{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2025,10,31]],"date-time":"2025-10-31T14:10:10Z","timestamp":1761919810645,"version":"3.40.3"},"reference-count":42,"publisher":"Oxford University Press (OUP)","issue":"4","license":[{"start":{"date-parts":[[2002,8,1]],"date-time":"2002-08-01T00:00:00Z","timestamp":1028160000000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/academic.oup.com\/pages\/standard-publication-reuse-rights"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":[],"published-print":{"date-parts":[[2002,8,15]]},"abstract":"<jats:title>Abstract<\/jats:title>\n               <jats:p>Persistent cross-linking of hen egg lysozyme (HEL)-specific B cell membrane Ig (mIg) in double transgenic mice that express soluble HEL as a self Ag (HEL-Ig mice) decreases B cell mIgM expression, responsiveness, and life span. Because in vitro treatment with IL-4 inhibits T cell apoptosis through a Stat6-independent mechanism, increases mIg expression, and suppresses activation-induced B cell death, we studied IL-4 effects on B cell mIg expression, survival, and Ab secretion in Stat6-sufficient and deficient HEL-Ig mice. IL-4 treatment nearly normalized B cell number and greatly increased the percentage of mature B cells in HEL-Ig mice, but failed to normalize mIgM expression or spontaneous LPS-induced IgM secretion. IL-4 effects on B cell survival and maturation were CD4+ T cell independent, but Stat6 dependent, and did not involve receptor editing. IL-4 had to be present while B cells were generated to have a detectable effect on autoreactive B cell survival; however, the survival of B cells generated in the presence of IL-4 was substantially increased even after IL-4 was withdrawn. These observations suggest that: 1) activation-induced B cell death and anergy are independent processes; 2) B cells that survive to maturity develop increased resistance to Ag-induced deletion; and 3) IL-4 promotes B and T cell survival through different mechanisms.<\/jats:p>","DOI":"10.4049\/jimmunol.169.4.1696","type":"journal-article","created":{"date-parts":[[2014,4,20]],"date-time":"2014-04-20T22:19:11Z","timestamp":1398032351000},"page":"1696-1704","source":"Crossref","is-referenced-by-count":15,"title":["IL-4 Promotes Stat6-Dependent Survival of Autoreactive B Cells In Vivo Without Inducing Autoantibody Production"],"prefix":"10.1093","volume":"169","author":[{"given":"Suzanne C","family":"Morris","sequence":"first","affiliation":[{"name":"Cincinnati Veterans Affairs Medical Center , Cincinnati, OH 45220"},{"name":"Division of Immunology, University of Cincinnati College of Medicine , Cincinnati, OH 45267"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Nanette L","family":"Dragula","sequence":"additional","affiliation":[{"name":"Cincinnati Veterans Affairs Medical Center , Cincinnati, OH 45220"},{"name":"Division of Immunology, University of Cincinnati College of Medicine , Cincinnati, OH 45267"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Fred D","family":"Finkelman","sequence":"additional","affiliation":[{"name":"Cincinnati Veterans Affairs Medical Center , Cincinnati, OH 45220"},{"name":"Division of Immunology, University of Cincinnati College of Medicine , Cincinnati, OH 45267"},{"name":"Division of Immunology, Children\u2019s Hospital Medical Center , Cincinnati, OH 45229"}],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"286","published-online":{"date-parts":[[2002,8,15]]},"reference":[{"volume-title":"Immunol. 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