{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,1,29]],"date-time":"2026-01-29T03:52:56Z","timestamp":1769658776830,"version":"3.49.0"},"reference-count":64,"publisher":"Oxford University Press (OUP)","issue":"3","license":[{"start":{"date-parts":[[2007,2,1]],"date-time":"2007-02-01T00:00:00Z","timestamp":1170288000000},"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":[[2007,2,1]]},"abstract":"<jats:title>Abstract<\/jats:title>\n                  <jats:p>Immunological mechanisms leading to increased asthma susceptibility in early life remain obscure. In this study, we examined the effects of neonatal Ab treatments targeting T cell populations on the development of an asthma syndrome. We used a model of increased asthma susceptibility where offspring of asthmatic BALB\/c mother mice are more prone (than normal pups) to develop the disease. Neonatal pretreatment of naive pups with mAb directed against the IL-2R\u03b1 chain (CD25), the costimulatory molecule glucocorticoid-induced TNFR family related gene, and the inhibitory molecule CTLA-4 elicited contrasting effects in offspring depending on the mother\u2019s asthma status. Specifically, neonatal CD25high T cell depletion stimulated asthma susceptibility in normal offspring whereas it ameliorated the condition of pups born of asthmatic mothers. Conversely, glucocorticoid-induced TNFR family related gene ligation as a primary signal reduced the spleen cellularity and largely abrogated asthma susceptibility in asthma-prone offspring, without inducing disease in normal pups. Striking changes in Th1\/Th2 cytokine levels, especially IL-4, followed mAb pretreatment and were consistent with the impact on asthma susceptibility. These results point to major differences in neonatal T cell population and responsiveness related to maternal asthma history. Interventions that temporarily remove and\/or inactivate specific T cell subsets may therefore prove useful to attenuate early life asthma susceptibility and prevent the development of Th2-driven allergic airway disease.<\/jats:p>","DOI":"10.4049\/jimmunol.178.3.1477","type":"journal-article","created":{"date-parts":[[2014,4,18]],"date-time":"2014-04-18T19:08:45Z","timestamp":1397848125000},"page":"1477-1487","source":"Crossref","is-referenced-by-count":23,"title":["Targeting of CD25 and Glucocorticoid-Induced TNF Receptor Family-Related Gene-Expressing T Cells Differentially Modulates Asthma Risk in Offspring of Asthmatic and Normal Mother Mice"],"prefix":"10.1093","volume":"178","author":[{"given":"Cedric","family":"Hubeau","sequence":"first","affiliation":[{"name":"Department of Environmental Health, Harvard School of Public Health , Boston, MA 02115"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Irina","family":"Apostolou","sequence":"additional","affiliation":[{"name":"Department of Cancer Immunology and AIDS, Dana-Farber Cancer Institute , Boston, MA 02115"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Lester","family":"Kobzik","sequence":"additional","affiliation":[{"name":"Department of Environmental Health, Harvard School of Public Health , Boston, MA 02115"},{"name":"Department of Pathology, Brigham & Women\u2019s Hospital , Boston, MA 02115"}],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"286","published-online":{"date-parts":[[2007,2,1]]},"reference":[{"key":"2026012810525046600_R1","first-page":"789","volume-title":"Annu. 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