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Massachusetts Institute of Technology

Interleukin-2 Engineering for improved therapeutic effectiveness

Abstract

dc:description.abstract

(cont.) (K[d] [approximately] 10pM) for its private alpha receptor subunit, unlike wild-type IL-2 (K[d] [approximately] 10 nM). IL-2 mutants with picomolar affinity for IL-2Rα stimulate T cell growth responses quantitatively equivalent to those mediated by IL-15. Our results suggest that the contrasting effects of IL-2 and IL-15 on T cells in vivo are largely due to the 1,000-fold different affinities of wild-type IL-2 and IL-15 for their respective private alpha receptor subunits.

Degree

thesis:*
Department dc:contributor.department
Massachusetts Institute of Technology. Dept. of Chemical Engineering.
Grantor dc:publisher
Massachusetts Institute of Technology
Year dc:date.issued
2004

Author and committee

dc:creator, dc:contributor.*
Author dc:creator
  • Rao, Balaji Madhav, 1978-
Advisor dc:contributor.advisor
  • K. Dane Wittrup and Douglas A. Lauffenburger.

Subjects

dc:subject × 1

Rights

dc:rights
Statement dc:rights
  • M.I.T. theses are protected by copyright. They may be viewed from this source for any purpose, but reproduction or distribution in any format is prohibited without written permission. See provided URL for inquiries about permission.
Language dc:language.iso
en_US

Identifiers

dc:identifier.*
Handle dc:identifier.uri
http://hdl.handle.net/1721.1/28664
OAI identifier oai:identifier
oai:dspace.mit.edu:1721.1/28664

Chain of custody

source
Harvested from
MIT
Base URL
dspace.mit.edu/oai/request
Last updated
2026-07-22
Source record
OAI-PMH GetRecord
citation

Rao, Balaji Madhav, 1978-. Interleukin-2 Engineering for improved therapeutic effectiveness. Massachusetts Institute of Technology, 2004. http://hdl.handle.net/1721.1/28664