• Title/Summary/Keyword: Disease Network

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Alteration of Innate Immune T and B Cells in the NC/Nga Mouse (아토피성 피부질환 동물 모델 NC/Nga 생쥐에서 내재면역 T와 B 세포의 변형)

  • Kim, Jung-Eun;Kim, Hyo-Jeong;Kim, Tae-Yoon;Park, Se-Ho;Hong, Seok-Mann
    • IMMUNE NETWORK
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    • v.5 no.3
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    • pp.137-143
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    • 2005
  • Background: Millions of people in the world are suffering from atopic dermatitis (AD), which is a chronic inflammatory skin disease triggered by Th2 immune responses. The NC/Nga mouse is the most extensively studied animal model of AD. Like human AD, NC/Nga mice demonstrate increased levels of IgE, a hallmark of Th2 immune responses. Adaptive immunity cannot be generated without help of innate immunity. Especially natural killer T (NKT) cells and marginal zone B (MZB) cells have been known to play important roles in linking innate immunity to adaptive immunity. Methods: Through flow cytometric analysis and ELISA assay, we investigated whether these lymphocytes might be altered in number in NC/Nga mice. Results: Our data demonstrated that the number of NKT cells was reduced in NC/Nga mice and IFN${\gamma}$ production by NKT cells upon ${\alpha}-GalCer$ stimulation decreased to the levels of CD1d KO mice lacking in NKT cells. However, reduction of NKT cells in NC/Nga mice was not due to CD1d expression, which was normal in the thymus. Interestingly, there was a significant increase of $CD1d^{high}B220^+$ cells in the spleen of NC/Nga mice. Further, we confirmed that $CD1d^{high}B220^+$ cells are B cells, not dendritic cells. These $CD1d^{high}B220^+$ B cells show $IgM^{high}CD21^{high}CD23^{low}$, a characteristic phenotype of MZB cells. Conclusion: We provide the evidence that there are decreased activities of NKT cells and increased number of MZB cells in the NC/Nga mice. Our findings may thus explain why NC/Nga mice are susceptible to AD.

Effects of Physical Training on Defence Mechanism of Aging and Memory Impairment of Senescence-accelerated SAMP8 (운동이 SAMP8 마우스의 노화와 기억장애에 미치는 영향)

  • Ku, Woo-Young;Lee, Jong-Soo;Kwak, Yi-Sub
    • IMMUNE NETWORK
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    • v.5 no.4
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    • pp.252-257
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    • 2005
  • Background: This study was designed to investigate the effect of exercise training on defense mechanism of chronic degenerative disease, aging, and memory impairments of senescence-accelerated mouse (SAM)P8 under the hypothesis that "Senile dementia may be prevented by regular exercises". Methods: To evaluate the effects of exercise training on the defense mechanism of aging and memory impairment, SAMP8 were divided into two groups, the control group and exercise training groups. the exercise training group were performed with low $(\dot{V}O_2max\;25{\sim}33%)$, middle ($\dot{V}O_2max$ 50%) and high $(\dot{V}O_2max\;66{\sim}75%)$ intensity exercise. All SAMP8 mice were fed experimental diet ad libitum until 4, 8 months, and dead period. Results: Median lifespan in middle exercise group resulted in a significantly increased (23.5% and 18.7%, respectively), whereas these lifespan in high exercise group resulted in an unexpectedly decreased (13.5% and 12.1%, respectively) compared with control group. Body fat levels in 4 and 8 months of age were significantly decreased 43% to 51% in middle exercise group, whereas were remarkably deceased to 57% in high exercise group compared with control group. It is believed that extended median and maximum lifespan may be effected by calory restriction through the exercise training. Acetylcholine (ACh) levels were significantly increased 6.7% and 8.5% in middle and high exercise groups, and also choline acetyltransfease (ChAT) activities were significantly increased 10.3% and 11.9% in middle and high exercise groups. Conclusion: These results suggest that proper and regular exercises such as middle group ($\dot{V}O_2max$ 50%) may play an effective role in attenuating an oxygen radicals and may play an important role in improving a learning and memory impairments of senile dementia.

Immune Responses to Viral Infection (바이러스 감염에 대한 면역반응)

  • Hwang, Eung-Soo;Park, Chung-Gyu;Cha, Chang-Yong
    • IMMUNE NETWORK
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    • v.4 no.2
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    • pp.73-80
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    • 2004
  • Viruses are obligate intracellular parasites which cause infection by invading and replicating within cells. The immune system has mechanisms which can attack the virus in extracellular and intracellular phase of life cycle, and which involve both non-specific and specific effectors. The survival of viruses depends on the survival of their hosts, and therefore the immune system and viruses have evolved together. Immune responses to viral infection may be variable depending on the site of infection, the mechanism of cell-to-cell spread of virus, physiology of the host, host genetic variation, and environmental condition. Viral infection of cells directly stimulates the production of interferons and they induce antiviral state in the surrounding cells. Complement system is also involved in the elimination of viruses and establishes the first line of defence with other non-specific immunity. During the course of viral infection, antibody is most effective at an early stage, especially before the virus enters its target cells. The virus- specific cytotoxic T lymphocytes are the principal effector cells in clearing established viral infections. But many viruses have resistant mechanism to host immune responses in every step of viral infection to cells. Some viruses have immune evasion mechanism and establish latency or persistency indefinitely. Furthermore antibodies to some viruses can enhance the disease by the second infection. Immune responses to viral infection are very different from those to bacterial infection.

Fcγ Receptors Modulate Pulmonary Inflammation by Activating Innate Immune Cells in Murine Hypersensitivity Pneumonitis

  • Park, Hyo Jin;Kim, Hye Sung;Chung, Doo Hyun
    • IMMUNE NETWORK
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    • v.10 no.1
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    • pp.26-34
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    • 2010
  • Background: Hypersensitivity pneumonitis (HP) is an interstitial lung disease that develops following repeated exposure to inhaled particulate antigens. The family of $Fc{\gamma}$ receptors ($Fc{\gamma}Rs$) has emerged as central regulators for modulating both pro-and anti-inflammatory responses. However, the role of $Fc{\gamma}Rs$ in the development of HP has not been investigated yet. Methods: To explore the functional roles of $Fc{\gamma}Rs$ in HP, $Fc{\gamma}R^{-/-}$ and B6 mice were challenged with Saccharopolyspora rectivirgula (SR) antigen intranasally, and compared these mice in terms of the histological change, infiltrated immune cells in BALF and in vitro immune responses. Results: $Fc{\gamma}R^{-/-}$ mice exhibited attenuation of HP in terms of histological alterations, and reduced numbers of neutrophils and macrophages in and the increased CD4 : CD8 ratio of bronchoalveolar lavage fluid. The lungs of $Fc{\gamma}R^{-/-}$ mice showed high production of Th2 cytokine such as IL-4 and slightly low production of Th1 cytokine, INF-${\gamma}$ compared to those of B6 mice. However, SR-specific adaptive immune responses of $Fc{\gamma}R^{-/-}$ mice were similar to those of B6 mice. Conclusion: These results demonstrate that activating $Fc{\gamma}$ receptors play an important role in activating neutrophils and macrophages in pulmonary inflammation and inducing Th1 differentiation by regulating cytokine expression in SR-induced HP.

Priming of Autoreactive $CD8^+T$ Cells Is Inhibited by Immunogenic Peptides Which Are Competitive for Major Histocompatibility Complex Class I Binding

  • You, Sooseong;Choi, Yoon Seok;Hong, Seokchan;Shin, Eui-Cheol
    • IMMUNE NETWORK
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    • v.13 no.3
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    • pp.86-93
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    • 2013
  • In the present study, we investigated if priming of autoreactive $CD8^+T$ cells would be inhibited by competitive peptides for major histocompatibility complex (MHC) class I binding. We used a mouse model of vitiligo which is induced by immunization of $K^b$-binding tyrosinase-related protein 2 (TRP2)-180 peptide. Competitive peptides for $K^b$ binding inhibited IFN-${\gamma}$production and proliferation of TRP2-180-specific $CD8^+T$ cells upon ex vivo peptide restimulation, while other MHC class I-binding peptides did not. In mice, the capability of inhibition was influenced by T-cell immunogenicity of the competitive peptides. The competitive peptide with a high T-cell immunogenicity efficiently inhibited priming of TRP2-180-specific $CD8^+T$ cells in vivo, whereas the competitive peptide with a low T-cell immunogenicity did not. Taken together, the inhibition of priming of autoreactive $CD8^+T$ cells depends on not only competition of peptides for MHC class I binding but also competitive peptide-specific $CD8^+T$ cells, suggesting that clonal expansion of autoreactive T cells would be affected by expansion of competitive peptide-specific T cells. This result provides new insights into the development of competitive peptides-based therapy for the treatment of autoimmune diseases.

Transcatheter Embolotherapy of Giant Pulmonary Arteriovenous Malformation Using Amplatzer® Vascular Plug (Amplatzer® 혈관폐색장치를 이용한 거대 폐동정맥기형 색전술 1예)

  • Jung, Ki Hwan;Lee, Seung Hwa;Shin, Chol;Kim, Je Hyeong
    • Tuberculosis and Respiratory Diseases
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    • v.67 no.1
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    • pp.52-58
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    • 2009
  • Pulmonary arteriovenous malformation (PAVM) is a rare pulmonary vascular anomaly due to an abnormal communication between the pulmonary artery and vein. The most common presenting symptom is a dyspnea on exertion related to this right-to-left shunt. If left untreated, PAVM has been known to result in serious complications. Incomplete pulmonary capillary network can be the cause of cerebral abscesses and other noninfectious neurological complications, such as stroke and transient ischemic attacks due to paradoxic embolism Transcatheter embolotherapy, using coils or balloons, has replaced surgical resection as the treatment of choice for PAVM. However, the risk of device embolization has limited the use of coil embolotherapy, while the size of PAVM is huge. Recently, Amplatzer$^{(R)}$ Vascular Plug has been proposed as an alternative endovascular occlusion device for arteriovenous malformation. We report a case of 81-year-old male patient with a giant PAVM, which was successfully treated by transcatheter embolotherapy using the Amplatzer$^{(R)}$ Vascular Plug.

Apo-1/Fas (CD95) Gene Polymorphism in Korean Knee Osteoarthritis Patients (한국인 무릎 골 관절염 환자들의 임상 양상과 Apo-1/Fas (CD95) 유전자 다형성과의 상관관계에 관한 연구)

  • Hong, Seung-Jae;Yang, Hyung-In;Yim, Sung-Vin;Chung, Joo-Ho;Jung, Young-Ok;Kim, Ho-Youn
    • IMMUNE NETWORK
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    • v.3 no.2
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    • pp.145-149
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    • 2003
  • Background: Apoptosis has been implicated in pathogenesis of various disease. Apo-1/Fas (CD95) is one of the main pathway of apoptosis. To examine the possible relationship between Apo-1/Fas (CD95) and primary knee osteoarthritis, MvaI restriction length polymorphism (RFLP) in human Apo-1/Fas (CD95) gene was assessed. Methods: Genotype and allele frequencies in promoter region in the Apo-1/Fas (CD95) gene were studied by PCR-RFLP in 226 Korean controls and 148 Korean patients with primary knee osteoarthritis. Results: No statistically significant difference in the genotypic distribution and allelic frequencies was found between the control and the knee oateoarthritis patients. But in the severe grade (grade 3, 4) Kellgren-Lawrence score patients, the frequency of $MvaI^*1$ (G) allele was significantly decreased (P=0.0392) and the of $MvaI^*2$ (A) allele frequency was significantly increased (P=0.0473) compared to the normal controls. Conclusion: Apo-1/Fas (CD95) gene polymorphism is a part a determinant factor of severity in knee osteoarthritis, the patients with $MvaI^*2$ (A) allele is more severe radiologic progression. Further substantiation studies are needed in larger patient samples and various other apoptosis related genes to elucidate the mechanism of osteoarthritis, including the Fas ligand gene analysis.

Immunostimulatory Effects of Cordyceps militaris on Macrophages through the Enhanced Production of Cytokines via the Activation of NF-${\kappa}B$

  • Shin, Seul-Mee;Kwon, Jeong-Hak;Lee, Sung-Won;Kong, Hyun-Seok;Lee, Seung-Jeong;Lee, Chong-Kil;Cho, Kyung-Hae;Ha, Nam-Joo;Kim, Kyung-Jae
    • IMMUNE NETWORK
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    • v.10 no.2
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    • pp.55-63
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    • 2010
  • Background: Cordyceps militaris has been used in traditional medicine to treat numerous diseases and has been reported to possess both antitumor and immunomodulatory activities in vitro and in vivo. However, the pharmacological and biochemical mechanisms of Cordyceps militaris extract (CME) on macrophages have not been clearly elucidated. In the present study, we examined how CME induces the production of proinflammatory cytokines, transcription factor, and the expression of co-stimulatory molecules. Methods: We confirmed the mRNA and protein levels of proinflammatory cytokines through RT-PCR and western blot analysis, followed by a FACS analysis for surface molecules. Results: CME dose dependently increased the production of NO and proinflammatory cytokines such as IL-$1{\beta}$, IL-6, TNF-${\alpha}$, and $PGE_2$, and it induced the protein levels of iNOS, COX-2, and proinflammatory cytokines in a concentrationdependent manner, as determined by western blot and RT-PCR analysis, respectively. The expression of co-stimulatory molecules such as ICAM-1, B7-1, and B7-2 was also enhanced by CME. Furthermore, the activation of the nuclear transcription factor, NF-${\kappa}B$ in macrophages was stimulated by CME. Conclusion: Based on these observations, CME increased proinflammatory cytokines through the activation of NF-${\kappa}B$, further suggesting that CME may prove useful as an immune-enhancing agent in the treatment of immunological disease.

Burden Assessment of Thyroid cancer in Iran from 1990 to 2010: Lessons Obtained from Global Burden of Disease Report 2010

  • Modirian, Mitra;Cheraghi, Zahra;Rahimzadeh, Shadi;Moghaddam, Sahar Saeedi;Jarrahi, Alireza Mosavi
    • Asian Pacific Journal of Cancer Prevention
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    • v.16 no.17
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    • pp.7743-7748
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    • 2015
  • Background: Thyroid tumors are generally regarded as rare malignancies. Nowadays, however, their global incidence is growing continuously partially due to western life style and utilization of more sensitive methods of early detection. It is approximately three times more prevalent in females than in males. Most cases of thyroid cancer are asymptomatic nodules or just have local cervical symptoms or adenopathy in early stages. Materials and Methods: The Global Burden of Diseases report 2010 study (released 3/2013) profited from 100 collaborators worldwide and used a vast network of data on health outcomes, vital registries, and population surveys. It shared many of the Global Burden of Diseases 1990 principal databases such as all available data on injuries, diseases, risk factors, as well as comparable metrics, and used different scientific approved methods to estimate important health status data like: death rate, life expectancy, healthy adjusted life expectancy, disability-adjusted life years (DALY), years of living lost due to premature death and years of life with disabilities. Results: DALY as thyroid cancer burden per 100,000 Iranian populations had increased by about 14% during 1990 to 2010 in all ages; from 6.1 (95% UI 4.2-9.74) years in 1990 to 6.95 (95% UI 5.06-9.18) years in 2010 in both sex. The 2010 peak age-group was estimated at 45-49 years in males and 40-45 years in females.

The Climate Change and Zoonosis (Zoonotic Disease Prevention and Control) (기후변화와 인수공통전염병 관리)

  • Jung, Suk-Chan
    • 한국환경농학회:학술대회논문집
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    • 2009.07a
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    • pp.228-239
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    • 2009
  • The observations on climate change show a clear increase in the temperature of the Earth's surface and the oceans, a reduction in the land snow cover, and melting of the sea ice and glaciers. The effects of climate change are likely to include more variable weather, heat waves, increased mean temperature, rains, flooding and droughts. The threat of climate change and global warming on human and animal health is now recognized as a global issue. This presentation is described an overview of the latest scientific knowledge on the impact of climate change on zoonotic diseases. Climate strongly affects agriculture and livestock production and influences animal diseases, vectors and pathogens, and their habitat. Global warming are likely to change the temporal and geographical distribution of infectious diseases, including those that are vector-borne such as West Nile fever, Rift Valley fever, Japanese encephalitis, bluetongue, malaria and visceral leishmaniasis, and other diarrheal diseases. The distribution and prevalence of vector-borne diseases may be the most significant effect of climate change. The impact of climate change on the emergence and re-emergence of animal diseases has been confirmed by a majority of countries. Emerging zoonotic diseases are increasingly recognized as a global and regional issue with potential serious human health and economic impacts and their current upward trends are likely to continue. Coordinated international responses are therefore essential across veterinary and human health sectors, regions and countries to control and prevent emerging zoonoses. A new early warning and alert systems is developing and introducing for enhancing surveillance and response to zoonotic diseases. And international networks that include public health, research, medical and veterinary laboratories working with zoonotic pathogens should be established and strengthened. Facing this challenging future, the long-term strategies for zoonotic diseases that may be affected by climate change is need for better prevention and control measures in susceptible livestock, wildlife and vectors in Korea. In conclusion, strengthening global, regional and national early warning systems is extremely important, as are coordinated research programmes and subsequent prevention and control measures, and need for the global surveillance network essential for early detection of zoonotic diseases.

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