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1 hibition also promoted TH(2) polarization in memory CD4 cells.
2 dent CD80/CD86 expression, and activation of memory CD4 cells.
3  costimulatory molecule OX40 is expressed on memory CD4 cells.
4 ir by promoting homeostatic proliferation of memory CD4+ cells.
5 ve influence on memory CD8(+) cells, but not memory CD4(+) cells.
6 roductive state within a small population of memory CD4(+) cells.
7 e that iTreg can be efficiently induced from memory CD4 cells, a subset enriched in relevant specific
8 only once induced a maximal pool of effector/memory CD4(+) cells and protective immunity by 4 wk afte
9                              Jug r 2 central memory CD4(+) cells and terminal effector T cells were d
10 mmunosuppression mediated by CD25(-)Foxp3(-) memory CD4(+) cells and, in the absence of those cells,
11                         CCR4 was on 5-21% of memory CD4 cells, and 20% were also ESL(+).
12 emory populations were comparable to that in memory CD4 cells, and both Tc1 and Tc2 memory cells beca
13 lymphopenic hosts where IL-7 levels are low, memory CD4 cells are heavily dependent on IL-15.
14                                      Resting memory CD4(+) cells are dependent on signals from contac
15              In vitro evidence suggests that memory CD4(+) cells are preferentially infected by human
16 echanisms that control memory CD8+ cells and memory CD4+ cells are quite distinct.
17 pigeon cytochrome c from TCR transgenics and memory CD4 cells derived by in vivo priming with KLH.
18 ve examined the synapses formed by naive and memory CD4 cells during Ag-specific cognate interactions
19                                              Memory CD4 cells engrafted and responded to antigen both
20                                Dermal homing memory CD4 cells express CCR4 and depend more on alpha(4
21 y CD4 lymphocytes, including almost all skin memory CD4(+) cells expressing the cutaneous lymphocyte
22 cing cells were also observed among effector memory CD4(+) cells for two of these donors.
23                           The ratio of naive:memory CD4+ cells from PB positively correlated with tha
24 ytokines are required for the maintenance of memory CD4 cells has not been rigorously assessed.
25                     In contrast, Ag-specific memory CD4 cells have a slow turnover rate and are MHC I
26                              Past studies of memory CD4(+) cells have relied heavily on the use of na
27 ralization of these beta-chemokines rendered memory CD4(+) cells highly sensitive to infection with R
28 nd CD40L-dependent bulk B cell activation of memory CD4 cells in HCV infection.
29 ts in a latent reservoir of infected resting memory CD4 cells in patients receiving antiretroviral th
30 rvival and up-regulation of Bcl-2 by resting memory CD4 cells in vitro in the absence of proliferatio
31 lls pulsed with defined doses of Ag anergize memory CD4 cells in vivo.
32  In vivo, there is an expansion of activated/memory CD4(+) cells in p27(Kip1)-deficient mice before a
33 rtmentalization of antigen-specific effector memory CD4(+) cells in the lungs of CBD patients.
34        The differentiation from activated to memory CD4 cells increases the dependence on CCR4 for sk
35                    Strikingly, we found that memory CD4 cells induced neither clinical nor histologic
36 ory CD8+ cells, homeostatic proliferation of memory CD4+ cells is independent of IL-7 and IL-15 (also
37 suggest that the threshold for activation of memory CD4+ cells is lower than that of naive cells.
38                                      CCR4(+) memory CD4 cells migrated 4- to 7-fold more to dermal in
39 nversion of naive responder cells to central memory CD4 cells (P<0.001 at 96 hr) and effector CD8 cel
40                                              Memory CD4 cells persisted for extended periods upon ado
41 hymus is not critical for maintenance of the memory CD4 cell pool in the periphery.
42              The development of effector and memory CD4 cell populations depends upon both T cell rec
43 seline age, CD4 cells, HIV RNA, and naive-to-memory CD4 cell ratio, haplogroup L2 was associated with
44 ce of B cells did not affect the survival of memory CD4 cells since frequencies remained stable.
45 remaining naive (CD44(low) or CD44(int)) and memory CD4(+) cell subsets in reconstituting the overall
46 rvival of resting T cell receptor transgenic memory CD4 cells that were generated in vivo.
47 onally, DL1 potentiated FOXP3 acquisition by memory CD4 cells through the modulation of the TGF-beta
48 (+) and CD8(+) cells were activated but only memory CD4(+) cells were cycling at increased frequency.
49 these subjects exhibit a higher frequency of memory CD4 cells with the capacity to transition into IL

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