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At least 991 records · Page 55Linked to original sources
PubMed1987

Complications and efficacy of transsternal thymectomy in myasthenia gravis.

Between January 1977 and September 1985, 75 patients in our department underwent elective surgery for myasthenia gravis through a median sternotomy. The main prerequisite was optimal stabilization by medical treatment with the best possible vital capacity. The Osseman types were as follows: type I (22), type IIa (19), type IIb (26), type III (7), and type IV (1). All patients, except for 3 who were mechanically ventilated for a few hours after surgery, were immediately extubated at the end of the operation. The most frequent histologic finding was thymic hyperplasia (36%); 21.3% of the patients had thymomas. No surgery-related deaths occurred. Wound healing was impaired in 6.7% of the patients, including one patient with complete sternal instability, while 5.3% developed pneumonia. The most serious complications were myasthenic (9.3%) and cholinergic (2.7%) crises. Paresis of the phrenic (2.7%) and recurrent laryngeal (1.3%) nerves occurred only in the thymoma patients, who also had a higher frequency of all other complications. The effect on the myasthenic symptoms 3 months after surgery was as follows: 7.5% of the patients were in complete remission, 61.2% had improved, 9% had deteriorated. In a logistic regression model, the parameters age, sex, duration of disease, Osserman type, histology, pre-operative antibody titer to acetylcholine receptors, and post-operative change in titer were examined with respect to their influence on the effect of surgery. Only thymic histology had an appreciable influence (p = 0.057). The effect of these parameters on the success of surgery as well as the type and frequency of complications in relation to perioperative procedure are discussed in detail.

Adolescent↗
PubMed1977

Suppressor cell regulation of immune response to tumors: abrogation by adult thymectomy.

The regulatory role of the adult thymus on the appearance of cytotoxic and suppressor T cells (thymus-derived lymphocytes) to allogeneic and autochthonous virus-induced tumors in mice was investigated. It was demonstrated that C57BL/6 mice challenged with allogeneic P815 mastocytoma cells and complete Freund's adjuvant failed to develop cytotoxic cells but instead developed suppressor T cells which inhibited cytotoxic T cell function. Further, adjuvant-induced suppressor cells prevented the primary in vitro induction of cytotoxic T cells to P815 mastocytoma cells. In contrast, adult thymectomized animals, when challenged with adjuvant and allogeneic cells, had a normal cytotoxic response in vivo and their cells could not inhibit the generation of cytotoxic T cells in vitro. These studies suggested that the intact adult thymus was necessary for the induction of suppressor cells. Moreover, suppressor cells regulated cytotoxic T cell activity both in vivo and in vitro. Further, it was shown that adjuvant could prevent the normal immune response to virus-induced tumors. BALB/c mice treated with murine sarcoma virus developed tumors which reached a maximal size by day 14 and then regressed. Sham thymectomized animals treated with virus and complete Freund's adjuvant to generate suppressor cells died from progressive tumor growth. In contrast, thymectomized animals similarly treated had normal regression of tumor and survived. These studies lead to the conclusion that the adult thymus may regulate immune responsiveness by the export of suppressor T cells which regulate other T cell responses to both allogeneic and tumor antigens.

Animals↗
PubMed1995

Aod1, the immunoregulatory locus controlling abrogation of tolerance in neonatal thymectomy-induced autoimmune ovarian dysgenesis, maps to mouse chromosome 16.

Mice thymectomized at three days of age (D3Tx) develop during adulthood a variety of organ-specific autoimmune diseases, including autoimmune ovarian dysgenesis (AOD). The phenotypic spectrum of AOD is characterized by the development of anti-ovarian autoantibodies, oophoritis, and atrophy. The D3Tx model of AOD is unique in that disease induction depends exclusively on perturbation of the normal developing immune system, is T-cell-mediated, and is strain specific. For example, D3Tx A/J mice are highly susceptible to AOD, whereas C57BL/6J mice are resistant. After D3Tx, self ovarian antigens, expressed at physiological levels, trigger an autoimmune response capable of eliciting disease. The D3Tx model provides, therefore, the opportunity to focus on the mechanisms of self-tolerance that are relevant to disease pathogenesis. Previous studies indicate that the principal mechanisms involved in AOD susceptibility are genetically controlled and govern developmental processes associated with the induction and maintenance of peripheral tolerance. We report here the mapping of the Aod1 locus to mouse chromosome 16 within a region encoding several loci of immunologic relevance, including scid, Igl1, VpreB, Igll, Igl1r, Mtv6 (Mls-3), Ly-7, Ifnar, and Ifgt.

Animals↗