• 제목/요약/키워드: Immunity, Cellular

검색결과 298건 처리시간 0.023초

Co-infection of Canine Distemper Virus and Toxoplasma gondii in Dog.

  • Kang, Hong-won;Kang, Sang-Chul;Yang, Hyoung-Seok;Bae, Jong-Hee;Kim, Jae-Hoon
    • 한국수의병리학회:학술대회논문집
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    • 한국수의병리학회 2003년도 추계학술대회초록집
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    • pp.44-44
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    • 2003
  • Canine distemper virus (CDV) is a member of the genus Morbillivirus and the family Paramyxoviridae [3]. CDV is known to induce immunosuppression in affected animals by disrupting both humoral and cellular immunity [3]. This often results in secondary opportunistic infections. Activated toxoplasmosis develops in dogs whose immune systems have been damaged by CDV [3]. (omitted)

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Brazilin Augments Cellular Immunity in Multiple Low Dose Streptozotocin (MLD-STZ) Induced Type I Diabetic Mice

  • Yang, Kyoung-Mee;Jeon, Sun-Duck;So, Dhong-Soo;Moon, Chang-Kiu
    • Archives of Pharmacal Research
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    • 제23권6호
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    • pp.626-632
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    • 2000
  • Brazilin, an active principle of Caesalprenia sappan, was examined for its immunopotentiating effects in multiple low dose streptozotocin (MLD-STZ) induced type diabetic mice. Brazilin was intraperitoneally administered for 5 consecutive days to MLD-STZ induced type 1 diabetic mice. Delayed type hypersensitivity, Con A-induced proliferation of splenocytes and mixed lymphocyte reaction, which had been decreased in diabetic mice, were significantly recovered by the administration of brazilin. Brazilin increased IL-2 production without affecting suppressor cell activity. Con A-induced and IL-2-induced expression of high affinity IL-2 receptors were also enhanced by brazilin. These results indicate that brazilin augments cellular immune responses, which are suppressed in the MLD-STZ induced type I diabetic mice, by increasing IL-2 production and responsiveness of immune cells to IL-2.

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랏트에 있어서 에탄올과 삭카린이 면역반응에 미치는 영향 (Effects of Ethanol and Saccharin on the Immune Response in Rats)

  • 안영근;김주영;김정훈;염정열
    • Environmental Analysis Health and Toxicology
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    • 제2권1_2호
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    • pp.33-42
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    • 1987
  • Experiments were performed to investigate effects of ethanol and saccharin on the immune system in rats. 4% ethanol and 0.02, 0.20, 2.00% saccharin solution in 4% ethanol were provided ad libitum by tap water for 4 weeks. Rats were sensitized and challenged with sheep red blood cells (S-RBC). Immune responses were evaluated by relative immuno organ weight, antibody production, Arthus reaction, delayed type hypersensitivity, and rosette forming cell. Ethanol exposure decreased thymus weight and delayed type hypersensitivity. A combined solution of ethanol and saccharin decreased water intake, growth rate, spleen weight, thymus weight, humoral and cellular immune response. Especially, a 2% saccharin solution in 4% ethanol very significantly suppressed cellular immunity.

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Innate Immune Response of NNV Infection in Fish and Its Disease Prevention

  • Lu, Ming-Wei;Wu, Jen-Leih
    • 한국해양바이오학회지
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    • 제2권3호
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    • pp.127-132
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    • 2007
  • The innate immune response which is seen as the initial defense mechanism induced upon foreign invasion has been well documented in higher vertebrates. This has also been observed in fish infected with NNV. However, the fish immune system based on fully established genome project has not been fully elucidated. Therefore, in this review, we hope to correlate NNV infection in fish that has devastated the aquaculture industry, to its host immune system. Further, we discuss the potential preventive measures in overcoming the widespread of this neurodisease.

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Respiratory Syncytial Virus (RSV) Modulation at the Virus-Host Interface Affects Immune Outcome and Disease Pathogenesis

  • Tripp, Ralph A.
    • IMMUNE NETWORK
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    • 제13권5호
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    • pp.163-167
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    • 2013
  • The dynamics of the virus-host interface in the response to respiratory virus infection is not well-understood; however, it is at this juncture that host immunity to infection evolves. Respiratory viruses have been shown to modulate the host response to gain a replication advantage through a variety of mechanisms. Viruses are parasites and must co-opt host genes for replication, and must interface with host cellular machinery to achieve an optimal balance between viral and cellular gene expression. Host cells have numerous strategies to resist infection, replication and virus spread, and only recently are we beginning to understand the network and pathways affected. The following is a short review article covering some of the studies associated with the Tripp laboratory that have addressed how respiratory syncytial virus (RSV) operates at the virus-host interface to affects immune outcome and disease pathogenesis.

Dead cell phagocytosis and innate immune checkpoint

  • Yoon, Kyoung Wan
    • BMB Reports
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    • 제50권10호
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    • pp.496-503
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    • 2017
  • The human body loses several billions of cells daily. When cells die in vivo, the corpse of each dead cell is immediately cleared. Specifically, dead cells are efficiently recognized and cleared by multiple types of neighboring phagocytes. Early research on cell death focused more on molecular mechanisms of cell death regulation while the cellular corpses were merely considered cellular debris. However, it has come to light that various biological stimuli following cell death are important for immune regulation. Clearance of normal dead cells occurs silently in immune tolerance. Exogenous or mutated antigens of malignant or infected cells can initiate adaptive immunity, thereby inducing immunogenicity by adjuvant signals. Several pathogens and cancer cells have strategies to limit the adjuvant signals and escape immune surveillance. In this review, we present an overview of the mechanisms of dead cell clearance and its immune regulations.

The Zinc Transport Systems and Their Regulation in Pathogenic Fungi

  • Jung, Won Hee
    • Mycobiology
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    • 제43권3호
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    • pp.179-183
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    • 2015
  • Zinc is an essential micronutrient required for many enzymes that play essential roles in a cell. It was estimated that approximately 3% of the total cellular proteins are required for zinc for their functions. Zinc has long been considered as one of the key players in host-pathogen interactions. The host sequesters intracellular zinc by utilizing multiple cellular zinc importers and exporters as a means of nutritional immunity. To overcome extreme zinc limitation within the host environment, pathogenic microbes have successfully evolved a number of mechanisms to secure sufficient concentrations of zinc for their survival and pathogenesis. In this review, we briefly discuss the zinc uptake systems and their regulation in the model fungus Saccharomyces cerevisiae and in major human pathogenic fungi such as Aspergillus fumigatus, Candida albicans, and Cryptococcus gattii.

Moderating Effects and Maintenance of Lung Cancer Cellular Immune Functions by CIK Cell Therapy

  • Jin, Cong-Guo;Chen, Xiao-Qun;Li, Jia;Wu, Zhi-Pin;Liu, Xin;Wang, Xi-Cai
    • Asian Pacific Journal of Cancer Prevention
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    • 제14권6호
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    • pp.3587-3592
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    • 2013
  • Aims: To study the CIK cell treatment effects on regulation of cellular immune function disorders in patients with lung cancer, and to analyze the time characteristics. Methods: Cellular immune function was assessed by FCM, and patients with functional disorders were randomly divided into two groups, one given CIK cell therapy within 18 months (5 courses) and the other the controls, which were followed up for 1 year with cellular immune functions tested once a month. Results: There were 5 types of cellular immunity, 4 of which are disorders; after CIK treatment, the improvement rate of the 4 groups were 79.1%, 70.8%, 76.0% and 70.0%, intergroup differences not being statistically significant (P=0.675), all significantly higher than in the control group (P=0.000). The median maintenance times for the 4 groups were 10.4 months (9.76-11.04), 8.4 months (7.86-8.94), 9.8 months (9.20-10.4) and 7.9 months (6.25-9.55), respectively. Conclusions: CIK cells were able to improve the immune functions of patients with lung cancer, the rate of improvement and maintenance time being related to the immune function before the treatment and CIK-cell-therapy courses.

페렴구균 전신감염에 대한 협막. 표면단백질 접합백신의 효과 (A Pneumococcal Conjugate Vaccine Formula Induces Protection in Mice Against Disseminated Disease due to Streptococcus pneumoniae)

  • 한용문;이주희
    • 약학회지
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    • 제48권6호
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    • pp.345-351
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    • 2004
  • ln the present work to determine effect of a Streptococcus pneumoniae conjugate vaccine, S.pneumoniae capsule attached to the surface protein (JY-Pol) was ex amined. This JY-Pol contained approximately 92% and 6% carbohydrate and protein, respectively. Gel electrophoresis revealed the presence of the surface protein in the JY-Pol. By the double immunodiffusion and isotyping ELISA analyses, administration of JY-Pol that was adsorbed to alum adjuvant (JY-Pol/Alum) into mice induced IgM, IgG, and IgA specific for the S.pneumoniae capsule. The ATCC capsular polysaccharide adsorbed to alum (ATCC-Pol/Alum) provoked only IgM in mice. In survival tests, mice that were immunized with the JY-Pol/Alum before intravenous challenge with live S.pneumoniae survived entire period of 46 day-observation, whereas all mice that received ATCC-Pol/Alum or only diluent instead of the vaccination died within 5 and 12 days, respectively. Results from footpad-edema test showed that JY-Pol/Alum formula provoked the cellular immunity as determined by swelling of the mouse footpad. These data indicate that the naturally conjugated JY- Pol enhances resistance of mice against disseminated pneumococcal disease due to S.pneumoniae by both humoral and cellular immune responses.

Mitochondria: multifaceted regulators of aging

  • Son, Jyung Mean;Lee, Changhan
    • BMB Reports
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    • 제52권1호
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    • pp.13-23
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    • 2019
  • Aging is accompanied by a time-dependent progressive deterioration of multiple factors of the cellular system. The past several decades have witnessed major leaps in our understanding of the biological mechanisms of aging using dietary, genetic, pharmacological, and physical interventions. Metabolic processes, including nutrient sensing pathways and mitochondrial function, have emerged as prominent regulators of aging. Mitochondria have been considered to play a key role largely due to their production of reactive oxygen species (ROS), resulting in DNA damage that accumulates over time and ultimately causes cellular failure. This theory, known as the mitochondrial free radical theory of aging (MFRTA), was favored by the aging field, but increasing inconsistent evidence has led to criticism and rejection of this idea. However, MFRTA should not be hastily rejected in its entirety because we now understand that ROS is not simply an undesired toxic metabolic byproduct, but also an important signaling molecule that is vital to cellular fitness. Notably, mitochondrial function, a term traditionally referred to bioenergetics and apoptosis, has since expanded considerably. It encompasses numerous other key biological processes, including the following: (i) complex metabolic processes, (ii) intracellular and endocrine signaling/communication, and (iii) immunity/inflammation. Here, we will discuss shortcomings of previous concepts regarding mitochondria in aging and their emerging roles based on recent advances. We will also discuss how the mitochondrial genome integrates with major theories on the evolution of aging.