ライフサイエンスコーパス: IL-3R

1 hinella-induced basophil responses were IL-3-IL-3R independent but critically dependent on TSLP-TSLPR

2 could elicit basophil responses in both IL-3-IL-3R-sufficient and -deficient environments, and genome

3 mice, we report in this study that the IL-3/IL-3R system is absolutely required to recruit circulati

4 on activates transcription factor CREB after IL-3R engagement.

5 he entire cytoplasmic domain of IL-3R alpha [IL-3R alpha(CD)] or carrying a substitution of trp for l

6 d to residues 306 through 379 of GM-R alpha [IL-3R alpha/GM-R alpha-DS] also failed to bind 125I-IL-3

7 subunit of the GM-CSF receptor (GM-R alpha) [IL-3R alpha/GM-R alpha] or the first 118 aa of GM-R alph

8 a 104 through 378 of IL-3R alpha [GM-R alpha/IL-3R alpha] failed to bind 125I-IL-3 in the presence of

9 n was potent because it inhibited FDC-P1, an IL-3R-expressing murine myelomonocytic tumor line (IC50

10 Preincubation of HUVECs with an IL-3R-blocking Ab (CD123) before the addition of IL-3 in

11 ile up-regulating alpha-chain mRNAs for both IL-3R and GM-CSFR as well as the beta-chain mRNA.

12 he CD11c+ DC subset (48-fold) and the CD11c- IL-3R+ DC precursors (13-fold).

13 1) resident eosinophils (Siglec-8(+)CD62L(+)IL-3R(lo)) or 2) inflammatory eosinophils (iEos; Siglec-

14 e G-CSF domain can alter the ratio of G-CSFR:IL-3R agonist activities, demonstrating that it is a use

15 l line (Ba/F3), which endogenously expresses IL-3R.

16 (+) lymphoid progenitor population expresses IL-3R and proliferates in response to IL-3 and that IL-3

17 Cell lines not expressing IL-3R were not inhibited by the fusion protein.

18 , whereas enhanced accumulation of mRNAs for IL-3R alpha and the beta-chain results from reduced mRNA

19 anisms that are distinct from those used for IL-3R alpha and GM-CSFR alpha.

20 The functional IL-3R expression on the surface was seen only after anti

21 Furthermore, IL-3R expressing and IL-3-secreting Th cells were high i

22 d basophil rolling and adhesion, implicating IL-3R activation on endothelial cells.

23 Interestingly, IL-3R(+) cells exhibit a Th2 cell-like phenotype and sho

24 atory eosinophils (iEos; Siglec-8(+)CD62L(lo)IL-3R(hi)).

25 f GM-R alpha joined to aa 104 through 378 of IL-3R alpha [GM-R alpha/IL-3R alpha] failed to bind 125I

26 omposed of the first 104 amino acids (aa) of IL-3R alpha joined to aa 118 through 400 of the alpha su

27 king almost the entire cytoplasmic domain of IL-3R alpha [IL-3R alpha(CD)] or carrying a substitution

28 ar domain of EpoR fused to the endodomain of IL-3R beta-chain (E/beta), while the other contained the

29 ha, respectively, fused to the endodomain of IL-3R beta-chain.

30 ficantly increases the surface expression of IL-3R and also increases the number of IL-3R(+) Th cells

31 human chondrocytes show strong expression of IL-3R at gene and protein levels.

32 de the first evidence that the expression of IL-3R on activated human Th cells is modulated by IL-4,

33 might be heterogenous in their expression of IL-3R.

34 ting state do not show surface expression of IL-3R; however, its expression was observed at transcrip

35 on of IL-3R and also increases the number of IL-3R(+) Th cells.

36 To identify regions of IL-3R alpha critical for ligand binding and receptor fun

37 his study, we investigated the regulation of IL-3R expression on human Th cells and also examined the

38 ceptor composed of the first 281 residues of IL-3R alpha fused to residues 306 through 379 of GM-R al

39 exhibited significant surface expression of IL-3Rs and GM-CSFRs, as well as ERK1/2 phosphorylation i

40 subunit of the human interleukin-3 receptor (IL-3R alpha) is a 70-kD glycoprotein member of the hemat

41 F (cpG-CSF) sequences with an IL-3 receptor (IL-3R) agonist moiety attached at locations that corresp

42 nd downregulation of interleukin-3 receptor (IL-3R) beta-chain expression, and accelerated G-CSF-stim

43 y cytokine receptor (interleukin-3 receptor [IL-3R], IL-5R, and granulocyte-macrophage colony stimula

44 lasm, in contrast to the mitogenic receptors IL-3R, IL-5R, GM-CSFR, which assemble as alphabeta heter

45 ukemias can express interleukin-3 receptors (IL-3R).

46 anulocyte-macrophage CSF (GM-CSF) receptors (IL-3R and GM-CSFR).

47 econdary transfer experiments indicated that IL-3R is not uniformly expressed on all primitive progen

48 We have recently shown that IL-3R occupancy activates a phosphatidylcholine-specific

49 atment of myeloid leukemias that express the IL-3R.

50 Approximately 38% of BMCPs expressed the IL-3R alpha-chain.

51 to be more potent than the coaddition of the IL-3R agonist and G-CSF in stimulating the production of

52 are distinguishable by the expression of the IL-3R alpha chain, the receptor of an early-acting hemat

53 3 cross-linking is due to stimulation of the IL-3R and induction of PDC maturation.

54 tions were found in which the linkage to the IL-3R agonist domain either restored (e.g., attachment a

55 of the beta subunit but, in contrast to the IL-3R alpha/GM-R alpha hybrid, demonstrated weak surface

56 The MPOs retained the ability to bind to the IL-3R with affinities similar to that of the parental MP

57 MPO in which the IL-3R agonist domain is attached to the cpG-CSF(L1)[133/

58 MPOs with the IL-3R agonist domain linked to cpG-CSFs in the first (re

59 3 with nearly the same affinity as wild-type IL-3R alpha.