ライフサイエンスコーパス: LFA-3

1 and leukocyte function-associated antigen-3 (LFA-3).

2 e costimulatory molecules (B7.1, ICAM-1, and LFA-3).

3 a high degree of sequence homology to CD58 (LFA-3).

4 e function-associated antigen 1 (LFA-1), and LFA-3.

5 human accessory molecules B7.1, ICAM-1, and LFA-3.

6 immunogen and adhesion molecules ICAM-1 and LFA-3.

7 s containing purified, fluorescently labeled LFA-3.

8 Anti-LFA-3 Abs, in the absence or presence of IL-12, inhibit

9 LFA-3 accumulated at sites of contact with a half-time o

10 to or better than PBAMCs, which use both the LFA-3 and B7 molecules, at costimulating IL-2 and IL-4 p

11 Therefore, receptors for LFA-3 and CD48 on resting NK cells strengthen the adhesi

12 imulatory molecules (CD80, CD86, ICAM-1, and LFA-3) and Fas expression.

13 (ICAM-1), lymphocyte function associated-3 (LFA-3), and vascular cell adhesion molecule-1 (VCAM-1) a

14 en 1alpha (LFA-1alpha), CD18/LFA-1beta, CD58/LFA-3, and CD54/intercellular adhesion molecule, CD8 for

15 Interactions with ICAM-1, LFA-3, and to a lesser extent CD80/CD86 contribute to th

16 A-3 (CD58) mAb or pretreatment of EC with an LFA-3 antisense oligonucleotide blocks EC-induced increa

17 region, encoding the costimulatory molecule LFA-3, are associated with risk of developing MS.

18 l costimulatory molecules (B7-1, ICAM-1, and LFA-3) as a result of individual early avipox promoters

19 othelial cells (PAEC) via the second signals LFA-3/CD2 and B7-2 (CD86), respectively.

20 ded intercellular adhesion molecule-1/LFA-1, LFA-3/CD2, and class I/CD8.

21 Inclusion of anti-human LFA-3 (CD58) mAb or pretreatment of EC with an LFA-3 ant

22 Coexpression of either LFA-3 (CD58) or CD48 with ICAM-1 resulted in strong adhe

23 CD2 interactions with its principal ligand, LFA-3 (CD58), can inhibit immune reactions in vivo.

24 in lymphocyte function-associated antigen-3 (LFA-3) (CD58) and CD44 motifs modified with CS or a comb

25 , lymphocyte function-associated molecule-3 (LFA-3, CD58), or intercellular adhesion molecule-1 (ICAM

26 ression of the costimulatory molecules CD58 (LFA-3), CD80 (B7-1), and CD86 (B7-2) by using flow cytom

27 impaired by low levels of ICAM-1, LFA-1, and LFA-3 cell surface expression, a functional attribute th

28 Thus, formation of CD2/LFA-3 complexes should be highly favored in physiologica

29 ity was reduced by 80 and 70% after B7-1 and LFA-3 costimulation, respectively.

30 l costimulatory molecules (B7-1, ICAM-1, and LFA-3 (designated TRICOM)) enhances the level and avidit

31 l costimulatory molecules [B7-1, ICAM-1, and LFA-3, designated recombinant vaccinia (rV)-CEA/TRICOM],

32 imulatory molecule transgenes (B7-1, ICAM-1, LFA-3, designated rF-CEA/TRICOM) was more potent in indu

33 RIad of COstimulatory Molecules (B7-1/ICAM-1/LFA-3, designated TRICOM) induced the activation of T ce

34 -cell costimulatory molecules (B7-1, ICAM-1, LFA-3, designated TRICOM) results in a significant impro

35 and leukocyte-function-associated antigen 3 [LFA-3], designated TRICOM), to stimulate effective antit

36 These data provide the first evidence that LFA-3 functions in vivo and establish the ability of thi

37 omposed of the first extracellular domain of LFA-3 fused to the human IgG1 hinge, C(H)2, and C(H)3 do

38 mCD2-hCD2+ mice treated with anti-T11(1) or LFA-3 fusion proteins also showed significant prolongati

39 sion receptor CD2 with its counter-receptor, LFA-3, has a high solution-phase Kd (16 microM at 37 deg

40 costimulatory molecule CD80, while I-CAM-1, LFA-3, HLA-DR, and CD86 expression were unaffected.

41 cells, the virus progeny bore high levels of LFA-3, ICAM-1, and major histocompatibility complex clas

42 by mAb blocking of costimulation provided by LFA-3, ICAM-1, or CD40, by addition of comitogenic anti-

43 Both Amevive, an LFA-3-Ig fusion protein targeting CD2, and Xanelim, a hu

44 anti-tumor necrosis factor antibodies, anti-LFA-3-IgG fusion protein, extracorporeal photopheresis,

45 Murine Mab to human LFA-3 or human LFA-3-IgG1 fusion protein, but not isotype-matched contr

46 We have studied the interaction of CD2 with LFA-3 in the contact area between Jurkat T lymphoblasts

47 Kd (16 microM at 37 degrees C), yet the CD2/LFA-3 interaction serves as an effective adhesion mechan

48 dS suggest that cell-cell contact favors CD2/LFA-3 interaction to a greater extent than that predicte

49 The two-dimensional Kd for the CD2/LFA-3 interaction was 21 molecules/microns 2, which is l

50 of costimulatory molecules, particularly CD2-LFA-3 interaction.

51 on of the structurally related protein CD58 (LFA-3) is associated with disease remission in MS.

52 Coexpression of ICAM-1 or LFA-3 molecules along with DNA immunogens resulted in a

53 LFA-3 molecules in the contact site were capable of late

54 SW480 cells express both ICAM-1 and LFA-3 molecules, and the addition of Abs to these recept

55 the surface densities of CD2 on T cells and LFA-3 on most target or stimulator cells.

56 lymphocyte function-associated antigen-3, or LFA-3) on the ECs and were mediated by production of sol

57 n between CD2 and its counterreceptor, CD58 (LFA-3), on opposing cells optimizes immune recognition,

58 Murine Mab to human LFA-3 or human LFA-3-IgG1 fusion protein, but not isotyp

59 31 (PE-CAM), and CD54 (ICAM-I) but not CD58 (LFA-3) or CD95 (Fas).

60 Analysis of the CD44-modified LFA-3 protein showed that it retains the ability to enga

61 These results suggest that ICAM-1 and LFA-3 provide direct T-cell costimulation.

62 of TCs (e.g. LFA-1 and ICAM-1-ICAM3, CD2 and LFA-3; receptors for TNF and corresponding ligand etc.0;

63 calize in a new lipid microdomain from which LFA-3 remains excluded and the TCR is now dissociated.

64 f costimulatory molecules (B7-1, ICAM-1, and LFA-3), respectively.

65 r CD28 or CD2 by its cognate ligands B7-1 or LFA-3, respectively, greatly aids the Ag-induced up-regu

66 Moreover, mAb to LFA-3 reverses the capacity of EC to prolong the half-li

67 latory molecules (TRICOM): B7.1, ICAM-1, and LFA-3 (rV-CEA-TRICOM); and (b) a booster vaccine using C

68 Blockade of LFA-3 strongly inhibits both IL-2 and IFN-gamma secretio

69 in contact areas as functions of the initial LFA-3 surface density and of time after contact of the c

70 ransduced to express human B7.1, ICAM-1, and LFA-3 that each stably express one of a series of six co

71 We conclude that EC use LFA-3 to increase early CD40L protein expression on newl

72 minantly leukocyte-function associated Ag 3 (LFA-3) to provide costimulation.

73 B7.1, intercellular adhesion molecule-1, and LFA-3, together with either p540 and p865 minigenes or t

74 Redistribution and lateral mobility of LFA-3 were measured in contact areas as functions of the

75 and CD59, while beta(1) integrin, CD43, and LFA-3 were not localized in the vesicle.

76 e costimulatory molecules (B7-1, ICAM-1, and LFA-3), with anti-CTLA-4 mAb, with GM-CSF, and combinati