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      Interleukin-10-deficient mice develop chronic enterocolitis

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      Cell

      Elsevier BV

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          Abstract

          Interleukin-10 (IL-10) affects the growth and differentiation of many hemopoietic cells in vitro; in particular, it is a potent suppressor of macrophage and T cell functions. In IL-10-deficient mice, generated by gene targeting, lymphocyte development and antibody responses are normal, but most animals are growth retarded and anemic and suffer from chronic enterocolitis. Alterations in intestine include extensive mucosal hyperplasia, inflammatory reactions, and aberrant expression of major histocompatibility complex class II molecules on epithelia. In contrast, mutants kept under specific pathogen-free conditions develop only a local inflammation limited to the proximal colon. These results indicate that the bowel inflammation in the mutants originates from uncontrolled immune responses stimulated by enteric antigens and that IL-10 is an essential immunoregulator in the intestinal tract.

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          Most cited references 35

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          TH1 and TH2 cells: different patterns of lymphokine secretion lead to different functional properties.

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            Targeted disruption of the mouse transforming growth factor-beta 1 gene results in multifocal inflammatory disease.

            Transforming growth factor-beta 1 (TGF-beta 1) is a multifunctional growth factor that has profound regulatory effects on many developmental and physiological processes. Disruption of the TGF-beta 1 gene by homologous recombination in murine embryonic stem cells enables mice to be generated that carry the disrupted allele. Animals homozygous for the mutated TGF-beta 1 allele show no gross developmental abnormalities, but about 20 days after birth they succumb to a wasting syndrome accompanied by a multifocal, mixed inflammatory cell response and tissue necrosis, leading to organ failure and death. TGF-beta 1-deficient mice may be valuable models for human immune and inflammatory disorders, including autoimmune diseases, transplant rejection and graft versus host reactions.
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              Use of avidin-biotin-peroxidase complex (ABC) in immunoperoxidase techniques: a comparison between ABC and unlabeled antibody (PAP) procedures.

               S. Hsu,  L Raine,  H Fanger (1981)
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                Author and article information

                Journal
                Cell
                Cell
                Elsevier BV
                00928674
                October 1993
                October 1993
                : 75
                : 2
                : 263-274
                Article
                10.1016/0092-8674(93)80068-P
                8402911
                © 1993

                https://www.elsevier.com/tdm/userlicense/1.0/

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