• 제목/요약/키워드: cell-mediated immune response

검색결과 246건 처리시간 0.023초

염증성 근질환의 발병기전 (Pathogenesis of Inflammatory Muscle Diseases)

  • 이동국
    • Annals of Clinical Neurophysiology
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    • 제4권1호
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    • pp.1-6
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    • 2002
  • The inflammatory myopathies are divided into three major and distinct subsets as polymyositis(PM), dermatomyositis(DM), and inclusion body myositis(IBM). This distinction is based on unique clinical, demographic, laboratory, histologic, therapeutic, prognostic, and immunopathologic criteria. Although the causes of PM, DM, and IBM are unknown, autoimmune mechanisms are implicated, as supported by their association with other putative or definite autoimmune diseases or viruses, the evidence for a T cell-mediated myocytotoxicity or complement-mediated microangiopathy, the presence of various autoantibodies and their response to immunotherapies. But in IBM the immune-mediated process is weaker and IBM patients do not readily respond to immunotherapies, there are convincing immunopathological signs to suggest that a definite autoimmune component, similar to that seen in PM, also plays a role in the cause of IBM.

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Exosome-mediated delivery of gga-miR-20a-5p regulates immune response of chicken macrophages by targeting IFNGR2, MAPK1, MAP3K5, and MAP3K14

  • Yeojin Hong;Jubi Heo;Suyeon Kang;Thi Hao Vu;Hyun S. Lillehoj;Yeong Ho Hong
    • Animal Bioscience
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    • 제36권6호
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    • pp.851-860
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    • 2023
  • Objective: This study aims to evaluate the target genes of gga-miR-20a-5p and the regulated immune responses in the chicken macrophage cell line, HD11, by the exosome-mediated delivery of miR-20a-5p. Methods: Exosomes were purified from the chicken macrophage cell line HD11. Then, mimic gga-miR-20p or negative control miRNA were internalized into HD11 exosomes. HD11 cells were transfected with gga-miR-20a-5p or negative control miRNA containing exosomes. After 44 h of transfection, cells were incubated with or without 5 ㎍/mL poly(I:C) for 4 h. Then, expression of target genes and cytokines was evaluated by quantitative realtime polymerase chain reaction. Results: Using a luciferase reporter assay, we identified that gga-miR-20a-5p directly targeted interferon gamma receptor 2 (IFNGR2), mitogen-activated protein kinase 1 (MAPK1), mitogen-activated protein kinase kinase kinase 5 (MAP3K5), and mitogen-activated protein kinase kinase kinase 14 (MAP3K14). Moreover, the exosome-mediated delivery of gga-miR-20a-5p successfully repressed the expression of IFNGR2, MAPK1, MAP3K5, and MAP3K14 in HD11 cells. The expressions of interferon-stimulated genes (MX dynamin like GTPase 1 [MX1], eukaryotic translation initiation factor 2A [EIF2A], and oligoadenylate synthase-like [OASL]) and proinflammatory cytokines (interferon-gamma [IFNG], interleukin-1 beta [IL1B], and tumor necrosis factor-alpha [TNFA]) were also downregulated by exosomal miR-20a-5p. In addition, the proliferation of HD11 cells was increased by exosomal miR-20a-5p. Conclusion: The exosome-mediated delivery of gga-miR-20a-5p regulated immune responses by controlling the MAPK and apoptotic signaling pathways. Furthermore, we expected that exosomal miR-20a-5p could maintain immune homeostasis against highly pathogenic avian influenza virus H5N1 infection by regulating the expression of proinflammatory cytokines and cell death.

인체의 영양상태가 세포매개성 및 체액성 면역 반응에 미치는 영향 (Effect of Nutritional Status on Cell-mediated and Humoral Immunity in Female College Students)

  • 김현미
    • Journal of Nutrition and Health
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    • 제27권5호
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    • pp.483-494
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    • 1994
  • The purpose of this study was to investigate the effect of nutritional status on the cell-mediated and humoral immunity in female college students. The nutritional status of twenty subjects was determined by six-days food records, anthropometric measurements, and biochemical assessments of serum nutrients. Cell-mediated and humoral immunity of the subjects was analyzed by in vivo and in vitro assessments. The results were summerized as follows : First, The average daily energy intake was 1437Kcal(CHO : PRO : FAT = 61:13:26), which corresponds to 71.9% of RDA. Anthropometric measurements showed that 50% of the subjects was under-weight(BMI<20), only 5% was over-weight(25

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CD72 is a Negative Regulator of B Cell Responses to Nuclear Lupus Self-antigens and Development of Systemic Lupus Erythematosus

  • Takeshi Tsubata
    • IMMUNE NETWORK
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    • 제19권1호
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    • pp.1.1-1.13
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    • 2019
  • Systemic lupus erythematosus (SLE) is the prototypic systemic autoimmune disease characterized by production of autoantibodies to various nuclear antigens and overexpression of genes regulated by IFN-I called IFN signature. Genetic studies on SLE patients and mutational analyses of mouse models demonstrate crucial roles of nucleic acid (NA) sensors in development of SLE. Although NA sensors are involved in induction of antimicrobial immune responses by recognizing microbial NAs, recognition of self NAs by NA sensors induces production of autoantibodies to NAs in B cells and production of IFN-I in plasmacytoid dendritic cells. Among various NA sensors, the endosomal RNA sensor TLR7 plays an essential role in development of SLE at least in mouse models. CD72 is an inhibitory B cell co-receptor containing an immunoreceptor tyrosine-based inhibition motif (ITIM) in the cytoplasmic region and a C-type lectin like-domain (CTLD) in the extracellular region. CD72 is known to regulate development of SLE because CD72 polymorphisms associate with SLE in both human and mice and CD72-/- mice develop relatively severe lupus-like disease. CD72 specifically recognizes the RNA-containing endogenous TLR7 ligand Sm/RNP by its extracellular CTLD, and inhibits B cell responses to Sm/RNP by ITIM-mediated signal inhibition. These findings indicate that CD72 inhibits development of SLE by suppressing TLR7-dependent B cell response to self NAs. CD72 is thus involved in discrimination of self-NAs from microbial NAs by specifically suppressing autoimmune responses to self-NAs.

림프절 스트로마 유래 Fibroblastic Reticular Cell의 면역학적 위치 (The Immunological Position of Fibroblastic Reticular Cells Derived From Lymph Node Stroma)

  • 이종환
    • 생명과학회지
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    • 제34권5호
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    • pp.356-364
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    • 2024
  • 림프절은 인체에 침입한 감염원에 대하여 면역반응을 일으키는 곳이다. 림프절은 스트로마세포에 의해 뚜렷하게 구획화되어 있다. 스트로마세포들은 면역세포의 이동, 활성화, 분화를 야기하기 위해 상호작용을 위해 미세환경을 제공한다. FRC는 림프절의 T zone에서 3차원 구조물을 형성하여 면역세포의 통로를 제공한다. FRC는 림프절 구조, 면역세포 리쿠르트, 면역세포와의 상호작용, 항원제시 등을 촉진시키는 역할을 한다. 염증반응 동안, FRC는 면역세포들의 면역반응을 조절하기 위해 국부적이며 분비성 물질을 통해 면역반응을 조절하고 있다. 본문 면역반응 조절을 위해 FRC가 면역반응의 setup, support 그리고 suppress 단계로 3부분에 관여하여 면역반응을 조절하고 있는 것으로 나누어 설명하였다. 전체적으로 FRC는 T 세포생물학적 효율성 증대를 위해 기능을 하는 것으로 보인다. 더불어, FRC는 식작용을 통해 선천성 면역반응에 영향을 미치고 있는 것으로 나타났다. 따라서 FRC는 림프절에서 면역반응의 immune gate-keepers로써 위치적 역할을 하는 것으로 사료된다. 전체적으로 FRC는 선천성면역과 적응면역의 조절기능에 대한 내용으로 설명하다. 이러한 협력적 피드백 루프는 염증반응 동안 림프절의 기능을 유지하는데 기여를 할 것으로 사료된다.

음양곽분획물이 생쥐의 면역반응에 미치는 영향 (Effects of Epimedii Herba Fraction on Response in ICR Mice)

  • 김정훈;김인훈;채병숙;강태욱;박찬봉;안영근
    • 약학회지
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    • 제40권2호
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    • pp.230-237
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    • 1996
  • The fractions of Epimedii Herba were examined for the immunological effects in ICR mice. Mice were divided into 4 groups and administered orally the fractions of Epimedii Herba for 10 days. The results of this study were summarized as following: (1) The fraction 1 (EtOAc layer) administered group as compared with control group significantly decreased spleen weight, Arthus reaction and hemagglutination (HA) titer but significantly increased circulating white blood cells (WBC). (2) The fraction 2 ($H_20$ layer) administered group as compared with control group significantly decreased liver weight, Arthus reaction and HA titer but significantly increased WBC. (3) The fraction 3 (ppt) administered group as compared with control group significantly increased liver weight, thymus weight rate, delayed type hypersensitivity, phagocytic activity and WBC. The results showed that Frs. 1 and 2 administered groups reduced humoral immune response but increased WBC, and that Fr. 3 administered group increased cell-mediated immune response, phagocytic activity and WBC.

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Recent Advances of Vaccine Adjuvants for Infectious Diseases

  • Lee, Sujin;Nguyen, Minh Trang
    • IMMUNE NETWORK
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    • 제15권2호
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    • pp.51-57
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    • 2015
  • Vaccines are the most effective and cost-efficient method for preventing diseases caused by infectious pathogens. Despite the great success of vaccines, development of safe and strong vaccines is still required for emerging new pathogens, re-emerging old pathogens, and in order to improve the inadequate protection conferred by existing vaccines. One of the most important strategies for the development of effective new vaccines is the selection and usage of a suitable adjuvant. Immunologic adjuvants are essential for enhancing vaccine potency by improvement of the humoral and/or cell-mediated immune response to vaccine antigens. Thus, formulation of vaccines with appropriate adjuvants is an attractive approach towards eliciting protective and long-lasting immunity in humans. However, only a limited number of adjuvants is licensed for human vaccines due to concerns about safety and toxicity. We summarize current knowledge about the potential benefits of adjuvants, the characteristics of adjuvants and the mechanisms of adjuvants in human vaccines. Adjuvants have diverse modes of action and should be selected for use on the basis of the type of immune response that is desired for a particular vaccine. Better understanding of current adjuvants will help exploring new adjuvant formulations and facilitate rational design of vaccines against infectious diseases.

AT9283, 1-Cyclopropyl-3-(3-(5-(Morpholinomethyl)-1H-Benzo[d] Imidazole-2-yl)-1H-Pyrazol-4-yl) Urea, Inhibits Syk to Suppress Mast Cell-Mediated Allergic Response

  • Kim, Su Jeong;Choi, Min Yeong;Min, Keun Young;Jo, Min Geun;Kim, Jie Min;Kim, Hyung Sik;Kim, Young Mi
    • Biomolecules & Therapeutics
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    • 제30권6호
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    • pp.520-528
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    • 2022
  • Mast cells are an effector cell that plays a pivotal role in type I hypersensitive immune responses. Mast cells exist in connective tissues, such as skin and mucosal tissue, and contain granules which contain bioactive substances such as histamine and heparin in cells. The granules of mast cells are secreted by antigen stimulation to cause the type I allergic hypersensitivity. In addition, stimulated by antigen, mast cells synthesize and secrete various eicosanoids and cytokines. While AT9283 is known to have anticancer effects, the therapeutic effect of AT9283 on allergic disorders is completely unknown. In this study, it was found that AT9283 reversibly inhibited antigen-IgE binding-induced degranulation in mast cells (IC50, approx. 0.58 μM) and suppressed the secretion of the inflammatory cytokines IL-4 (IC50, approx. 0.09 μM) and TNF-α (IC50, approx. 0.19 μM). For a mechanism of mast cell inhibition, while not inhibiting Syk phosphorylation, AT9283 suppressed the activation of LAT, a downstream substrate protein of Syk, in a dose-dependent manner. As expected, AT9283 also inhibited the activation of PLCγ1 and Akt, downstream signaling molecules of Syk/LAT, and MAP kinases such as JNK, Erk1/2, and P38. In an in vitro protein tyrosine kinase assay, AT9283 directly inhibited Syk activity. Next, AT9283 dose-dependently inhibited passive cutaneous anaphylaxis (PCA), an IgE-mediated allergic acute response, in mice (ED50, approx. 34 mg/kg, p.o.). These findings suggest that AT9283 has potential to use as a new drug for alleviating the symptoms of IgE-mediated allergic disorders.

생혈단의 골수부전 치료효과에 대한 실험적 연구 (The Effects of Saenghyuldan(shengxiedan) on Bone Marrow Failure)

  • 이연월;손창규;조종관
    • 대한한의학회지
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    • 제22권1호
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    • pp.33-45
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    • 2001
  • Objectives: This experimental study was carried out to prove the effect of Saenghyuldan(SHD; shengxiedan) on bone marrow failure induced by cyclophosphamide(CY) and irradiation in mice. Methods: The following were performed; immunopathology, histopathlogical findings of bone marrow and in the smear of myelocyte. hematopoietic cytokine(IL-3, GM-CSF, TPO), hematopoietic stem cell colony assay, humoral immunity(LPS mitogen response), cell-mediated immunity (Con A mitogen response) and nonspecific immunity(macrophage adherence & phagocytosis) in vitro or vivo. Results: SHD showed a protective effect on bone marrow failure induced by cyclophosphamide(CY) and irradiation in mice. SHD increased lymphoproliferative responses to LPS and Con A, and activated macrophage adherence and phagocytosis to SRBC. Conclusions: We expect that SHD can be used to treat bone marrow failure and immune suppression induced by the chemotherapy or radiation.

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Maturation-Resistant Dendritic Cells Ameliorate Experimental Autoimmune Uveoretinitis

  • Oh, Keun-Hee;Kim, Yon-Su;Lee, Dong-Sup
    • IMMUNE NETWORK
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    • 제11권6호
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    • pp.399-405
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    • 2011
  • Background: Endogenous uveitis is a chronic inflammatory eye disease of human, which frequently leads to blindness. Experimental autoimmune uveoretinitis (EAU) is an animal disease model of human endogenous uveitis and can be induced in susceptible animals by immunization with retinal antigens. EAU resembles the key immunological characteristics of human disease in that both are $CD4^+$ T-cell mediated diseases. Dendritic cells (DCs) are specialized antigen-presenting cells that are uniquely capable of activating naive T cells. Regulation of immune responses through modulation of DCs has thus been tried extensively. Recently our group reported that donor strain-derived immature DC pretreatment successfully controlled the adverse immune response during allogeneic transplantation. Methods: EAU was induced by immunization with human interphotoreceptor retinoid-binding protein (IRBP) $peptide_{1-20}$. Dendritic cells were differentiated from bone marrow in the presence of recombinant GM-CSF. Results: In this study, we used paraformaldehyde-fixed bone marrow-derived DCs to maintain them in an immature state. Pretreatment with fixed immature DCs, but not fixed mature DCs, ameliorated the disease progression of EAU by inhibiting uveitogenic $CD4^+$ T cell activation and differentiation. Conclusion: Application of iBMDC prepared according to the protocol of this study would provide an important treatment modality for the autoimmune diseases and transplantation rejection.