{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,1]],"date-time":"2026-10-01T06:03:22Z","timestamp":1790834602957,"version":"4.1.0"},"reference-count":36,"publisher":"American Association for the Advancement of Science (AAAS)","issue":"4756","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Science"],"published-print":{"date-parts":[[1986,6,13]]},"abstract":"<jats:p>\n            Almost all B cells in autoimmune mice with the viable motheaten (\n            <jats:italic>me<\/jats:italic>\n            <jats:sup>v<\/jats:sup>\n            ) mutation express the Ly-1 cell surface antigen, which marks a minor population of B cells constituting a separate lineage in normal mice. Immunoglobulins primarily of the M and G3 classes, which in both normal and\n            <jats:italic>me<\/jats:italic>\n            <jats:sup>v<\/jats:sup>\n            mice contain high levels of lambda light chain, are produced in excess in\n            <jats:italic>me<\/jats:italic>\n            <jats:sup>v<\/jats:sup>\n            mice. These and other observations suggest that the development of B cells that express Ly-1 is regulated independently from the development of B cells that do not express Ly-1. B cells bearing the Ly-1 surface antigen may play specialized roles in the normal immune system and in autoimmunity by regulating other B cells via lymphokines, by producing antibodies to self and certain foreign antigens, and by preferentially secreting immunoglobulin M and immunoglobulin G3.\n          <\/jats:p>","DOI":"10.1126\/science.3487115","type":"journal-article","created":{"date-parts":[[2006,10,5]],"date-time":"2006-10-05T20:28:52Z","timestamp":1160080132000},"page":"1423-1425","source":"Crossref","is-referenced-by-count":226,"title":["Production of Immunoglobulin Isotypes by Ly-1\n            <sup>+<\/sup>\n            B Cells in Viable Motheaten and Normal Mice"],"prefix":"10.1126","volume":"232","author":[{"given":"Charles L.","family":"Sidman","sequence":"first","affiliation":[{"name":"The Jackson Laboratory, Bar Harbor, ME 04609."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Leonard D.","family":"Shultz","sequence":"additional","affiliation":[{"name":"The Jackson Laboratory, Bar Harbor, ME 04609."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Richard R.","family":"Hardy","sequence":"additional","affiliation":[{"name":"Department of Genetics, Stanford University Medical School, Stanford, CA 94305."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Kyoko","family":"Hayakawa","sequence":"additional","affiliation":[{"name":"Department of Genetics, Stanford University Medical School, Stanford, CA 94305."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Lee A.","family":"Herzenberg","sequence":"additional","affiliation":[{"name":"Department of Genetics, Stanford University Medical School, Stanford, CA 94305."}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"221","reference":[{"key":"e_1_2_1_1_1","doi-asserted-by":"crossref","first-page":"931","DOI":"10.1084\/jem.136.4.931","volume":"136","year":"1972","unstructured":"AMSBAUGH, D.F., GENETIC-CONTROL OF ANTIBODY-RESPONSE TO TYPE III PNEUMOCOCCAL POLYSACCHARIDE IN MICE .1. 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