title: Thymic atrophy in type 2 reovirus infected mice: immunosuppression and effects of thymic hormone. Thymic atrophy caused by reo-2.
abstract: Suckling mice infected with reovirus type 2 showed a thymic atrophy followed by a marked suppression of the antibody, production to SRBC (a T cell dependent antigen) and bacterial LPS, when measured by the splenic PFC assay. The PFCs produced were sometimes less than 1% of uninfected control animals. Histologically the thymus was usually smaller than normal, and atrophy of the cortex and increased number of Hassal's bodies were observed. Number of nucleated cells in the thymus of infected mice showed 90% decrease as compared to uninfected mice. The spleen, although larger in size, showed depletion of lymphocytes from the thymus-dependent and follicular areas. No viral replication was detected in lymphatic organs using virological methods. Virus-infected mice transferred with the splenocytes or thymocytes from age-matched uninfected mice restored the antibody production against SRBC to normal levels. Thymocytes were more efficient than splenocytes in enhancing the antibody production in virus-infected mice. Injection of several different kinds of immunopotentiating agents enhanced the antibody production to SRBC, although LPS exacerbated the unresponsiveness. Thymic hormones such as FTS and TP5 enhanced antibody production to SRBC and LPS more efficiently than MDP. Flow cytometric analysis showed that percentage of CD4+ single positive cells was slightly increased in virus-infected mice treated with FTS, while there was no difference in the phenotypic distributions of thymocyte subpopulations among virus-infected mice, FTS-untreated and FTS-treated normal mice.
authors.affiliation: National Institute of Animal Health, Ibaraki, Japan.
authors.forename: T
authors.initials: T
authors.lastname: Onodera
authors.forename: T
authors.initials: T
authors.lastname: Taniguchi
authors.forename: T
authors.initials: T
authors.lastname: Tsuda
authors.forename: K
authors.initials: K
authors.lastname: Yoshihara
authors.forename: S
authors.initials: S
authors.lastname: Shimizu
authors.forename: M
authors.initials: M
authors.lastname: Sato
authors.forename: A
authors.initials: A
authors.lastname: Awaya
authors.forename: T
authors.initials: T
authors.lastname: Hayashi
mesh_terms: D000367:Age Factors; D000818:Animals; D000833:Animals, Suckling; D000917:Antibody Formation / Q000187:drug effects; D001284:Atrophy; D001323:Autoantibodies / Q000032:analysis; D005260:Female; D007108:Immune Tolerance / Q000187:drug effects; D016219:Immunotherapy, Adoptive; D008297:Male; D051379:Mice; D008807:Mice, Inbred BALB C; D012087:Reoviridae; D012088:Reoviridae Infections / Q000503:physiopathology* / Q000628:therapy; D013154:Spleen / Q000187:drug effects / Q000276:immunology; D013935:Thymic Factor, Circulating / Q000627:therapeutic use*; D016305:Thymopentin / Q000627:therapeutic use; D013950:Thymus Gland / Q000187:drug effects / Q000473:pathology*
chemical_list: D001323:Autoantibodies; D013935:Thymic Factor, Circulating; D016305:Thymopentin