• Title/Summary/Keyword: immune tolerance

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Allograft Immune Reaction of Kidney Transplantation Part 1. Mechanism of Allograft Rejection (신이식 후 면역반응의 이해 - 1부. 이식 거부 반응의 기전 -)

  • Kang, Hee-Gyung
    • Childhood Kidney Diseases
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    • v.12 no.1
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    • pp.23-29
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    • 2008
  • Kidney allograft transplantation is the most effective method of renal replacement for end stage renal disease patients. Still, it is another kind of 'disease', requiring immunosuppression to keep the allograft from rejection(allograft immune reaction). Immune system of the allograft recipient recognizes the graft as a 'pathogen (foreign or danger)', and the allograft-recognizing commanderin-chief of adaptive immune system, T cell, recruits all the components of immune system for attacking the graft. Proper activation and proliferation of T cell require signals from recognizing proper epitope(processed antigen by antigen presenting cell) via T cell receptor, costimulatory stimuli, and cytokines(IL-2). Thus, most of the immunosuppressive agents suppress the process of T cell activation and proliferation.

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The Role of Dendritic Cells in Central Tolerance

  • Oh, Jaehak;Shin, Jeoung-Sook
    • IMMUNE NETWORK
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    • v.15 no.3
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    • pp.111-120
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    • 2015
  • Dendritic cells (DCs) play a significant role in establishing self-tolerance through their ability to present self-antigens to developing T cells in the thymus. DCs are predominantly localized in the medullary region of thymus and present a broad range of self-antigens, which include tissue-restricted antigens expressed and transferred from medullary thymic epithelial cells, circulating antigens directly captured by thymic DCs through coticomedullary junction blood vessels, and peripheral tissue antigens captured and transported by peripheral tissue DCs homing to the thymus. When antigen-presenting DCs make a high affinity interaction with antigen-specific thymocytes, this interaction drives the interacting thymocytes to death, a process often referred to as negative selection, which fundamentally blocks the self-reactive thymocytes from differentiating into mature T cells. Alternatively, the interacting thymocytes differentiate into the regulatory T (Treg) cells, a distinct T cell subset with potent immune suppressive activities. The specific mechanisms by which thymic DCs differentiate Treg cells have been proposed by several laboratories. Here, we review the literatures that elucidate the contribution of thymic DCs to negative selection and Treg cell differentiation, and discusses its potential mechanisms and future directions.

Expression of Co-stimulatory Molecules and STAT/SOCS Signaling Factors in the Splenocytes of Mice Tolerized against Arthritis by Oral Administration of Type II Collagen (제2형 콜라겐으로 경구관용을 유도한 관절염 모델 마우스의 비장림프구내의 보조자극인자 및 STAT/SOCS 신호전달 인자의 발현 양상조사)

  • Lee, Kang-Eun;Hwang, Sue-Yun;Min, So-Youn;Kim, Ho-Youn
    • IMMUNE NETWORK
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    • v.3 no.3
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    • pp.248-254
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    • 2003
  • Oral administration of antigen has long been used in the induction of immune tolerance in various animal models of autoimmune diseases including rheumatoid arthritis (RA). Alleveation of arthritogenic symptoms has been reported from RA patients who received oral administration of type II collagen (CII) without side effects, however its rather inconsistent therapeutic efficacy and variation among patients calls for more detailed investigation on the mechanism of oral tolerance to be settled as regular treatment for RA. In an attempt to understand the immunogenic processes underpinning tolerance induction by orally administered CII, we analyzed changes in the expression of costimulatory molecules and STAT/SOCS signaling messengers in the mouse model of collagen induced arthritis (CIA). We found thatin the spleen of CIA mice, that has been undergone repeated oral feeding of CII prior to the induction of arthritis, showed increased promortion of CTLA4 expressing lymphocytes than in the spleen of PBS fed control. On the other hand, cells expressing CD28 or ICOS were decreased in the spleen of tolerized mice. Tolerance induction by oral CII administration also enhanced the expression of STAT6 in both RNA and protein level, while not affecting the expression of STAT3. The expression of SOCS3, which hasbeen known to transmit STAT-mediated signals from Th2 type cytokines, remained unchanged in the spleen of tolerized mice. Interestingly transcript of SOCS1, which has been associated with Th1 related pathways, was only visible in the spleen of tolerized but not of control mice, suggesting that as in the case of IL-6 signaling, it may exert a feed back inhibition toward the Th1 type stimulation.

Immune Regulatory Function of Dendritic Cells Expressing Indoleamine 2,3-Dioxygenase in Orally Tolerance to Type II Collagen-induced Animal Model (제2형 콜라겐 경구관용 유도 동물모델에서 수지상 세포의 Indoleamine 2,3-dioxygenase의 의존성 관절염 항원 특이 T세포 증식반응 제어 연구)

  • Park, Min-Jung;Min, So-Youn;Park, Kyoung-Su;Cho, Mi-La;CHo, Young-Gyu;Min, Jun-Ki;Yoon, Chong-Hyeon;Park, Sung-Hwa;Kim, Ho-Youn
    • IMMUNE NETWORK
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    • v.5 no.4
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    • pp.221-231
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    • 2005
  • Background: Immune regulatory dendritic cells (DCs) play an important role in maintaining self-tolerance. Recent evidences demonstrate that DCs expressing indoleamine 2,3-dioxygenase (IDO), which is involved in tryptophan catabolism, play an important role in immunoregulation and tolerance and induce T cell apoptosis. This study was devised to examine the role of IDO in the oral tolerance induction in collagen-induced arthritis (CIA) mouse model. Methods: Beginning 2 weeks before immunization, CII was fed six times to DBA/1 mice and the effect on arthritis was assessed. In tolerized mice, $CD11c^+$ DCs were isolated and stimulated with CII, IFN-${\gamma}$, and LPS with or without IDO inhibitor, 1-methyl-DL-tryptophan (1-MT) and IDO expression by $CD11c^+$ DCs was analyzed using FACS and RT-PCR. The expression of IDO, MHC II, CD80, and CD86 by $CD11c^+$ DCs were examined using confocal microscopy. Regulatory effect of $CD11c^+$ DCs on Ag-specific T cell proliferative response to CII was examined by mixed lymphocyte reaction (MLR) with or without 1-MT. Results: The proportion of IDO-expressing $CD11c^+$ DCs was slightly higher in tolerized mice than in CIA mice and significantly increased after stimulation with CII, IFN-${\gamma}$, and LPS in an IDO-dependent manner. On confocal microscopic examination, the expression of IDO was higher and those of MHC II and CD86 were lower in CD11c + DCs from tolerized mice compared to those from CIA mice. On MLR, $CD11c^+$ DCs from tolerized mice inhibited T cell proliferative response to CII in an IDO-dependent manner. Conclusion: Enhanced IDO expression by $CD11c^+$ DCs from tolerized mice may contribute to the regulation of proliferative response of CII-reactive T cells and could be involved in the induction of oral tolerance to CII.

A New Immunotronic Approach to Hardware Fault Detection Using Symbiotic Evolution (공생 진화를 이용한 Immunotronic 접근 방식의 하드웨어 오류 검출)

  • Lee, Sang-Hyung;Kim, Eun-Tai;Lee, Hee-Jin;Park, Mignon
    • Journal of the Institute of Electronics Engineers of Korea CI
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    • v.42 no.5
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    • pp.59-68
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    • 2005
  • A novel immunotronic approach to fault detection in hardware based on symbiotic evolution is proposed in this paper. In the immunotronic system, the generation of tolerance conditions corresponds to the generation of antibodies in the biological immune system. In this paper, the principle of antibody diversity, one of the most important concepts in the biological immune system, is employed and it is realized through symbiotic evolution. Symbiotic evolution imitates the generation of antibodies in the biological immune system morethan the traditional GA does. It is demonstrated that the suggested method outperforms the previous immunotronic methods with less running time. The suggested method is applied to fault detection in a decade counter (typical example of finite state machines) and MCNC finite state machines and its effectiveness is demonstrated by the computer simulation.

Practical Swarm Optimization based Fault-Tolerance Algorithm for the Internet of Things

  • Luo, Shiliang;Cheng, Lianglun;Ren, Bin
    • KSII Transactions on Internet and Information Systems (TIIS)
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    • v.8 no.3
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    • pp.735-748
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    • 2014
  • The fault-tolerance routing problem is one of the most important issues in the application of the Internet of Things, and has been attracting growing research interests. In order to maintain the communication paths from source sensors to the macronodes, we present a hybrid routing scheme and model, in which alternate paths are created once the previous routing is broken. Then, we propose an improved efficient and intelligent fault-tolerance algorithm (IEIFTA) to provide the fast routing recovery and reconstruct the network topology for path failure in the Internet of Things. In the IEIFTA, mutation direction of the particle is determined by multi-swarm evolution equation, and its diversity is improved by the immune mechanism, which can improve the ability of global search and improve the converging rate of the algorithm. The simulation results indicate that the IEIFTA-based fault-tolerance algorithm outperforms the EARQ algorithm and the SPSOA algorithm due to its ability of fast routing recovery mechanism and prolonging the lifetime of the Internet of Things.

A Biologically Inspired New Hardware Fault Detection: immunotronic and Genetic Algorithm-Based Approach

  • Lee, Sanghyung;Kim, Euntai;Park, Mignon
    • International Journal of Fuzzy Logic and Intelligent Systems
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    • v.4 no.1
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    • pp.7-11
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    • 2004
  • This paper proposes a new immunotronic approach for the fault detection in hardware. The suggested method is, inspired by biology and its implementation is based on genetic algorithm. Tolerance conditions in the immunotronic system for fault detection correspond to the antibodies in the biological immune system. A novel algorithm of generating tolerance conditions is suggested based on the principle of the antibody diversity and GA optimization is employed to select mature tolerance conditions in immunotronic fault detection system. The suggested method is applied to the fault detection for MCNC benchmark FSMs (finite state machines) and its effectiveness is demonstrated by the computer simulation.

Practical Swarm Optimization based Fault-Tolerance Algorithm for the Internet of Things

  • Luo, Shiliang;Cheng, Lianglun;Ren, Bin
    • KSII Transactions on Internet and Information Systems (TIIS)
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    • v.8 no.4
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    • pp.1178-1191
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    • 2014
  • The fault-tolerance routing problem is one of the most important issues in the application of the Internet of Things, and has been attracting growing research interests. In order to maintain the communication paths from source sensors to the macronodes, we present a hybrid routing scheme and model, in which alternate paths are created once the previous routing is broken. Then, we propose an improved efficient and intelligent fault-tolerance algorithm (IEIFTA) to provide the fast routing recovery and reconstruct the network topology for path failure in the Internet of Things. In the IEIFTA, mutation direction of the particle is determined by multi-swarm evolution equation, and its diversity is improved by the immune mechanism, which can improve the ability of global search and improve the converging rate of the algorithm. The simulation results indicate that the IEIFTA-based fault-tolerance algorithm outperforms the EARQ algorithm and the SPSOA algorithm due to its ability of fast routing recovery mechanism and prolonging the lifetime of the Internet of Things.

Immune Evasion Mechanism as a Guide for Immunotherapy in Head and Neck Cancer (두경부암에서 면역회피 기전과 면역항암제 치료)

  • Chang, Hyun
    • Korean Journal of Head & Neck Oncology
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    • v.33 no.1
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    • pp.1-5
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    • 2017
  • Head and neck squamous cell carcinoma (HNSCC) is the sixth most common cancer globally with high morbidity and mortality. Immune surveillance is well recognized as an important mechanism to prevent development or progression of HNSCC. HNSCC can escape the immune system through multiple mechanisms including development of tolerance in T cells and inhibition of T-cell-related pathways, generally referred to as checkpoint inhibitors. Recent clinical trials have demonstrated a clear advantage in advanced HNSCC patients treated with immune checkpoint blockade. Right at the front of the new era of immunotherapy, we will review current knowledge of immune escape mechanisms and clinical implication for HNSCC.

Interplay between Inflammatory Responses and Lymphatic Vessels

  • Shin, Kihyuk;Lee, Seung-Hyo
    • IMMUNE NETWORK
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    • v.14 no.4
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    • pp.182-186
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    • 2014
  • Lymphatic vessels are routes for leukocyte migration and fluid drainage. In addition to their passive roles in migration of leukocytes, increasing evidence indicates their active roles in immune regulation. Tissue inflammation rapidly induces lymphatic endothelial cell proliferation and chemokine production, thereby resulting in lymphangiogenesis. Furthermore, lymphatic endothelial cells induce T cell tolerance through various mechanisms. In this review, we focus on the current knowledge on how inflammatory cytokines affect lymphangiogenesis and the roles of lymphatic vessels in modulating immune responses.