{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,1,31]],"date-time":"2026-01-31T08:04:56Z","timestamp":1769846696316,"version":"3.49.0"},"reference-count":20,"publisher":"The Endocrine Society","issue":"9","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":[],"published-print":{"date-parts":[[2014,9,1]]},"abstract":"<jats:sec>\n                  <jats:title>Context:<\/jats:title>\n                  <jats:p>Anti-pituitary-specific transcriptional factor 1 (PIT-1) antibody syndrome is characterized by acquired growth hormone (GH), prolactin (PRL), and thyroid-stimulating hormone (TSH) deficiencies associated with circulating anti-PIT-1 antibodies. Although autoimmunity to PIT-1 has been suggested as a pathogenesis, the precise mechanism of the syndrome remains unclarified.<\/jats:p>\n               <\/jats:sec>\n               <jats:sec>\n                  <jats:title>Objective:<\/jats:title>\n                  <jats:p>To elucidate the involvement of antibody- or cell-mediated immunity in anti-PIT-1 antibody syndrome.<\/jats:p>\n               <\/jats:sec>\n               <jats:sec>\n                  <jats:title>Materials and Methods:<\/jats:title>\n                  <jats:p>To investigate a direct effect of anti-PIT-1 antibody on pituitary cells, cell proliferation, and cytotoxicity detection assays were performed using patient serum. Enzyme-linked immunospot (ELISpot) assay was performed to evaluate the involvement of PIT-1-reactive cytotoxic T lymphocytes (CTLs). An immunohistochemical analysis using anti-CD4 or anti-CD8 antibody was performed to examine tissue infiltration by CTLs.<\/jats:p>\n               <\/jats:sec>\n               <jats:sec>\n                  <jats:title>Results:<\/jats:title>\n                  <jats:p>Patient serum did not exhibit any inhibitory effect on cell proliferation and secretion of GH and PRL in GH3 cells. In addition, complement-dependent cytotoxicity was not detected in patient serum on GH3 cells or primary pituitary cells. The ELISpot assay revealed the presence of CTLs that specifically reacted to the recombinant PIT-1 protein in the patient's peripheral lymphocytes. CD8+ cell infiltrations, which is the characteristic of CTLs, were observed in the pituitary gland, adrenal gland, stomach, thyroid gland, liver, and pancreas of the patient with anti-PIT-1 antibody syndrome.<\/jats:p>\n               <\/jats:sec>\n               <jats:sec>\n                  <jats:title>Conclusions:<\/jats:title>\n                  <jats:p>These results suggest that the anti-PIT-1 antibody is not a cause but a marker of anti-PIT-1 antibody syndrome, in which CTLs play a pivotal role in the pathogenesis.<\/jats:p>\n               <\/jats:sec>","DOI":"10.1210\/jc.2014-1769","type":"journal-article","created":{"date-parts":[[2014,6,17]],"date-time":"2014-06-17T17:01:30Z","timestamp":1403024490000},"page":"E1744-E1749","source":"Crossref","is-referenced-by-count":28,"title":["Involvement of PIT-1-Reactive Cytotoxic T Lymphocytes in Anti-PIT-1 Antibody Syndrome"],"prefix":"10.1210","volume":"99","author":[{"given":"Hironori","family":"Bando","sequence":"first","affiliation":[{"name":"Division of Diabetes and Endocrinology, Department of Internal Medicine (H.B., G.I., H.F., M.Y., R.H., R.M., K.S., H.N., M.T., Y.T.), Kobe University Graduate School of Medicine, Kobe 650-0017, Japan"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Genzo","family":"Iguchi","sequence":"first","affiliation":[{"name":"Division of Diabetes and Endocrinology, Department of Internal Medicine (H.B., G.I., H.F., M.Y., R.H., R.M., K.S., H.N., M.T., Y.T.), Kobe University Graduate School of Medicine, Kobe 650-0017, Japan"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Hidenori","family":"Fukuoka","sequence":"first","affiliation":[{"name":"Division of Diabetes and Endocrinology, Department of Internal Medicine (H.B., G.I., H.F., M.Y., R.H., R.M., K.S., H.N., M.T., Y.T.), Kobe University Graduate School of Medicine, Kobe 650-0017, 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654-8585"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Ryusaku","family":"Matsumoto","sequence":"first","affiliation":[{"name":"Division of Diabetes and Endocrinology, Department of Internal Medicine (H.B., G.I., H.F., M.Y., R.H., R.M., K.S., H.N., M.T., Y.T.), Kobe University Graduate School of Medicine, Kobe 650-0017, Japan"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Kentaro","family":"Suda","sequence":"first","affiliation":[{"name":"Division of Diabetes and Endocrinology, Department of Internal Medicine (H.B., G.I., H.F., M.Y., R.H., R.M., K.S., H.N., M.T., Y.T.), Kobe University Graduate School of Medicine, Kobe 650-0017, Japan"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Hitoshi","family":"Nishizawa","sequence":"first","affiliation":[{"name":"Division of Diabetes and Endocrinology, Department of Internal Medicine (H.B., G.I., H.F., M.Y., R.H., R.M., K.S., H.N., M.T., Y.T.), Kobe University Graduate School of Medicine, 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