Processing by CD26/dipeptidyl-peptidase IV reduces the chemotactic and anti-HIV-1 activity of stromal-cell-derived factor-1α

被引：186

作者：

Proost, P

Struyf, S

Schols, D

Durinx, C

Wuyts, A

Lenaerts, JP

De Clercq, E

De Meester, I

Van Damme, J

机构：

[1] Katholieke Univ Leuven, Rega Inst Med Res, Lab Mol Immunol, B-3000 Leuven, Belgium

[2] Katholieke Univ Leuven, Rega Inst Med Res, Lab Expt Chemotherapy, B-3000 Leuven, Belgium

[3] Univ Instelling Antwerp, Lab Clin Biochem, B-2610 Wilrijk, Belgium

来源：

FEBS LETTERS | 1998年 / 432卷 / 1-2期

关键词：

chemokine; CXCR4; HIV-1; inhibitor; desensitization; SDF-1; alpha; exopeptidase;

D O I：

10.1016/S0014-5793(98)00830-8

中图分类号：

Q5 [生物化学]; Q7 [分子生物学];

学科分类号：

071010 ; 081704 ;

摘要：

The chemokine stromal-cell-derived factor-let (SDF-1 alpha) chemoattracts lymphocytes and CD34(+) haematopoietic progenitors and is the ligand for CXCR4 (CXC chemokine receptor 4), the main co-receptor for T-tropic HIV-1 strains. SDF-1 alpha was NH2-terminally cleaved to SDF-1 alpha?(3-68) by dipeptidyl-peptidase IV (CD26/DPP IV), which is present in blood in soluble and membrane-bound form. SDF-1 alpha(3-68) lost both lymphocyte chemotactic and CXCR4-signaling properties. However, SDF-1 alpha(3-68) still desensitized the SDF-1 alpha(1-68)-induced Ca2+ response. In contrast to CD26/DPP IV-processed RANTES(3-68), SDF-1 alpha(3-68) had diminished potency to inhibit HIV-I infection. Thus, CD26/DPP IV impairs the inflammatory and haematopoietic potency of chemokines but plays a dual role in AIDS. (C) 1998 Federation of European Biochemical Societies.

引用

页码：73 / 76

页数：4

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