研究者詳細 - 松崎　吾朗

論文 - 松崎　吾朗

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In Vivo Analysis of the Anti-allergic Activities of Camellia japonica Extract and Okicamelliaside, a Degranulation Inhibitor

Kuba Megumi, Tsuha Kazuyo, Tsuha Keiko, MATSUZAKI Goro, YASUMOTO Takeshi

ＪＯＵＲＮＡＬ　ＯＦ　ＨＥＡＬＴＨ　ＳＣＩＥＮＣＥ ( 公益社団法人日本薬学会 ) 54 ( 5 ) 584 - 588 2008年 [ 査読有り ]

掲載種別: 研究論文（学術雑誌）

Based on the previous finding of okicamelliaside (OCS), a highly potent anti-degranulation ellagic acid glucoside, in the leaves of Camellia japonica (C. japonica), we evaluated an extract of these leaves and OCS itself for their potential to suppress allergic reactions in vivo. Two conventional animal allergy models were used. In the allergic conjunctivitis model, male S.D. rats were stimulated with anti-ovalbumin (OVA) serum and challenged with OVA/Evans blue mixture. Oral administration of extracts from C. japonica at 1000 mg/kg for 10 days significantly reduced the vascular permeability of conjunctivas. In the second model, male BALB/c mice were stimulated with a Japanese cedar pollen extract and challenged by nasal instillation of the antigen. The sneezing frequency during the 10 min immediately after the challenge tended to decrease by intraperitoneal administration of 0.2 mg/kg of OCS for 24 days. These results suggest that C. japonica extracts (CJE) and OCS prepared from them could be useful to alleviate the symptoms of an immediate-type allergy.

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IL-17-mediated regulation of innate and acquired immune response against pulmonary Mycobacterium bovis bacille Calmette-Guerin infection.

Umemura M, Yahagi A, Hamada S, Begum MD, Watanabe H, Kawakami K, Suda T, Sudo K, Nakae S, Iwakura Y, Matsuzaki G

Journal of immunology (Baltimore, Md. : 1950) ( The American Association of Immunologists ) 178 ( 6 ) 3786 - 96 2007年03月

掲載種別: 研究論文（学術雑誌）

<jats:title>Abstract</jats:title> <jats:p>IL-17 is a cytokine that induces neutrophil-mediated inflammation, but its role in protective immunity against intracellular bacterial infection remains unclear. In the present study, we demonstrate that IL-17 is an important cytokine not only in the early neutrophil-mediated inflammatory response, but also in T cell-mediated IFN-γ production and granuloma formation in response to pulmonary infection by Mycobacterium bovis bacille Calmette-Guérin (BCG). IL-17 expression in the BCG-infected lung was detected from the first day after infection and the expression depended on IL-23. Our observations indicated that γδ T cells are a primary source of IL-17. Lung-infiltrating T cells of IL-17-deficient mice produced less IFN-γ in comparison to those from wild-type mice 4 wk after BCG infection. Impaired granuloma formation was also observed in the infected lungs of IL-17-deficient mice, which is consistent with the decreased delayed-type hypersensitivity response of the infected mice against mycobacterial Ag. These data suggest that IL-17 is an important cytokine in the induction of optimal Th1 response and protective immunity against mycobacterial infection.</jats:p>

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結核菌の肺感染局所における免疫システムの解明と新たなワクチン開発への応用

新川　武,梅村　正幸

研究報告書（遺伝子実験センター） ( 松﨑吾朗 ) 2007年03月

掲載種別: 研究論文（その他学術会議資料等）

平成16-17年度科学研究費補助金(基盤研究(C))研究成果報告書 / 研究概要：本研究では、肺結核における肺での免疫応答誘導機構を検討するために、結核菌抗原Ag85B特異的CD4陽性T細胞のT細胞抗原レセプター遺伝子を発現するトランスジェニック(P25-TCRTg)マウスを用いた実験系を確立した。無処置のP25-TCR TgマウスのT細胞は、ほぼ全てが結核菌抗原特異的なナイーブT細胞であるため、このT細胞を養子移入した宿主マウスに結核菌を肺感染させた後に移入T細胞を追跡すれば、肺におけるT細胞活性化過程がモニターできる。この方法により結核菌肺感染後の肺及び肺所属リンパ節における結核菌特異的T細胞の動態・活性化及びインターフェロンγ(IFN-γ)産生を検討した。その結果、肺・リンパ節ともに結核菌抗原特異的T細胞の増加および活性化マーカーCD69発現増加が同様な経過で認められたが、細胞内IFN-γ発現は、肺でのみ選択的に強く検出された。従って、肺における免疫応答の誘導は、必ずしも所属リンパ節の免疫応答とは平行しないことが示唆された。上記の実験系では、検出されるTgT細胞数が非常に少なく明瞭な解析が困難であった。この点を改善するためにP25-TCR Tgマウスに正常T細胞を移入するという逆の移入実験を行なった。これにより、大多数のT細胞がP25-TCR TgT細胞であるが、その他の特殊なT細胞(例えばNKT細胞など)も存在するマウスが作成される。このマウスに結核菌を肺感染させた場合も、肺・リンパ節とも感染後に結核菌抗原特異的T細胞の増加・活性化マーカーの獲得が明瞭に検出されたが、IFN-γ産生は肺においてのみ強く認められ、上記の仮説が支持された。今後は、これらの実験系を用いて、結核感染時に肺と所属リンパ節との間で認められた獲得免疫誘導の乖離のメカニズムを詳細に解析するとともに、この実験系を組換え結核抗原ワクチンの効果検討に応用する。（管理者追加）リポジトリ登録情報を移行しました。確認のうえ、加除修正をしてください。

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IL-17-mediated regulation of innate and acquired immune response against pulmonary Mycobacterium bovis bacille Calmette-Guerin infection

Masayuki Umemura, Ayano Yahagi, Satoru Hamada, Mst Dilara Begum, Hisami Watanabe, Kazuyoshi Kawakami, Takashi Suda, Katsuko Sudo, Susumu Nakae, Yoichiro Iwakura, Goro Matsuzaki

JOURNAL OF IMMUNOLOGY ( AMER ASSOC IMMUNOLOGISTS ) 178 ( 6 ) 3786 - 3796 2007年03月 [ 査読有り ]

掲載種別: 研究論文（学術雑誌）

IL-17 is a cytokine that induces neutrophil-mediated inflammation, but its role in protective immunity against intracellular bacterial infection remains unclear. In the present. study; we demonstrate that IL-17 is an important cytokine not only in the early neutrophil-mediated inflammatory response, but also in T cell-mediated IFN-gamma production and granuloma formation in response to pulmonary infection by Mycobacterium bovis bacille Calmette-Guerin (BCG). IL-17 expression in the BCG-infected lung was detected from the first day after infection and the expression depended on IL-23. Our observations indicated that gamma delta T cells are a primary source of IL-17. Lung-infiltrating T cells of IL-17-deficient mice produced less IFN-gamma in comparison to those from wild-type mice 4 wk after BCG infection. Impaired granuloma formation was also observed in the infected lungs of IL-17-deficient mice, which is consistent with the decreased delayed-type hypersensitivity response of the infected mice against mycobacterial Ag. These data suggest that IL-17 is an important cytokine in the induction of optimal Th1 response and protective immunity against mycobacterial infection.

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Interleukin-17 as an effector molecule of innate and acquired immunity against infections

Goro Matsuzaki, Masayuki Umemura

MICROBIOLOGY AND IMMUNOLOGY ( BLACKWELL PUBLISHING ) 51 ( 12 ) 1139 - 1147 2007年 [ 査読有り ]

掲載種別: 研究論文（学術雑誌）

Interleukin (IL)-17 is a proinflammatory cytokine which induces differentiation and migration of neutrophils through induction of cytokines and chemokines including granulocyte-colony stimulating factor and CXCL8/IL-8. IL-17-producing CD4(+) T cells (Th17) have pivotal role in pathogenesis of autoimmune diseases. IL-17 is also involved in protective immunity against various infections. IL-17 has important role in induction of neutrophil-mediated protective immune response against extracellular bacterial or fungal pathogens such as Klebsiella pneumoniae and Candida albicans. Importance of IL-17 in protection against intracellular pathogens including Mycobacterium has also been reported. Interestingly, not only CD4(+) T cells but atypical CD4(-)CD8(-) T cells expressing T cell receptor (TCR) gamma delta produce IL-17, and IL-17 producing cells participate in both innate and acquired immune response to infections. Furthermore, neutrophil induction may not be the only mechanism of IL-17-mediated protective immunity. IL-17 seems to participate in host defense through regulation of cell-mediated immunity or induction of antimicrobial peptides such as beta-defensins. In this review, we summarize recent progress on the role of IL-17 in immune response against infections, and discuss possible application of IL-17 in prevention and treatment of infectious diseases.

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Suppression of the bacterial antigen-specific T cell response and the dendritic cell migration to the lymph nodes by osteopontin.

Begum MD, Umemura M, Kon S, Yahagi A, Hamada S, Oshiro K, Gotoh K, Nishizono A, Uede T, Matsuzaki G

Microbiology and immunology ( Wiley ) 51 ( 1 ) 135 - 47 2007年

掲載種別: 研究論文（学術雑誌）

Osteopontin (OPN) has been reported to enhance the interferon (IFN)-gamma-producing Th1-type T cell response through the induction of interleukin (IL)-12 and the suppression of IL-10. We therefore investigated whether OPN could enhance Th1 induction by vaccination against bacterial antigen in vivo. Unexpectedly, the co-inoculation of OPN suppressed the induction of IFN-gamma-producing CD4(+) T cells and T cell proliferative response after the subcutaneous heat-killed Listeria monocytogenes (HKLM) immunization. These results suggest that OPN down-regulates T cell priming. Since dendritic cells (DC) play a pivotal role in T cell priming, we next analyzed the effects of OPN on DC. The addition of OPN into the culture of either bone marrow-derived immature DC or an immature DC line JAWSII showed no effects on the expression of MHC class II, CD80, and CD86 molecules before and after HKLM stimulation. Consistently, in vitro OPN-treated DC showed a normal antigen-presenting function to an established Listeria-specific Th1-type T cells. However, when the DC were transferred into the footpad with HKLM and OPN, the migration of the transferred DC into the regional LN was suppressed in comparison to the DC transferred with HKLM alone. Furthermore, the addition of OPN into the culture of the DC line and HKLM severely suppressed the HKLM-induced expression of CCR7 chemokine receptor which is an important factor in the migration of DC into LN. All the results suggest the existence of an OPN-mediated negative feedback mechanism in the T cell immune response through the regulation of DC migration.

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Suppressor of cytokine signalling 1 in lymphocytes regulates the development of intestinal inflammation in mice

Inagaki-Ohara K, Sasaki A, Matsuzaki G, Ikeda T, Hotokezaka M, Chijiiwa K, Kubo M, Yoshida H, Nawa Y, Yoshimura A

GUT ( Gut ) 55 ( 2 ) 212 - 219 2006年02月 [ 査読有り ]

掲載種別: 研究論文（学術雑誌）

Background and aims: Imbalance between pro- and anti-inflammatory cytokines produced by intestinal T cells induces inflammatory bowel diseases (IBD). However, the importance of regulation of cytokine signalling in IBD has not been fully clarified. We have demonstrated that suppressor of cytokine signalling 1 (SOCS1) is expressed in inflamed tissues in an experimental colitis model. In the present study, we investigated the role of SOCS1 in colitis models to clarify the mechanism of IBD development. Methods: Intestinal T cells in transgenic mice expressing high levels of SOCS1 in lymphocytes (SOCS1Tg mice) were characterised by flow cytometric analysis and cytokine production from intestinal T cells was determined by ELISA. 2,4,6-Trinitrobenzene sulphonic acid (TNBS) induced colitis was induced in SOCS1Tg mice and severity was compared with control littermates by measurement of survival rates. Intracellular signalling was assessed by western blotting analysis. Results: SOCS1Tg mice developed colitis spontaneously with age. Young SOCS1Tg mice less than 15 weeks of age, before the onset of colitis, were susceptible to TNBS induced colitis. Intestinal T cells of SOCS1Tg mice showed increased interferon c and tumour necrosis factor a production and decreased transforming growth factor beta production. Expression of cytotoxic T lymphocyte associated antigen 4 (CTLA-4), a negative regulator of T cell activation, in SOCS1Tg mice was severely impaired at the protein level although mRNA levels of CTLA-4 in SOCS1Tg mice were comparable with those in control mice. Conclusions: Our data suggest that SOCS1 plays an important role in the regulation of colitis by controlling intestinal T cell activation mediated through CTLA-4 expression.

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Fas Ligand Induces Cell-Autonomous IL-23 Production in Dendritic Cells, a Mechanism for Fas Ligand-Induced IL-17 Production

Hiroyasu Kidoya, Masayuki Umemura, Takaya Kawabe, Goro Matsuzaki, Ayano Yahagi, Ryu Imamura, Takashi Suda

The Journal of Immunology ( The American Association of Immunologists ) 175 ( 12 ) 8024 - 8031 2005年12月

掲載種別: 研究論文（学術雑誌）

<jats:title>Abstract</jats:title> <jats:p>Fas ligand (FasL) has the potential to induce inflammation accompanied by massive neutrophil infiltration. We previously reported that FasL rapidly induces the production of various inflammatory cytokines including IL-1β and IL-17. In this study, we investigated the mechanism of the FasL-induced IL-17 production. We found that the culture supernatant of mouse resident peritoneal exudate cells (PEC) cocultured with FasL-expressing tumor (FFL) cells induced IL-17 production in freshly isolated resident PEC. Anti-IL-1β Ab strongly inhibited the IL-17-inducing activity. However, rIL-1β by itself induced only weak IL-17 production. Intriguingly, anti-IL-12 Ab but not an IL-15-neutralizing agent, IL15R-Fc, strongly inhibited the FasL-induced IL-17-inducing activity. IL-23, which shares the p40 subunit with IL-12, but not IL-12 itself, induced IL-17 production synergistically with IL-1β in resident PEC. FasL induced the production of IL-23 in PEC in vivo and in vitro, and IL-17 production following the i.p. injection of FFL cells was severely impaired in p40−/− mice, indicating that IL-23 plays an important role in the FasL-induced IL-17 production. FFL also induced the production of IL-23 in bone marrow- or PEC-derived dendritic cells (DCs). Finally, FasL induced only weak p40 production in a mixture of p40−/− and Fas−/− DC, indicating that FasL induces IL-23 production in DC mainly in a cell-autonomous manner.</jats:p>

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Fas ligand induces cell-autonomous IL-23 production in dendritic cells, a mechanism for Fas ligand-induced IL-17 production

H Kidoya, M Umemura, T Kawabe, G Matsuzaki, A Yahagi, R Imamura, T Suda

JOURNAL OF IMMUNOLOGY ( AMER ASSOC IMMUNOLOGISTS ) 175 ( 12 ) 8024 - 8031 2005年12月 [ 査読有り ]

掲載種別: 研究論文（学術雑誌）

Fas ligand (FasL) has the potential to induce inflammation accompanied by massive neutrophil infiltration. We previously reported that FasL rapidly induces the production of various inflammatory cytokines including IL-1 beta and IL-17. In this study, we investigated the mechanism of the FasL-induced IL-17 production. We found that the culture supernatant of mouse resident peritoneal exudate cells (PEC) cocultured with FasL-expressing tumor (FFL) cells induced IL-17 production in freshly isolated resident PEC. Anti-IL-1 beta Ab strongly inhibited the IL-17-inducing activity. However, rIL-1 beta by itself induced only weak IL-17 production. Intriguingly, anti-IL-12 Ab but not an IL-15-neutralizing agent, IL15R-Fc, strongly inhibited the FaSL-induced IL-17-inducing activity. IL-23, which shares the p40 subunit with IL-12, but not IL-12 itself, induced IL-17 production synergistically with IL-1 beta in resident PEC. FasL induced the production of IL-23 in PEC in vivo and in vitro, and IL-17 production following the i.p. injection of FFL cells was severely impaired in p40(-/-) mice, indicating that IL-23 plays an important role ill the FasL-induced IL-17 production. FFL, also induced the production of IL-23 in bone marrow- or PEC-derived dendritic cells (DCs). Finally, FasL induced only weak p40 production in a mixture of p40(-/-) and Fas(-/-) DC, indicating that FasL induces IL-23 production in DC mainly in a cell-autonomous manner.

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The regulatory functions of Ly-49A, Ly-49D and Ly-49G2 on NK cells in the recognition and rejection of the alloantigen in vivo

Shimizu I, Tomita Y, Iwai T, Zhang QW, Matsuzaki G, Nomoto K, Yasui H

TRANSPLANT INTERNATIONAL ( Transplant International ) 18 ( 9 ) 1090 - 1099 2005年09月 [ 査読有り ]

掲載種別: 研究論文（学術雑誌）

Ly-49A is an inhibitory receptor that binds H-2D(d) and H-2D(.)(k) The downregulation of Ly-49A is thought to mediate NK self tolerance in vivo. In this study, we analyzed the regulation of Ly-49A, D and G2 on NK cells in an in vivo rejection model. After injection with 1 x 10(8) B10.D2 spleen cells (SC) into B 10 mice, we found Ly-49A downregulated within 3 h on NK cells of B10 mice, whereas expressions of Ly-49D and G2 were augmented. To investigate effects of different expression patterns of Ly-49 receptors on NK cells, Ly-49A, D or G2-depleted B10 mice were inoculated with B10.D2 SC. NK cells from SC of Ly-49A-depleted and B10.D2 SC-injected B10 mice showed enhanced cytotoxicity to D-d-positive targets in vitro. Furthermore, reduced numbers of B10.D2 SC were observed in Ly-49A or G2-depleted B10 mice, whereas increased numbers of B10.D2 SC were observed in Ly-49D-depleted B10 mice after inoculation with B10.D2 SC in vivo. These findings indicated that the downregulation of Ly-49A and the augmentation of Ly-49D expression may mediate NK cells to recognize and kill D-d antigen efficiently. In conclusion, each Ly-49 isoform may play independent roles in the regulation of activation or inhibition on NK cells.

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Intraepithelial lymphocytes express junctional molecules in murine small intestine

Inagaki-Ohara K.

Biochemical and Biophysical Research Communications ( Biochemical and Biophysical Research Communications ) 331 ( 4 ) 977 - 983 2005年06月 [ 査読有り ]

掲載種別: 研究論文（学術雑誌）

Intestinal intraepithelial lymphocytes (IEL) that reside at basolateral site regulate the proliferation and differentiation of epithelial cells (EC) for providing a first line of host defense in intestine. However, it remains unknown how IEL interact and communicate with EC. Here, we show that IEL express junctional molecules like EC. We identified mRNA expression of the functional molecules in IEL such as zonula occludens (ZO)-1, occludin and junctional adhesion molecule (JAM) (tight junction), beta-catenin and E-cadherin (adherens junction), and connexin26 (gap junction). IEL constitutively expressed occludin and E-cadherin at protein level, while other T cells in the thymus, spleen, liver, mesenteric lymph node, and Peyer's patches did not. gamma delta IEL showed higher level of these expressions than alpha beta IEL. The expression of occludin was augmented by anti-CD3 Ab stimulation. These results suggest the possibility of a novel role of IEL concerning epithelial barrier and communication between IEL and EC. (c) 2005 Elsevier Inc. All rights reserved.

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Absent mRNA Accumulation of Th1 or Th2 Cytokines in Heart Allografts with Chimerism-Based Drug-Induced Tolerance

TOMITA YUKIHIRO, ZHANG QI-WEI, MATSUZAKI GORO, SHIMIZU ICHIRO, IWAI TOSHIRO, OKANO SHINJI, NOMOTO KIKUO, YASUI HISATAKA

Surgery today : the Japanese journal of surgery 35 ( 5 ) 364 - 370 2005年05月 [ 査読有り ]

掲載種別: 研究論文（学術雑誌）

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Absent mRNA accumulation of Th1 or Th2 cytokines in heart allografts with chimerism-based drug-induced tolerance

Tomita Y, Zhang QW, Matsuzaki G, Shimizu I, Iwai T, Okano S, Nomoto K, Yasui H

SURGERY TODAY ( Surgery Today ) 35 ( 5 ) 364 - 370 2005年05月 [ 査読有り ]

掲載種別: 研究論文（学術雑誌）

Purpose. We recently described using cyclophosphamide (CP) plus busulfan (BU) to create drug-induced skin and heart allograft tolerance capable of regularly overcoming fully H-2 mismatched barriers in mice. The present study investigates the intragraft mRNA expressions of Th1 and Th2 cytokines. Methods. This method consists of the intravenous (i.v.) injection of 1 x 10(8) allogeneic spleen cells on day 0, the intraperitoneal injection of 200 mg/ kg CP and 30 mg/ kg BU on day 2, and the i.v. injection of 1 x 10(7) T cell-depleted allogeneic bone marrow cells from the same strain of mice on day 3. Heart grafting (HG) was performed on day 28. Chimerism in the peripheral blood was monitored by flow cytometric (FCM) analysis. The frequency of certain Vβ families was determined by FCM to assess deletion of donor-reactive T cells. Th1 ( interleukin [IL]-2, interferon [IFN]-γ) and Th2 (IL-4, IL-10) cytokine expression in the heart grafts was analyzed with reverse transcription - polymerase chain reaction. Results. In a fully MHC mismatched combination of B10. D2 (H-2(d), IE+) --> B10 (H-2(b), IE-), B10. D2 heart grafts were accepted permanently in a donor-specific manner, mixed chimerism was observed, and IE-reactive Vβ 11(+) T cells were specifically reduced in the periphery from the recipient B10 mice. In the donor B10. D2 heart grafts, there was no accumulation of Th1 (IL-2, IFN-γ) or Th2 (IL-4, IL-10) cytokines. Conclusions. These results show that the drug-induced tolerance we established can regularly induce long-lasting heart allograft tolerance without intragraft mRNA accumulation of Th1 or Th2.

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Anti-tumour activity of heat-shock protein 60-recognizing CD4(+) T cells against syngeneic murine renal cell carcinoma

Eto M, Harada M, Tatsugami K, Harano M, Koga H, Matsuzaki G, Naito S

BJU INTERNATIONAL ( BJU International ) 95 ( 3 ) 420 - 423 2005年02月 [ 査読有り ]

掲載種別: 研究論文（学術雑誌）

To determine whether heat-shock protein (HSP) 60-recognizing CD4(+) T cells show antitumour activity against renal carcinoma (RENCA) cells, as HSP is highly expressed by tumour cells and induced in cells by various stresses, including transformation. RENCA, a renal cortical adenocarcinoma cell line of BALB/c origin, was used. Expression of major histocompatibility complex (MHC) class I, class II and HSP-60 on RENCA tumour cells was analysed by flow cytometry. BASL1.1, an autoreactive T-helper type 1 type CD4(+) T cell clone established by us, and that recognises HSP-60, was also used for a tumour-neutralising assay. The RENCA cells were negative for MHC class II, but expressed intracellular HSP-60. In the tumour-neutralising assay, BASL1.1 cells significantly suppressed the in vivo growth of RENCA cells. Three of five mice rejected RENCA cells when co-inoculated with BASL1.1 cells. These results indicate that HSP-60-recognizing CD4(+) T cells have the potential to eliminate renal cell carcinoma in vivo and that the eliciting of an anti-self T cell response at the tumour site can lead to regression of renal cancer.

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Vdelta1+ gammadelta T cells producing CC chemokines may bridge a gap between neutrophils and macrophages in innate immunity during Escherichia coli infection in mice.

Tagawa T, Nishimura H, Yajima T, Hara H, Kishihara K, Matsuzaki G, Yoshino I, Maehara Y, Yoshikai Y

Journal of immunology (Baltimore, Md. : 1950) ( The American Association of Immunologists ) 173 ( 8 ) 5156 - 64 2004年10月 [ 査読有り ]

掲載種別: 研究論文（学術雑誌）

<jats:title>Abstract</jats:title> <jats:p>An influx of neutrophils followed a short time later by an influx of macrophages to the infected site plays a key role in innate immunity against Escherichia coli infection. We found in this study that Vδ1−/− mice exhibited impaired accumulation of peritoneal macrophages but not neutrophils and delayed bacterial clearance after i.p. inoculation with E. coli. Peritoneal γδ T cells from E. coli-infected wild-type mice produced CCL3/MIP-1α and CCL5/RANTES in response to γδ TCR triggering in vitro, whereas such production was not evident in γδ T cells from E. coli-infected Vδ1−/− mice. Neutralization of CCL3/MIP-1α by a specific mAb in vivo significantly inhibited the accumulation of macrophages in the peritoneal cavity after E. coli infection, resulting in exacerbated bacterial growth in the peritoneal cavity. These results suggest that Vδ1+ γδ T cells bridge a gap between neutrophils and macrophages in innate immunity during E. coli infection mediated by production of CC chemokines, enhancing macrophage trafficking to the site of infection.</jats:p>

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V delta 1(+) gamma delta T cells producing CC chemokines may bridge a gap between neutrophils and macrophages in innate immunity during Escherichia coli infection in mice

T Tagawa, H Nishimura, T Yajima, H Hara, K Kishihara, G Matsuzaki, Yoshino, I, Y Maehara, Y Yoshikai

JOURNAL OF IMMUNOLOGY ( AMER ASSOC IMMUNOLOGISTS ) 173 ( 8 ) 5156 - 5164 2004年10月 [ 査読有り ]

掲載種別: 研究論文（学術雑誌）

An influx of neutrophils followed a short time later by an influx of macrophages to the infected site plays a key role in innate immunity against Escherichia coli infection. We found in this study that Vdelta1(-/-) mice exhibited impaired accumulation of peritoneal macrophages but not neutrophils and delayed bacterial clearance after i.p. inoculation with E. coli. Peritoneal gammadelta T cells from E. coli-infected wild-type mice produced CCL3/MIP-1alpha and CCL5/RANTES in response to gammadelta TCR triggering in vitro, whereas such production was not evident in gammadelta T cells from E. coli-infected Vdelta1(-/-) mice. Neutralization of CCL3/MIP-1alpha by a specific mAb in vivo significantly inhibited the accumulation of macrophages in the peritoneal cavity after E. coli infection, resulting in exacerbated bacterial growth in the peritoneal cavity. These results suggest that Vdelta1(+) gammadelta T cells bridge a gap between neutrophils and macrophages in innate immunity during E. coli infection mediated by production of CC chemokines, enhancing macrophage tracking to the site of infection.

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Involvement of IL-17 in Fas ligand-induced inflammation

UMEMURA Masayuki, KAWABE Takaya, SHUDO Koyo, KIDOYA Hiroyasu, FUKUI Masayuki, ASANO Masahide, IWAKURA Yoichiro, MATSUZAKI Goro, IMAMURA Ryu, SUDA Takashi

International immunology 16 ( 8 ) 1099 - 1108 2004年08月 [ 査読有り ]

掲載種別: 研究論文（学術雑誌）

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Involvement of IL-17 in Fas ligand-induced inflammation

Umemura M.

International Immunology ( International Immunology ) 16 ( 8 ) 1099 - 1108 2004年08月 [ 査読有り ]

掲載種別: 研究論文（学術雑誌）

Fas ligand (FasL) has been well characterized as a death factor. However, recent studies revealed that ectopic expression of FasL induces inflammation associated with massive neutrophil infiltration. We previously demonstrated that the neutrophil infiltration-inducing activity of FasL is partly dependent on, but partly independent of, IL-1beta. Here we investigated the cytokine profile of peritoneal lavage fluid obtained from mice that received i.p. injections of FFL, a FasL-expressing tumor cell line. We found that FFL injection caused a marked increase of not only IL-1beta but also IL-6, IL-17, IL-18, KC/chemokine CXC ligand 1 and macrophage inflammatory protein (MIP)-2, but not of IL-1alpha, IFN-gamma, TGF-beta or TNF-alpha. The FFL-induced cytokine production was not observed in Fas-deficient Ipr mice. Among cells transfected to express individually IL-1beta, IL-6, IL-17, or IL-18, only those expressing IL-1beta and IL-17 induced neutrophil infiltration. In these analyses, as little as 20 pg of peritoneal IL-17 induced neutrophil infiltration. The peritoneal IL-17 levels after FFL-injection were greatly diminished in IL-1-deficient mice. However, the IL-17 level was still above the threshold for neutrophil infiltration. Consistent with this, co-administration of the anti-IL-17 antibody with FFL diminished the peritoneal KC levels and neutrophil infiltration in IL-1-deficient mice. In addition, the expression of IL-17 by the tumor cells inhibited tumor growth in wild-type and nude mice. These results indicate that FasL is an upstream inflammatory factor that induces a variety of other inflammatory cytokines in vivo, and suggest that IL-17 is involved in FasL-induced inflammation in the absence of IL-1beta.

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PubMed

Mucosal T Cells Bearing TCRγδ Play a Protective Role in Intestinal Inflammation

Kyoko Inagaki-Ohara, Takatoshi Chinen, Goro Matsuzaki, Atsuo Sasaki, Yukiko Sakamoto, Kenji Hiromatsu, Fukumi Nakamura-Uchiyama, Yukifumi Nawa, Akihiko Yoshimura

The Journal of Immunology ( The American Association of Immunologists ) 173 ( 2 ) 1390 - 1398 2004年07月

掲載種別: 研究論文（学術雑誌）

<jats:title>Abstract</jats:title> <jats:p>Intestinal intraepithelial lymphocytes (IEL) bearing TCRγδ represent a major T cell population in the murine intestine. However, the role of γδ IEL in inflammatory bowel diseases (IBD) remains controversial. In this study, we show that γδ IEL is an important protective T cell population against IBD. γδ T cell-deficient (Cδ−/−) mice developed spontaneous colitis with age and showed high susceptibility to Th1-type 2,4,6-trinitrobenzene sulfonic acid (TNBS)-induced colitis at a young age. Transfer of γδ IEL to Cδ−/− mice ameliorated TNBS-induced colitis, which correlated with decrease of IFN-γ and TNF-α production and an increase of TGF-β production by IEL. Furthermore, a high level of IL-15, which inhibits activation-induced cell death to terminate inflammation, was expressed more in intestinal epithelial cells (EC) from TNBS-treated Cδ−/− mice than in those from wild-type mice. EC from wild-type mice significantly suppressed the IFN-γ production of IEL from TNBS-treated Cδ−/− mice, whereas EC from TNBS-treated Cδ−/− mice did not. These data indicate that γδ IEL play important roles in controlling IBD by regulating mucosal T cell activation cooperated with EC function. Our study suggests that enhancement of regulatory γδ T cell activity is a possible new cell therapy for colitis.</jats:p>

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CiNii Research

Mucosal T cells bearing TCR gamma delta play a protective role in intestinal inflammation

K Inagaki-Ohara, T Chinen, G Matsuzaki, A Sasaki, Y Sakamoto, K Hiromatsu, F Nakamura-Uchiyama, Y Nawa, A Yoshimura

JOURNAL OF IMMUNOLOGY ( AMER ASSOC IMMUNOLOGISTS ) 173 ( 2 ) 1390 - 1398 2004年07月 [ 査読有り ]

掲載種別: 研究論文（学術雑誌）

Intestinal intraepithelial lymphocytes (IEL) bearing TCRgammadelta represent a major T cell population in the murine intestine. However, the role of gammadelta IEL in inflammatory bowel diseases (IBD) remains controversial. In this study, we show that gammadelta IEL is an important protective T cell population against IBD. gammadelta T cell-deficient (CS-/-) mice developed spontaneous colitis with age and showed high susceptibility to Th1-type 2,4,6-trinitrobenzene sulfonic acid (TNBS)-induced colitis at a young age. Transfer of gammadelta IEL to Cdelta(-/-) mice ameliorated TNBS-induced colitis, which correlated with decrease of IFN-gamma and TNF-alpha production and an increase of TGF-beta production by IEL. Furthermore, a high level of IL-15, which inhibits activation-induced cell death to terminate inflammation, was expressed more in intestinal epithelial cells (EC) from TNBS-treated Cdelta(-/-) mice than in those from wild-type mice. EC from wild-type mice significantly suppressed the IFN-gamma production of IEL from TNBS-treated Cdelta(-/-) mice, whereas EC from TNBS-treated Cdelta(-/-) mice did not. These data indicate that gammadelta IEL play important roles in controlling IBD by regulating mucosal T cell activation cooperated with EC function. Our study suggests that enhancement of regulatory gammadelta T cell activity is a possible new cell therapy for colitis.

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