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Representative data from a single subject treated at 60 μg/kg/d are shown

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posted on 2011-12-31, 13:54 authored by Claude Sportès, Frances T. Hakim, Sarfraz A. Memon, Hua Zhang, Kevin S. Chua, Margaret R. Brown, Thomas A. Fleisher, Michael C. Krumlauf, Rebecca R. Babb, Catherine K. Chow, Terry J. Fry, Julie Engels, Renaud Buffet, Michel Morre, Robert J. Amato, David J. Venzon, Robert Korngold, Andrew Pecora, Ronald E. Gress, Crystal L. Mackall
(A) Two-dimensional plots illustrating the rhIL-7 therapy–induced increased frequency of CD4 RTEs (CD31/CD45RA; red boxes in first row of graphs), and changes in CD4 and CD8 naive, memory, and effector subsets (respectively CD45RA/CD27, CD45RA/CD27, and CD45RA/CD27 sections on second and third rows). (B) Overlay histograms of Ki-67 expression on CD4 RTEs (CD31/CD45RA) and CD4 and CD8 naive (CD45RA/CD27), memory (CD45RA/CD27), and effector (CD45RA/CD27) subsets. Percent Ki-67 cells are indicated in each frame. Red lines, pretreatment; blue lines, day 7; green lines, day 14; orange lines, day 21. Note that at the end of treatment (green line), the percentage of Ki67 memory and effector CD8 populations drop to lower levels than the naive CD8. (C) Two-dimensional plots illustrating the rhIL-7 therapy–induced changes in CD4 (top row) and CD8 (bottom row) naive, central memory, effector memory, and effectors (respectively CD45RA/CCR7, CD45RA/CCR7, CD45RA/CCR7, and CD45RA/CCR7 sections).

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Taken from "Administration of rhIL-7 in humans increases in vivo TCR repertoire diversity by preferential expansion of naive T cell subsets"

The Journal of Experimental Medicine 2008;205(7):1701-1714.

Published online 7 Jul 2008

PMCID:PMC2442646.

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