WordNet

the 3rd letter of the Roman alphabet (同)c
(music) the keynote of the scale of C major
a general-purpose programing language closely associated with the UNIX operating system
any substance (as a toxin or enzyme) that stimulates an immune response in the body (especially the production of antibodies)

PrepTutorEJDIC

carbonの化学記号
抗原(生物の体内にはいって免疫体を作る物質)
certificate of deposit / (また『C.D.』)Civil Defense民間防衛

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1. 前立腺癌のスクリーニング screening for prostate cancer
2. 前立腺特異的抗原（PSA）の測定 measurement of prostate specific antigen
3. 抗原提示細胞 antigen presenting cells
4. 胎児および新生児における免疫細胞の発達 the development of immune cells in the fetus and neonate
5. 消化管疾患によるリウマチ症状の誘導のメカニズム mechanisms for the induction of rheumatic symptoms by gastrointestinal disease

English Journal

Innate mucosal-associated invariant T (MAIT) cells are activated in inflammatory bowel diseases.

Serriari NE1, Eoche M, Lamotte L, Lion J, Fumery M, Marcelo P, Chatelain D, Barre A, Nguyen-Khac E, Lantz O, Dupas JL, Treiner E.Author information 1Avenir Inserm UMR925 Group, Amiens, France.AbstractInflammatory bowel diseases are characterized by a deregulated immune response targeting the gut bacterial flora. Mucosal-associated invariant T (MAIT) cells are major histocompatibility complex (MHC) class Ib-restricted innate-like lymphocytes with anti-bacterial functions. They display an effector/memory phenotype and are found in large numbers in the blood, mucosae and liver. They have also been implicated in inflammatory diseases such as multiple sclerosis. Therefore, we aimed to analyse the possible involvement of MAIT cells in Crohn's disease (CD) and ulcerative colitis (UC). To this end, a phenotypical and functional analysis of MAIT cells isolated from the blood of healthy subjects, CD and UC patients was undertaken. MAIT cells were also quantified in ileal biopsies of CD patients. The frequency of blood MAIT cells was specifically reduced in IBD patients compared with healthy donors, whereas it was dramatically greater in the inflamed versus healthy tissue. MAIT cells were activated as they expressed significantly more the Ki67 antigen, and this was accompanied by phenotypical changes such as increased expression of natural killer (NK)G2D and B and T lymphocyte attenuator (BTLA). Finally, in-vitro-activated MAIT cells from CD and UC patients secreted significantly more interleukin (IL)-17, together with a decreased interferon (IFN)-γ in CD but an increased IL-22 in UC. These data show that MAIT cells are activated in IBD, which results in an increased recruitment towards the inflamed tissues, an altered phenotype and a switch in the pattern of cytokine secretion. This is the first demonstration that MAIT cells are immune players in IBD, whose precise functions in this context need to be addressed.
Clinical and experimental immunology.Clin Exp Immunol.2014 May;176(2):266-74. doi: 10.1111/cei.12277.
Inflammatory bowel diseases are characterized by a deregulated immune response targeting the gut bacterial flora. Mucosal-associated invariant T (MAIT) cells are major histocompatibility complex (MHC) class Ib-restricted innate-like lymphocytes with anti-bacterial functions. They display an effector
PMID 24450998

The central renin-angiotensin system and sympathetic nerve activity in chronic heart failure.

Zucker IH, Xiao L, Haack KK.Author information *Department of Cellular and Integrative Physiology, University of Nebraska Medical Center, Omaha, NE 68198, U.S.A.AbstractCHF (chronic heart failure) is a multifactorial disease process that is characterized by overactivation of the RAAS (renin-angiotensin-aldosterone system) and the sympathetic nervous system. Both of these systems are chronically activated in CHF. The RAAS consists of an excitatory arm involving AngII (angiotensin II), ACE (angiotensin-converting enzyme) and the AT1R (AngII type 1 receptor). The RAAS also consists of a protective arm consisting of Ang-(1-7) [angiotensin-(1-7)], the AT2R (AngII type 2 receptor), ACE2 and the Mas receptor. Sympatho-excitation in CHF is driven, in large part, by an imbalance of these two arms, with an increase in the AngII/AT1R/ACE arm and a decrease in the AT2R/ACE2 arm. This imbalance is manifested in cardiovascular-control regions of the brain such as the rostral ventrolateral medulla and paraventricular nucleus in the hypothalamus. The present review focuses on the current literature that describes the components of these two arms of the RAAS and their imbalance in the CHF state. Moreover, the present review provides additional evidence for the relevance of ACE2 and Ang-(1-7) as key players in the regulation of central sympathetic outflow in CHF. Finally, we also examine the effects of exercise training as a therapeutic strategy and the molecular mechanisms at play in CHF, in part, because of the ability of exercise training to restore the balance of the RAAS axis and sympathetic outflow.
Clinical science (London, England : 1979).Clin Sci (Lond).2014 May;126(10):695-706. doi: 10.1042/CS20130294.
CHF (chronic heart failure) is a multifactorial disease process that is characterized by overactivation of the RAAS (renin-angiotensin-aldosterone system) and the sympathetic nervous system. Both of these systems are chronically activated in CHF. The RAAS consists of an excitatory arm involving AngI
PMID 24490814

Modulation of the action of insulin by angiotensin-(1-7).

Dominici FP1, Burghi V1, Muñoz MC1, Giani JF2.Author information 1*IQUIFIB, Facultad de Farmacia y Bioquímica, Universidad de Buenos Aires, Buenos Aires, Argentina.2†Department of Biomedical Sciences and Department of Pathology and Laboratory Medicine, Cedars-Sinai Medical Center, Los Angeles, CA, U.S.A.AbstractThe prevalence of Type 2 diabetes mellitus is predicted to increase dramatically over the coming years and the clinical implications and healthcare costs from this disease are overwhelming. In many cases, this pathological condition is linked to a cluster of metabolic disorders, such as obesity, systemic hypertension and dyslipidaemia, defined as the metabolic syndrome. Insulin resistance has been proposed as the key mediator of all of these features and contributes to the associated high cardiovascular morbidity and mortality. Although the molecular mechanisms behind insulin resistance are not completely understood, a negative cross-talk between AngII (angiotensin II) and the insulin signalling pathway has been the focus of great interest in the last decade. Indeed, substantial evidence has shown that anti-hypertensive drugs that block the RAS (renin-angiotensin system) may also act to prevent diabetes. Despite its long history, new components within the RAS continue to be discovered. Among them, Ang-(1-7) [angiotensin-(1-7)] has gained special attention as a counter-regulatory hormone opposing many of the AngII-related deleterious effects. Specifically, we and others have demonstrated that Ang-(1-7) improves the action of insulin and opposes the negative effect that AngII exerts at this level. In the present review, we provide evidence showing that insulin and Ang-(1-7) share a common intracellular signalling pathway. We also address the molecular mechanisms behind the beneficial effects of Ang-(1-7) on AngII-mediated insulin resistance. Finally, we discuss potential therapeutic approaches leading to modulation of the ACE2 (angiotensin-converting enzyme 2)/Ang-(1-7)/Mas receptor axis as a very attractive strategy in the therapy of the metabolic syndrome and diabetes-associated diseases.
Clinical science (London, England : 1979).Clin Sci (Lond).2014 May;126(9):613-30. doi: 10.1042/CS20130333.
The prevalence of Type 2 diabetes mellitus is predicted to increase dramatically over the coming years and the clinical implications and healthcare costs from this disease are overwhelming. In many cases, this pathological condition is linked to a cluster of metabolic disorders, such as obesity, sy
PMID 24450744

Japanese Journal

CAR-T遺伝子治療の現状と今後の展開 (第77回日本血液学会学術集会教育講演特集号) -- (免疫・細胞・遺伝子治療/輸血)

小澤敬也
臨床血液 56(10), 2180-2185, 2015-10
NAID 40020597370

High-dose cyclophosphamide induces specific tumor immunity with concomitant recruitment of LAMP1/CD107a-expressing CD4-positive T cells into tumor sites

Naito Tatsushi,Baba Tomohisa,Takeda Kazuyoshi,Sasaki Soichiro,Nakamoto Yasunari,Mukaida Naofumi
Cancer Letters 336(1), 93-96, 2015-09-28
… Depletion of T cells, specifically CD4+ T cells, abrogated the CTX-mediated tumor regression. … CTX treatment induced the rapid recruitment of CD4+ T cells into the tumors, and these recruited cells initiated expression of LAMP1/CD107a, a cytotoxic granule molecule, and granzyme B in the absence of antigen presentation at draining lymph nodes and proliferation in the tumor tissues. …
NAID 120005646680

Mucosal-Associated Invariant T Cell Is a Potential Marker to Distinguish Fibromyalgia Syndrome from Arthritis

Sugimoto Chie,Konno Takahiko,Wakao Rika,Fujita Hiroko,Fujita Hiroyoshi,Wakao Hiroshi
PLOS ONE 10(4), e0121124, 2015-04-09
… The percentage of mucosal-associated invariant T (MAIT) cells in PBMCs and the mean fluorescent intensity (MFI) of cell surface antigen expression in MAIT cells were analyzed. …
NAID 120005611266