Int. J. Med. Sci. 2009, 6 http://www.medsci.org 85IInntteerrnnaattiioonnaall JJoouurrnnaall ooff MMeeddiiccaall SScciieenncceess 2009; 6(2):85-92 © Ivyspring International Publisher. All rights reserved Research Paper Induction and effector phase of allergic lung inflammation is independent of CCL21/CCL19 and LT-beta Corinne Ploix1, Riaz I. Zuberi2, Fu-Tong Liu3, Monica J. Carson4, and David D. Lo4 1. Roche Ltd., Basel, Switzerland 2. La Jolla Institute for Molecular Medicine, La Jolla, CA, USA 3. Department of Dermatology, School of Medicine, University of California, Davis, CA, USA 4. Division of Biomedical Sciences, University of California, Riverside, CA, USA Correspondence to: David D. Lo, M.D., Ph.D., Division of Biomedical Sciences, University of California, Riverside, CA. phone: 951-827-4553, fax: 951-827-5504, email: david.lo@ucr.edu Received: 2009.02.17; Accepted: 2009.03.06; Published: 2009.03.10 Abstract The chemokines CCL21 and CCL19, and cell bound TNF family ligand lymphotoxin beta (LTβ), have been associated with numerous chronic inflammatory diseases. A general role in chronic inflammatory diseases cannot be assumed however; in the case of allergic inflam-matory disease, CCL21/CCL19 and LTβ have not been associated with the induction, re-cruitment, or effector function of Th2 cells nor dendritic cells to the lung. We have exam-ined the induction of allergic inflammatory lung disease in mice deficient in CCL21/CCL19 or LTβ and found that both kinds of mice can develop allergic lung inflammation. To control for effects of priming differences in knockout mice, adoptive transfers of Th2 cells were also performed, and they showed that such effector cells had equivalent effects on airway hy-per-responsiveness in both knockout background recipients. Moreover, class II positive an-tigen presenting cells (B cells and CD11c+ dendritic cells) showed normal recruitment to the peribronchial spaces along with CD4 T cells. Thus, the induction of allergic responses and recruitment of both effector Th2 cells and antigen presenting cells to lung peribronchial spaces can develop independently of CCL21/CCL19 and LTβ. Key words: asthma, dendritic cell, Th2, chemokine Introduction The membrane-bound cytokine lymphotoxin beta (LTβ) is known to be important in the early stages of secondary lymphoid tissue development. Signaling by LTα1/β2 ligands through the LTβ-R in-duces development of the stromal cells of secondary lymphoid tissues [1]. The stromal cells provide or-ganization to these lymphoid tissues in large part by producing the chemotactic CCR7 ligand CCL21, which recruits both lymphocytes and dendritic cells, signaling through the chemokine receptor CCR7 [2,3]. LTβ-deficient mice show greatly impaired immune responses [4-6]; likewise, immune responses are sig-nificantly delayed in CCL21 deficient mice [7]. The tissue site and mechanism of induction of immune responses in these mutant mice remain unclear. Interestingly, several acute and chronic inflam-matory diseases also appear to have a strong de-pendence on LTβ and CCL21 during their effector phase. Thus, blockade of LTβ-R will significantly in-hibit graft-versus-host-disease [8,9], experimental colitis [10,11], and autoimmune diabetes [12]. Simi-larly, strong local CCL21 induction was found to be Int. J. Med. Sci. 2009, 6 http://www.medsci.org 86associated with autoimmune diabetes [13], chronic liver inflammation [14,15], multiple sclerosis [16] and CỘNG HÒA XÃ HỘI CHỦ NGHĨA VIỆT NAM ĐỘC LẬP - TỰ DO - HẠNH PHÚC TRƯỜNG ĐẠI HỌC GTVT PHÂN HIỆU TẠI TP.HỒ CHÍ MINH Tp Hồ Chí Minh, ngày 23 tháng 05 năm 2017 SỐ: 996 /TB-ĐHGTVT-PH.HCM LỊCH THI LẦN HỆ LIÊN THÔNG BỔ SUNG Lớp : LIÊN THÔNG - CẦU ĐƯỜNG BỘ K56 - QUẬN THI LẠI LẦN HỌC KỲ NĂM HỌC 2016-2017 TT Trắc địa Môn Số lượng Ngày thi Giờ thi Phòng thi 27/05/2017 8:45 502C2 Ghi TL.GIÁM ĐỐC KT.TRƯỞNG PHÒNG ĐÀO TẠO PHÓ TRƯỞNG PHÒNG TRẦN PHONG NHÃ QUY CHẾ THI TUYỂNCUỘC THI “LT-APTECH TÀI NĂNG VIỆT LẦN 2 – 2006”I. ĐỐI TƯNG – ĐIỀU KIỆN THAM DỰ- Tất cả các bạn sinh viên/học sinh đang theo học tại các trường đại học, cao đẳng, trung học chuyên nghiệp và các trường phổ thông trung học trên đòa bàn TPHCM.- Các thí sinh đã nhận được học bổng toàn phần trong chương trình “LT-APTECH Tài Năng Việt Lần 1 – 2005” không được tham dự kì tuyển lần này.- Các bạn sinh viên/học sinh khi đăng ký phải đem theo CMND, thẻ sinh viên/học sinh và điền nay đủ vào mẫu đăng ký.- Mỗi thí sinh sẽ đượïc cấp phát phiếu báo danh ghi mã số thi tuyển và thời gian thi tuyển.II. ĐỊA ĐIỂM ĐĂNG KÝ VÀ THI TUYỂN- Các bạn sinh viên/học sinh nhận mẫu đăng ký tham dự và thi tuyển tại:• Trung Tâm Đào Tạo Lập Trình Viên Quốc Tế LT-APTECH49H-49I Phan Đăng Lưu, P7, QPN, TPHCM 5109 648 - 5109 649III. MÔN THI- Các thí sinh sẽ thi tuyển 2 môn, mỗi môn 30 phút, thi trắc nghiệm trên máy:+ Tiếng Anh+ Toán LogicTổ chức thành 2 đợt thi:+ Đợt 1: 03,04/06/2006+ Đợt 2: 10,11/06/2006Thí sinh đăng ký thi vào đợt 1 trước ngày : 01/06/2006Thí sinh đăng ký thi vào đợt 2 trước ngày : 08/06/2006Mỗi thí sinh chỉ được tham gia 1 lần trong 2 đợt thi. Các thí sinh khi vào phòng thi phải xuất trình CMND, thẻ sinh viên, thẻ học sinh hoặc các giấy tờ có ảnh liên quan để đối chiếu với mẫu đăng ký.IV. CƠ CẤU GIẢI THƯƠÛNG- LT-APTECH trao 20 suất học bổng cho 20 thí sinh có số điểm cao nhất lấy từ trên xuống.• 10 suất học bổng toàn phần học năm nhất chương trình LTV Quốc tế ACCP 2005. Trò giá mỗi phần:720 USD• 10 suất học bổng học kỳ 1 năm nhất chương trình trình LTV Quốc tế ACCP 2005. Trò giá mỗi phần: 390 USD- Tổng giá trò học bổng của chương trình: 11.100 USD = 180.000.000 VNĐ ( Một trăm tám mươi triệu đồng).- Nếu có tranh chấp hoặc khiếu nại về cơ chế và cơ cấu giải thưởng thì phán quyết của ban tổ chức là quyết đònh cuối cùng.V. GIẢI ĐÁP THÔNG TIN- Để biết thêm thông tin vui lòng liên hệ Ban tư vấn:• Trung Tâm Đào Tạo Lập Trình Viên Quốc Tế LT-APTECH49H-49I Phan Đăng Lưu, P7, QPN, TPHCM 5109 648 - 5109 649 BAN TỔ CHỨC“LT-APTECH Tài Năng Việt Lần 2 – 2006” Int. J. Med. Sci. 2009, 6 http://www.medsci.org 85IInntteerrnnaattiioonnaall JJoouurrnnaall ooff MMeeddiiccaall SScciieenncceess 2009; 6(2):85-92 © Ivyspring International Publisher. All rights reserved Research Paper Induction and effector phase of allergic lung inflammation is independent of CCL21/CCL19 and LT-beta Corinne Ploix1, Riaz I. Zuberi2, Fu-Tong Liu3, Monica J. Carson4, and David D. Lo4 1. Roche Ltd., Basel, Switzerland 2. La Jolla Institute for Molecular Medicine, La Jolla, CA, USA 3. Department of Dermatology, School of Medicine, University of California, Davis, CA, USA 4. Division of Biomedical Sciences, University of California, Riverside, CA, USA Correspondence to: David D. Lo, M.D., Ph.D., Division of Biomedical Sciences, University of California, Riverside, CA. phone: 951-827-4553, fax: 951-827-5504, email: david.lo@ucr.edu Received: 2009.02.17; Accepted: 2009.03.06; Published: 2009.03.10 Abstract The chemokines CCL21 and CCL19, and cell bound TNF family ligand lymphotoxin beta (LTβ), have been associated with numerous chronic inflammatory diseases. A general role in chronic inflammatory diseases cannot be assumed however; in the case of allergic inflam-matory disease, CCL21/CCL19 and LTβ have not been associated with the induction, re-cruitment, or effector function of Th2 cells nor dendritic cells to the lung. We have exam-ined the induction of allergic inflammatory lung disease in mice deficient in CCL21/CCL19 or LTβ and found that both kinds of mice can develop allergic lung inflammation. To control for effects of priming differences in knockout mice, adoptive transfers of Th2 cells were also performed, and they showed that such effector cells had equivalent effects on airway hy-per-responsiveness in both knockout background recipients. Moreover, class II positive an-tigen presenting cells (B cells and CD11c+ dendritic cells) showed normal recruitment to the peribronchial spaces along with CD4 T cells. Thus, the induction of allergic responses and recruitment of both effector Th2 cells and antigen presenting cells to lung peribronchial spaces can develop independently of CCL21/CCL19 and LTβ. Key words: asthma, dendritic cell, Th2, chemokine Introduction The membrane-bound cytokine lymphotoxin beta (LTβ) is known to be important in the early stages of secondary lymphoid tissue development. Signaling by LTα1/β2 ligands through the LTβ-R in-duces development of the stromal cells of secondary lymphoid tissues [1]. The stromal cells provide or-ganization to these lymphoid tissues in large part by producing the chemotactic CCR7 ligand CCL21, which recruits both lymphocytes and dendritic cells, signaling through the chemokine receptor CCR7 [2,3]. LTβ-deficient mice show greatly impaired immune responses [4-6]; likewise, immune responses are sig-nificantly delayed in CCL21 deficient mice [7]. The tissue site and mechanism of induction of immune responses in these mutant mice remain unclear. Interestingly, several acute and chronic inflam-matory diseases also appear to have a strong de-pendence on LTβ and CCL21 during their effector phase. Thus, blockade of LTβ-R will significantly in-hibit graft-versus-host-disease [8,9], experimental colitis [10,11], and autoimmune diabetes [12]. Simi-larly, strong local CCL21 induction was found to be Int. J. Med. Sci. 2009, 6 http://www.medsci.org 86associated with autoimmune diabetes [13], chronic liver inflammation [14,15], multiple sclerosis [16] and TRƯỜNG ĐẠI HỌC GTVT PHÂN HIỆU TẠI TP.HỒ CHÍ MINH SỐ: /TB-ĐHGTVT-PH.HCM CỘNG HÒA XÃ HỘI CHỦ NGHĨA VIỆT NAM Độc lập - Tự - Hạnh phúc Tp Hồ Chí Minh, ngày 16 tháng 05 năm 2017 LỚP : TẠI CHỨC - XÂY DỰNG CẦU ĐƯỜNG K54 - CẦN THƠ (Hết hạn đăng ký + nộp tiền qua mạng ngày: 27/04/2017) I THI LẦN CÁC MÔN KỲ NĂM 2016-2017 TT Môn Đường sắt Thiết kế yếu tố hình học đường ô tô Thiết kế cầu bê tông cốt thép (TKMH) Thiết kế cầu thép (TKMH) Quản lý dự án xây dựng Kinh tế xây dựng Ngày thi Giờ thi 23/05/2017 24/05/2017 Int. J. Med. Sci. 2009, 6 http://www.medsci.org 85IInntteerrnnaattiioonnaall JJoouurrnnaall ooff MMeeddiiccaall SScciieenncceess 2009; 6(2):85-92 © Ivyspring International Publisher. All rights reserved Research Paper Induction and effector phase of allergic lung inflammation is independent of CCL21/CCL19 and LT-beta Corinne Ploix1, Riaz I. Zuberi2, Fu-Tong Liu3, Monica J. Carson4, and David D. Lo4 1. Roche Ltd., Basel, Switzerland 2. La Jolla Institute for Molecular Medicine, La Jolla, CA, USA 3. Department of Dermatology, School of Medicine, University of California, Davis, CA, USA 4. Division of Biomedical Sciences, University of California, Riverside, CA, USA Correspondence to: David D. Lo, M.D., Ph.D., Division of Biomedical Sciences, University of California, Riverside, CA. phone: 951-827-4553, fax: 951-827-5504, email: david.lo@ucr.edu Received: 2009.02.17; Accepted: 2009.03.06; Published: 2009.03.10 Abstract The chemokines CCL21 and CCL19, and cell bound TNF family ligand lymphotoxin beta (LTβ), have been associated with numerous chronic inflammatory diseases. A general role in chronic inflammatory diseases cannot be assumed however; in the case of allergic inflam-matory disease, CCL21/CCL19 and LTβ have not been associated with the induction, re-cruitment, or effector function of Th2 cells nor dendritic cells to the lung. We have exam-ined the induction of allergic inflammatory lung disease in mice deficient in CCL21/CCL19 or LTβ and found that both kinds of mice can develop allergic lung inflammation. To control for effects of priming differences in knockout mice, adoptive transfers of Th2 cells were also performed, and they showed that such effector cells had equivalent effects on airway hy-per-responsiveness in both knockout background recipients. Moreover, class II positive an-tigen presenting cells (B cells and CD11c+ dendritic cells) showed normal recruitment to the peribronchial spaces along with CD4 T cells. Thus, the induction of allergic responses and recruitment of both effector Th2 cells and antigen presenting cells to lung peribronchial spaces can develop independently of CCL21/CCL19 and LTβ. Key words: asthma, dendritic cell, Th2, chemokine Introduction The membrane-bound cytokine lymphotoxin beta (LTβ) is known to be important in the early stages of secondary lymphoid tissue development. Signaling by LTα1/β2 ligands through the LTβ-R in-duces development of the stromal cells of secondary lymphoid tissues [1]. The stromal cells provide or-ganization to these lymphoid tissues in large part by producing the chemotactic CCR7 ligand CCL21, which recruits both lymphocytes and dendritic cells, signaling through the chemokine receptor CCR7 [2,3]. LTβ-deficient mice show greatly impaired immune responses [4-6]; likewise, immune responses are sig-nificantly delayed in CCL21 deficient mice [7]. The tissue site and mechanism of induction of immune responses in these mutant mice remain unclear. Interestingly, several acute and chronic inflam-matory diseases also appear to have a strong de-pendence on LTβ and CCL21 during their effector phase. Thus, blockade of LTβ-R will significantly in-hibit graft-versus-host-disease [8,9], experimental colitis [10,11], and autoimmune diabetes [12]. Simi-larly, strong local CCL21 induction was found to be Int. J. Med. Sci. 2009, 6 http://www.medsci.org 86associated with autoimmune diabetes [13], chronic liver inflammation [14,15], multiple sclerosis [16] and TRƯỜNG ĐẠI HỌC GTVT PHÂN HIỆU TẠI TP.HỒ CHÍ MINH SỐ: /TB-ĐHGTVT-PH.HCM CỘNG HÒA XÃ HỘI CHỦ NGHĨA VIỆT NAM Độc lập - Tự - Hạnh phúc Tp Hồ Chí Minh, ngày 16 tháng 05 năm 2017 LỚP : TẠI CHỨC - KINH TẾ VẬN TẢI SẮT K54 - DĨ AN (Hết hạn đăng ký + nộp tiền qua mạng ngày: 27/04/2017) I THI LẦN CÁC MÔN KỲ NĂM 2016-2017 TT Môn Tổ chức chạy tàu đường sắt F1 (TKMH) Định mức vận tải đường sắt Marketing vận tải đường sắt Kế hoạch vận tải đường sắt F1 Tài - Kế toán vận tải đường sắt Chiến lược sản xuất kinh doanh vận tải Int. J. Med. Sci. 2009, 6 http://www.medsci.org 85IInntteerrnnaattiioonnaall JJoouurrnnaall ooff MMeeddiiccaall SScciieenncceess 2009; 6(2):85-92 © Ivyspring International Publisher. All rights reserved Research Paper Induction and effector phase of allergic lung inflammation is independent of CCL21/CCL19 and LT-beta Corinne Ploix1, Riaz I. Zuberi2, Fu-Tong Liu3, Monica J. Carson4, and David D. Lo4 1. Roche Ltd., Basel, Switzerland 2. La Jolla Institute for Molecular Medicine, La Jolla, CA, USA 3. Department of Dermatology, School of Medicine, University of California, Davis, CA, USA 4. Division of Biomedical Sciences, University of California, Riverside, CA, USA Correspondence to: David D. Lo, M.D., Ph.D., Division of Biomedical Sciences, University of California, Riverside, CA. phone: 951-827-4553, fax: 951-827-5504, email: david.lo@ucr.edu Received: 2009.02.17; Accepted: 2009.03.06; Published: 2009.03.10 Abstract The chemokines CCL21 and CCL19, and cell bound TNF family ligand lymphotoxin beta (LTβ), have been associated with numerous chronic inflammatory diseases. A general role in chronic inflammatory diseases cannot be assumed however; in the case of allergic inflam-matory disease, CCL21/CCL19 and LTβ have not been associated with the induction, re-cruitment, or effector function of Th2 cells nor dendritic cells to the lung. We have exam-ined the induction of allergic inflammatory lung disease in mice deficient in CCL21/CCL19 or LTβ and found that both kinds of mice can develop allergic lung inflammation. To control for effects of priming differences in knockout mice, adoptive transfers of Th2 cells were also performed, and they showed that such effector cells had equivalent effects on airway hy-per-responsiveness in both knockout background recipients. Moreover, class II positive an-tigen presenting cells (B cells and CD11c+ dendritic cells) showed normal recruitment to the peribronchial spaces along with CD4 T cells. Thus, the induction of allergic responses and recruitment of both effector Th2 cells and antigen presenting cells to lung peribronchial spaces can develop independently of CCL21/CCL19 and LTβ. Key words: asthma, dendritic cell, Th2, chemokine Introduction The membrane-bound cytokine lymphotoxin beta (LTβ) is known to be important in the early stages of secondary lymphoid tissue development. Signaling by LTα1/β2 ligands through the LTβ-R in-duces development of the stromal cells of secondary lymphoid tissues [1]. The stromal cells provide or-ganization to these lymphoid tissues in large part by producing the chemotactic CCR7 ligand CCL21, which recruits both lymphocytes and dendritic cells, signaling through the chemokine receptor CCR7 [2,3]. LTβ-deficient mice show greatly impaired immune responses [4-6]; likewise, immune responses are sig-nificantly delayed in CCL21 deficient mice [7]. The tissue site and mechanism of induction of immune responses in these mutant mice remain unclear. Interestingly, several acute and chronic inflam-matory diseases also appear to have a strong de-pendence on LTβ and CCL21 during their effector phase. Thus, blockade of LTβ-R will significantly in-hibit graft-versus-host-disease [8,9], experimental colitis [10,11], and autoimmune diabetes [12]. Simi-larly, strong local CCL21 induction was found to be Int. J. Med. Sci. 2009, 6 http://www.medsci.org 86associated with autoimmune diabetes [13], chronic liver inflammation [14,15], multiple sclerosis [16] and TRƯỜNG ĐẠI HỌC GTVT PHÂN HIỆU TẠI TP.HỒ CHÍ MINH SỐ: /TB-ĐHGTVT-PH.HCM CỘNG HÒA XÃ HỘI CHỦ NGHĨA VIỆT NAM Độc lập - Tự - Hạnh phúc Tp Hồ Chí Minh, ngày 16 tháng 05 năm 2017 Lớp : TẠI CHỨC - XÂY DỰNG CẦU ĐƯỜNG K54 - QUẬN (Hết hạn đăng ký + nộp tiền qua mạng ngày: 29/04/2017) I THI LẦN CÁC MÔN KỲ NĂM 2016-2017 Ngày thi Giờ thi Số lượng Phòng thi 22/05/2017 23/05/2017 24/05/2017 25/05/2017 7:00 7:00 7:00 7:00 8 10 504C2 503C2 501C2 504C2 Thiết kế cầu bê tông cốt thép (TKMH) 26/05/2017 7:00 10 504C2 7:00 502C2