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  • 1
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    ATP drives lamina propria T(H)17 cell differentiation (2008)
    Nature Publishing Group (NPG)
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    Publication Date: 2008-08-22
    Description: Interleukin (IL)-17-producing CD4(+) T lymphocytes (T(H)17 cells) constitute a subset of T-helper cells involved in host defence and several immune disorders. An intriguing feature of T(H)17 cells is their selective and constitutive presence in the intestinal lamina propria. Here we show that adenosine 5'-triphosphate (ATP) that can be derived from commensal bacteria activates a unique subset of lamina propria cells, CD70(high)CD11c(low) cells, leading to the differentiation of T(H)17 cells. Germ-free mice exhibit much lower concentrations of luminal ATP, accompanied by fewer lamina propria T(H)17 cells, compared to specific-pathogen-free mice. Systemic or rectal administration of ATP into these germ-free mice results in a marked increase in the number of lamina propria T(H)17 cells. A CD70(high)CD11c(low) subset of the lamina propria cells expresses T(H)17-prone molecules, such as IL-6, IL-23p19 and transforming-growth-factor-beta-activating integrin-alphaV and -beta8, in response to ATP stimulation, and preferentially induces T(H)17 differentiation of co-cultured naive CD4(+) T cells. The critical role of ATP is further underscored by the observation that administration of ATP exacerbates a T-cell-mediated colitis model with enhanced T(H)17 differentiation. These observations highlight the importance of commensal bacteria and ATP for T(H)17 differentiation in health and disease, and offer an explanation of why T(H)17 cells specifically present in the intestinal lamina propria.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Atarashi, Koji -- Nishimura, Junichi -- Shima, Tatsuichiro -- Umesaki, Yoshinori -- Yamamoto, Masahiro -- Onoue, Masaharu -- Yagita, Hideo -- Ishii, Naoto -- Evans, Richard -- Honda, Kenya -- Takeda, Kiyoshi -- England -- Nature. 2008 Oct 9;455(7214):808-12. doi: 10.1038/nature07240. Epub 2008 Aug 20.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratory of Immune Regulation, Graduate School of Medicine, Osaka University, 2-2 Yamadaoka, Suita, Osaka 565-0871, Japan.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/18716618" target="_blank"〉PubMed〈/a〉
    Keywords: Adenosine Triphosphate/metabolism/*pharmacology ; Animals ; Antigens, CD11c/metabolism ; Antigens, CD70/metabolism ; Cell Differentiation/*drug effects ; Cells, Cultured ; Colitis/chemically induced/immunology/pathology ; Disease Models, Animal ; Feces/microbiology ; Female ; Germ-Free Life ; Immunoglobulin A/analysis/immunology ; Interleukin-17/genetics/immunology/metabolism ; Male ; Mice ; Mucous Membrane/*cytology/*drug effects/immunology/microbiology ; Receptors, Purinergic P2/metabolism ; T-Lymphocytes, Helper-Inducer/*cytology/*drug effects/immunology
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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  • 2
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    HMGB proteins function as universal sentinels for nucleic-acid-mediated innate immune responses (2009)
    Nature Publishing Group (NPG)
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    Publication Date: 2009-11-06
    Description: The activation of innate immune responses by nucleic acids is crucial to protective and pathological immunities and is mediated by the transmembrane Toll-like receptors (TLRs) and cytosolic receptors. However, it remains unknown whether a mechanism exists that integrates these nucleic-acid-sensing systems. Here we show that high-mobility group box (HMGB) proteins 1, 2 and 3 function as universal sentinels for nucleic acids. HMGBs bind to all immunogenic nucleic acids examined with a correlation between affinity and immunogenic potential. Hmgb1(-/-) and Hmgb2(-/-) mouse cells are defective in type-I interferon and inflammatory cytokine induction by DNA or RNA targeted to activate the cytosolic nucleic-acid-sensing receptors; cells in which the expression of all three HMGBs is suppressed show a more profound defect, accompanied by impaired activation of the transcription factors interferon regulatory factor 3 (IRF3) and nuclear factor (NF)-kappaB. The absence of HMGBs also severely impairs the activation of TLR3, TLR7 and TLR9 by their cognate nucleic acids. Our results therefore indicate a hierarchy in the nucleic-acid-mediated activation of immune responses, wherein the selective activation of nucleic-acid-sensing receptors is contingent on the more promiscuous sensing of nucleic acids by HMGBs. These findings may have implications for understanding the evolution of the innate immune system and for the treatment of immunological disorders.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Yanai, Hideyuki -- Ban, Tatsuma -- Wang, ZhiChao -- Choi, Myoung Kwon -- Kawamura, Takeshi -- Negishi, Hideo -- Nakasato, Makoto -- Lu, Yan -- Hangai, Sho -- Koshiba, Ryuji -- Savitsky, David -- Ronfani, Lorenza -- Akira, Shizuo -- Bianchi, Marco E -- Honda, Kenya -- Tamura, Tomohiko -- Kodama, Tatsuhiko -- Taniguchi, Tadatsugu -- England -- Nature. 2009 Nov 5;462(7269):99-103. doi: 10.1038/nature08512.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Immunology, Graduate School of Medicine and Faculty of Medicine, University of Tokyo, Hongo 7-3-1, Bunkyo-ku, Tokyo 113-0033, Japan.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19890330" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Line ; Cytosol/immunology ; DNA/immunology ; HMGB Proteins/deficiency/genetics/*immunology/*metabolism ; HMGB1 Protein/deficiency/genetics/immunology/metabolism ; HMGB2 Protein/deficiency/genetics/immunology/metabolism ; Immunity, Innate/*immunology ; Interferon Regulatory Factor-3/metabolism ; Mice ; Mice, Inbred C57BL ; Models, Immunological ; NF-kappa B/metabolism ; Nucleic Acids/*immunology ; Nucleotides/chemistry/immunology/metabolism ; RNA/immunology ; Signal Transduction ; Toll-Like Receptors/immunology ; Virus Diseases/immunology/virology
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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  • 3
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    Gain-of-function of mutated C-CBL tumour suppressor in myeloid neoplasms (2009)
    Nature Publishing Group (NPG)
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    Publication Date: 2009-07-22
    Description: Acquired uniparental disomy (aUPD) is a common feature of cancer genomes, leading to loss of heterozygosity. aUPD is associated not only with loss-of-function mutations of tumour suppressor genes, but also with gain-of-function mutations of proto-oncogenes. Here we show unique gain-of-function mutations of the C-CBL (also known as CBL) tumour suppressor that are tightly associated with aUPD of the 11q arm in myeloid neoplasms showing myeloproliferative features. The C-CBL proto-oncogene, a cellular homologue of v-Cbl, encodes an E3 ubiquitin ligase and negatively regulates signal transduction of tyrosine kinases. Homozygous C-CBL mutations were found in most 11q-aUPD-positive myeloid malignancies. Although the C-CBL mutations were oncogenic in NIH3T3 cells, c-Cbl was shown to functionally and genetically act as a tumour suppressor. C-CBL mutants did not have E3 ubiquitin ligase activity, but inhibited that of wild-type C-CBL and CBL-B (also known as CBLB), leading to prolonged activation of tyrosine kinases after cytokine stimulation. c-Cbl(-/-) haematopoietic stem/progenitor cells (HSPCs) showed enhanced sensitivity to a variety of cytokines compared to c-Cbl(+/+) HSPCs, and transduction of C-CBL mutants into c-Cbl(-/-) HSPCs further augmented their sensitivities to a broader spectrum of cytokines, including stem-cell factor (SCF, also known as KITLG), thrombopoietin (TPO, also known as THPO), IL3 and FLT3 ligand (FLT3LG), indicating the presence of a gain-of-function that could not be attributed to a simple loss-of-function. The gain-of-function effects of C-CBL mutants on cytokine sensitivity of HSPCs largely disappeared in a c-Cbl(+/+) background or by co-transduction of wild-type C-CBL, which suggests the pathogenic importance of loss of wild-type C-CBL alleles found in most cases of C-CBL-mutated myeloid neoplasms. Our findings provide a new insight into a role of gain-of-function mutations of a tumour suppressor associated with aUPD in the pathogenesis of some myeloid cancer subsets.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Sanada, Masashi -- Suzuki, Takahiro -- Shih, Lee-Yung -- Otsu, Makoto -- Kato, Motohiro -- Yamazaki, Satoshi -- Tamura, Azusa -- Honda, Hiroaki -- Sakata-Yanagimoto, Mamiko -- Kumano, Keiki -- Oda, Hideaki -- Yamagata, Tetsuya -- Takita, Junko -- Gotoh, Noriko -- Nakazaki, Kumi -- Kawamata, Norihiko -- Onodera, Masafumi -- Nobuyoshi, Masaharu -- Hayashi, Yasuhide -- Harada, Hiroshi -- Kurokawa, Mineo -- Chiba, Shigeru -- Mori, Hiraku -- Ozawa, Keiya -- Omine, Mitsuhiro -- Hirai, Hisamaru -- Nakauchi, Hiromitsu -- Koeffler, H Phillip -- Ogawa, Seishi -- 2R01CA026038-30/CA/NCI NIH HHS/ -- England -- Nature. 2009 Aug 13;460(7257):904-8. doi: 10.1038/nature08240. Epub 2009 Jul 20.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Cancer Genomics Project, The University of Tokyo, 7-3-1 Hongo, Bunkyo-ku, Tokyo 113-8655, Japan.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19620960" target="_blank"〉PubMed〈/a〉
    Keywords: Allelic Imbalance ; Amino Acid Sequence ; Animals ; Base Sequence ; Chromosomes, Human, Pair 11/genetics ; Female ; *Genes, Tumor Suppressor ; Humans ; Leukemia, Myeloid/*genetics/metabolism/pathology ; Male ; Mice ; Mice, Knockout ; Mice, Nude ; Models, Molecular ; Molecular Sequence Data ; Mutant Proteins/chemistry/genetics/*metabolism ; Mutation ; NIH 3T3 Cells ; Neoplasm Transplantation ; Oncogenes/genetics ; Phosphorylation ; Protein Conformation ; Proto-Oncogene Proteins c-cbl/antagonists & ; inhibitors/chemistry/deficiency/*genetics/*metabolism ; Ubiquitination ; Uniparental Disomy/genetics ; ras Proteins/genetics/metabolism
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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  • 4
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    Commensal microbe-derived butyrate induces the differentiation of colonic regulatory T cells (2013)
    Nature Publishing Group (NPG)
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    Publication Date: 2013-11-15
    Description: Gut commensal microbes shape the mucosal immune system by regulating the differentiation and expansion of several types of T cell. Clostridia, a dominant class of commensal microbe, can induce colonic regulatory T (Treg) cells, which have a central role in the suppression of inflammatory and allergic responses. However, the molecular mechanisms by which commensal microbes induce colonic Treg cells have been unclear. Here we show that a large bowel microbial fermentation product, butyrate, induces the differentiation of colonic Treg cells in mice. A comparative NMR-based metabolome analysis suggests that the luminal concentrations of short-chain fatty acids positively correlates with the number of Treg cells in the colon. Among short-chain fatty acids, butyrate induced the differentiation of Treg cells in vitro and in vivo, and ameliorated the development of colitis induced by adoptive transfer of CD4(+) CD45RB(hi) T cells in Rag1(-/-) mice. Treatment of naive T cells under the Treg-cell-polarizing conditions with butyrate enhanced histone H3 acetylation in the promoter and conserved non-coding sequence regions of the Foxp3 locus, suggesting a possible mechanism for how microbial-derived butyrate regulates the differentiation of Treg cells. Our findings provide new insight into the mechanisms by which host-microbe interactions establish immunological homeostasis in the gut.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Furusawa, Yukihiro -- Obata, Yuuki -- Fukuda, Shinji -- Endo, Takaho A -- Nakato, Gaku -- Takahashi, Daisuke -- Nakanishi, Yumiko -- Uetake, Chikako -- Kato, Keiko -- Kato, Tamotsu -- Takahashi, Masumi -- Fukuda, Noriko N -- Murakami, Shinnosuke -- Miyauchi, Eiji -- Hino, Shingo -- Atarashi, Koji -- Onawa, Satoshi -- Fujimura, Yumiko -- Lockett, Trevor -- Clarke, Julie M -- Topping, David L -- Tomita, Masaru -- Hori, Shohei -- Ohara, Osamu -- Morita, Tatsuya -- Koseki, Haruhiko -- Kikuchi, Jun -- Honda, Kenya -- Hase, Koji -- Ohno, Hiroshi -- England -- Nature. 2013 Dec 19;504(7480):446-50. doi: 10.1038/nature12721. Epub 2013 Nov 13.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉1] RIKEN Center for Integrative Medical Sciences (IMS-RCAI), Kanagawa 230-0045, Japan [2] The Institute of Medical Science, The University of Tokyo, Tokyo 108-8639, Japan [3]. ; 1] RIKEN Center for Integrative Medical Sciences (IMS-RCAI), Kanagawa 230-0045, Japan [2] The Institute of Medical Science, The University of Tokyo, Tokyo 108-8639, Japan [3] Graduate School of Medicine, Chiba University, Chiba 260-8670, Japan [4]. ; 1] RIKEN Center for Integrative Medical Sciences (IMS-RCAI), Kanagawa 230-0045, Japan [2] Institute for Advanced Biosciences, Keio University, Yamagata 997-0052, Japan [3]. ; RIKEN Center for Integrative Medical Sciences (IMS-RCAI), Kanagawa 230-0045, Japan. ; Institute for Advanced Biosciences, Keio University, Yamagata 997-0052, Japan. ; 1] RIKEN Center for Integrative Medical Sciences (IMS-RCAI), Kanagawa 230-0045, Japan [2] Graduate School of Medical Life Science, Yokohama City University, Kanagawa 230-0045, Japan. ; Faculty of Agriculture, Shizuoka University, Shizuoka 422-8529, Japan. ; 1] RIKEN Center for Integrative Medical Sciences (IMS-RCAI), Kanagawa 230-0045, Japan [2] PRESTO, Japan Science and Technology Agency, Saitama 332-0012, Japan. ; The Institute of Medical Science, The University of Tokyo, Tokyo 108-8639, Japan. ; Preventative Health National Research Flagship, CSIRO Food and Nutritional Sciences, South Australia 5000, Australia. ; 1] RIKEN Center for Integrative Medical Sciences (IMS-RCAI), Kanagawa 230-0045, Japan [2] Graduate School of Medicine, Chiba University, Chiba 260-8670, Japan [3] Graduate School of Medical Life Science, Yokohama City University, Kanagawa 230-0045, Japan. ; 1] Graduate School of Medical Life Science, Yokohama City University, Kanagawa 230-0045, Japan [2] RIKEN Center for Sustainable Resource Science, Kanagawa 230-0045, Japan. ; 1] RIKEN Center for Integrative Medical Sciences (IMS-RCAI), Kanagawa 230-0045, Japan [2] CREST, Japan Science and Technology Agency, Saitama 332-0012, Japan. ; 1] RIKEN Center for Integrative Medical Sciences (IMS-RCAI), Kanagawa 230-0045, Japan [2] The Institute of Medical Science, The University of Tokyo, Tokyo 108-8639, Japan [3] PRESTO, Japan Science and Technology Agency, Saitama 332-0012, Japan [4].〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/24226770" target="_blank"〉PubMed〈/a〉
    Keywords: Acetylation/drug effects ; Adoptive Transfer ; Animals ; Butyrates/analysis/*metabolism/pharmacology ; *Cell Differentiation/drug effects ; Colitis/drug therapy/pathology ; Colon/cytology/*immunology/metabolism/*microbiology ; Conserved Sequence ; Female ; *Fermentation ; Forkhead Transcription Factors/genetics ; Germ-Free Life ; Histones/metabolism ; Homeostasis/drug effects ; Intestinal Mucosa/cytology/immunology ; Lymphocyte Count ; Magnetic Resonance Spectroscopy ; Male ; Metabolome ; Mice ; Promoter Regions, Genetic/drug effects ; *Symbiosis ; T-Lymphocytes, Regulatory/*cytology/drug effects/immunology
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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  • 5
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    Obesity-induced gut microbial metabolite promotes liver cancer through senescence secretome (2013)
    Nature Publishing Group (NPG)
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    Publication Date: 2013-06-28
    Description: Obesity has become more prevalent in most developed countries over the past few decades, and is increasingly recognized as a major risk factor for several common types of cancer. As the worldwide obesity epidemic has shown no signs of abating, better understanding of the mechanisms underlying obesity-associated cancer is urgently needed. Although several events were proposed to be involved in obesity-associated cancer, the exact molecular mechanisms that integrate these events have remained largely unclear. Here we show that senescence-associated secretory phenotype (SASP) has crucial roles in promoting obesity-associated hepatocellular carcinoma (HCC) development in mice. Dietary or genetic obesity induces alterations of gut microbiota, thereby increasing the levels of deoxycholic acid (DCA), a gut bacterial metabolite known to cause DNA damage. The enterohepatic circulation of DCA provokes SASP phenotype in hepatic stellate cells (HSCs), which in turn secretes various inflammatory and tumour-promoting factors in the liver, thus facilitating HCC development in mice after exposure to chemical carcinogen. Notably, blocking DCA production or reducing gut bacteria efficiently prevents HCC development in obese mice. Similar results were also observed in mice lacking an SASP inducer or depleted of senescent HSCs, indicating that the DCA-SASP axis in HSCs has key roles in obesity-associated HCC development. Moreover, signs of SASP were also observed in the HSCs in the area of HCC arising in patients with non-alcoholic steatohepatitis, indicating that a similar pathway may contribute to at least certain aspects of obesity-associated HCC development in humans as well. These findings provide valuable new insights into the development of obesity-associated cancer and open up new possibilities for its control.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Yoshimoto, Shin -- Loo, Tze Mun -- Atarashi, Koji -- Kanda, Hiroaki -- Sato, Seidai -- Oyadomari, Seiichi -- Iwakura, Yoichiro -- Oshima, Kenshiro -- Morita, Hidetoshi -- Hattori, Masahira -- Honda, Kenya -- Ishikawa, Yuichi -- Hara, Eiji -- Ohtani, Naoko -- England -- Nature. 2013 Jul 4;499(7456):97-101. doi: 10.1038/nature12347. Epub 2013 Jun 26.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Division of Cancer Biology, Cancer Institute, Japanese Foundation for Cancer Research, Koto-ku, Tokyo 135-8550, Japan.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/23803760" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Anti-Bacterial Agents/pharmacology ; Bacteria/metabolism ; Bile Acids and Salts/metabolism ; Carcinoma, Hepatocellular/complications/etiology/metabolism/prevention & control ; *Cell Aging/drug effects ; Cells, Cultured ; Cytokines/metabolism/secretion ; DNA Damage/drug effects ; Deoxycholic Acid/blood/*metabolism ; Dietary Fats/adverse effects/pharmacology ; Disease Models, Animal ; Fatty Liver/complications/pathology ; Gastrointestinal Tract/drug effects/*metabolism/*microbiology ; Hepatic Stellate Cells/cytology/drug effects/metabolism/*secretion ; Humans ; Interleukin-1beta/deficiency ; Liver Neoplasms/complications/etiology/*metabolism/prevention & control ; Male ; Mice ; Mice, Inbred C57BL ; Non-alcoholic Fatty Liver Disease ; Obesity/chemically induced/*metabolism ; Phenotype ; Risk Factors
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    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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  • 6
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    Treg induction by a rationally selected mixture of Clostridia strains from the human microbiota (2013)
    Nature Publishing Group (NPG)
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    Publication Date: 2013-07-12
    Description: Manipulation of the gut microbiota holds great promise for the treatment of inflammatory and allergic diseases. Although numerous probiotic microorganisms have been identified, there remains a compelling need to discover organisms that elicit more robust therapeutic responses, are compatible with the host, and can affect a specific arm of the host immune system in a well-controlled, physiological manner. Here we use a rational approach to isolate CD4(+)FOXP3(+) regulatory T (Treg)-cell-inducing bacterial strains from the human indigenous microbiota. Starting with a healthy human faecal sample, a sequence of selection steps was applied to obtain mice colonized with human microbiota enriched in Treg-cell-inducing species. From these mice, we isolated and selected 17 strains of bacteria on the basis of their high potency in enhancing Treg cell abundance and inducing important anti-inflammatory molecules--including interleukin-10 (IL-) and inducible T-cell co-stimulator (ICOS)--in Treg cells upon inoculation into germ-free mice. Genome sequencing revealed that the 17 strains fall within clusters IV, XIVa and XVIII of Clostridia, which lack prominent toxins and virulence factors. The 17 strains act as a community to provide bacterial antigens and a TGF-beta-rich environment to help expansion and differentiation of Treg cells. Oral administration of the combination of 17 strains to adult mice attenuated disease in models of colitis and allergic diarrhoea. Use of the isolated strains may allow for tailored therapeutic manipulation of human immune disorders.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Atarashi, Koji -- Tanoue, Takeshi -- Oshima, Kenshiro -- Suda, Wataru -- Nagano, Yuji -- Nishikawa, Hiroyoshi -- Fukuda, Shinji -- Saito, Takuro -- Narushima, Seiko -- Hase, Koji -- Kim, Sangwan -- Fritz, Joelle V -- Wilmes, Paul -- Ueha, Satoshi -- Matsushima, Kouji -- Ohno, Hiroshi -- Olle, Bernat -- Sakaguchi, Shimon -- Taniguchi, Tadatsugu -- Morita, Hidetoshi -- Hattori, Masahira -- Honda, Kenya -- England -- Nature. 2013 Aug 8;500(7461):232-6. doi: 10.1038/nature12331. Epub 2013 Jul 10.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉RIKEN Center for Integrative Medical Sciences (IMS-RCAI), 1-7-22 Suehiro-cho, Tsurumi-ku, Yokohama, Kanagawa 230-0045, Japan.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/23842501" target="_blank"〉PubMed〈/a〉
    Keywords: Adult ; Animals ; Cell Proliferation ; Clostridium/classification/genetics/*immunology ; Colitis/microbiology/pathology ; Colon/immunology/microbiology ; Disease Models, Animal ; Feces/microbiology ; Germ-Free Life ; Humans ; Inducible T-Cell Co-Stimulator Protein/metabolism ; Interleukin-10/metabolism ; Male ; Metagenome/genetics/*immunology ; Mice ; Mice, Inbred BALB C ; Mice, Inbred C57BL ; Mice, SCID ; RNA, Ribosomal, 16S/genetics ; Rats ; Rats, Inbred F344 ; T-Lymphocytes, Regulatory/cytology/*physiology
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    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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