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

机译:CD26 /二肽基肽酶IV处理可降低基质细胞衍生因子-1α的趋化性和抗HIV-1活性

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>The chemokine stromal-cell-derived factor-1α (SDF-1α) 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-1α was NH2-terminally cleaved to SDF-1α(3-68) by dipeptidyl-peptidase IV (CD26/DPP IV), which is present in blood in soluble and membrane-bound form. SDF-1α(3-68) lost both lymphocyte chemotactic and CXCR4-signaling properties. However, SDF-1α(3-68) still desensitized the SDF-1α(1-68)-induced Ca2+ response. In contrast to CD26/DPP IV-processed RANTES(3-68), SDF-1α(3-68) had diminished potency to inhibit HIV-1 infection. Thus, CD26/DPP IV impairs the inflammatory and haematopoietic potency of chemokines but plays a dual role in AIDS.
机译:>趋化因子基质细胞衍生因子1α(SDF-1α)吸引淋巴细胞和CD34 + 造血祖细胞,并且是主要共受体CXCR4(CXC趋化因子受体4)的配体。用于T-tropic HIV-1菌株。 SDF-1α是NH 2 端,被二肽基肽酶IV(CD26 / DPP IV)裂解成SDF-1α(3-68),它以可溶和膜结合的形式存在于血液中。 SDF-1α(3-68)失去了淋巴细胞趋化性和CXCR4信号转导特性。然而,SDF-1α(3-68)仍然使SDF-1α(1-68)诱导的Ca 2 + 响应减敏。与CD26 / DPP IV处理的RANTES(3-68)相反,SDF-1α(3-68)抑制HIV-1感染的能力减弱。因此,CD26 / DPP IV损害了趋化因子的炎症和造血能力,但在艾滋病中起着双重作用。

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