeled) were purchased from PharMingen. An annexin V PE staining kit was purchased from PharMingen.

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Section: Materials and Methods Mabs And Reagentsmentioning

confidence: 99%

Requirement for natural killer T (NKT) cells in the induction of allograft tolerance

Seino

Fukao

Muramoto

et al. 2001

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

234

185

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“…YNK1.3 cells were stained by antibodies against various cell surface molecules; anti-CD25 (anti-IL-2 receptor, 7D4, ATCC), anti-a4-integrin (R1-2), anti-CD28, antib 7-integrin, anti-CD69 (PharMingen, San Diego, Calif., USA), and anti-CD54 (KAT-1) mAbs [11]. FITC-conjugated antimouse IgM (Cappel, Westchester, Penn., USA) was used for anti-CD25, FITC-conjugated anti-hamster antibody (Cederlane, Homby, Ontario, Canada) for anti-CD28, and FITC-conjugated anti-rat IgG (Cappel) for anti-a4-integrin, anti-b7-integrin, anti-CD69, and anti-CD54 mAbs.…”

Section: Generation Of Islet-specific Cd8 T-cell Clones Cd8 T-cell Lmentioning

confidence: 99%

CD8 cytotoxic T-cell clone rapidly transfers autoimmune diabetes in very young NOD and MHC class I-compatible scid mice

et al. 1997

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Nonobese diabetic (NOD) mice spontaneously develop an autoimmune diabetes resembling human insulin-dependent diabetes mellitus (IDDM). Several lines of evidence suggest that T cells are responsible for mononuclear cell infiltration into the islets (insulitis) and destruction of beta cells in NOD mice. Disease transfer studies have shown that both splenic CD4 and CD8 T cells from diabetic NOD mice are necessary to transfer diabetes to newborn or sublethally irradiated NOD mice [1, 2] and islet-specific CD4 and CD8 T-cell clones are both required before significant insulitis develops in irradiated NOD mice [3]. However, islet-specific CD4 T-cell clones have been found to cause diabetes when injected into unmanipulated young NOD mice [4] or NOD F1 mice [5]. In addition, CD4 T cells from diabetic NOD donors have also been shown to transfer disease into NOD-severe combined immunodeficient (scid) mice

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“…It has been reported that excessive release of NO strongly damages myocardial cells (Mikami et al, 1996). Infiltration by inflammatory cells, including T cells and natural killer cells, peaks 7-14 days after viral infection and causes widespread necrosis of myocardial cells (Seko et al, 1993). As already noted, infected virus and released inflammatory cytokines are the main mechanisms in the development of myocardial dysfunction during the acute phase.…”

Section: Development and Strategy For Treatment During The Acute Phasementioning

confidence: 84%

Acute Myocarditis in Emergency Medicine

Ikegami¹,

Tase²

2011

Myocarditis

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Expression of intercellular adhesion molecule-1 in murine hearts with acute myocarditis caused by coxsackievirus B3.

Cited by 109 publications

References 37 publications

Requirement for natural killer T (NKT) cells in the induction of allograft tolerance

Requirement for natural killer T (NKT) cells in the induction of allograft tolerance

CD8 cytotoxic T-cell clone rapidly transfers autoimmune diabetes in very young NOD and MHC class I-compatible scid mice

Acute Myocarditis in Emergency Medicine

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