{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,2]],"date-time":"2026-10-02T10:34:52Z","timestamp":1790937292380,"version":"4.1.0"},"reference-count":63,"publisher":"Wiley","issue":"1","license":[{"start":{"date-parts":[[2007,3,12]],"date-time":"2007-03-12T00:00:00Z","timestamp":1173657600000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Immunological Reviews"],"published-print":{"date-parts":[[2007,4]]},"abstract":"<jats:p><jats:bold>Summary:\u2002<\/jats:bold> The control of T\u2010 and B\u2010cell proliferation following antigen stimulation lies at the heart of the adaptive immune response. The outcome of a response depends on the number of cells that are activated to go into cycle, the rates at which the cells divide and die, and the number of division cycles the cells undergo. Each of these processes may be under independent control, and the precise outcome of T\u2010 or B\u2010cell responses to antigen will depend on how the signals controlling the different events are integrated. In this article, the way different mathematical models in combination with data from carboxyfluorescein diacetate succinamidyl ester (CFSE) experiments can be used to investigate the mechanisms controlling T\u2010 and B\u2010cell proliferation is reviewed.<\/jats:p>","DOI":"10.1111\/j.1600-065x.2006.00498.x","type":"journal-article","created":{"date-parts":[[2015,10,13]],"date-time":"2015-10-13T15:10:46Z","timestamp":1444749046000},"page":"119-129","source":"Crossref","is-referenced-by-count":39,"title":["Modeling T\u2010 and B\u2010cell growth and 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