Abstract
Adult stem cell migration through human hematopoietic tissue requires the chemokine CXCL12 and its receptor CXCR4. In addition, human leukocyte elastase (HLE) plays a key role. When HLE is located on the cell surface (HLECS), it acts not as a proteinase, but as a receptor for α1proteinase inhibitor (α1PI, α1antitrypsin). Binding of α1PI to HLECS forms a motogenic complex. We previously demonstrated that α1PI deficiency attends HIV-1 disease. Here we investigate the mechanism and therapeutically address the α1PI deficiency of HIV-1 infection.
Highlights
Adult stem cell migration through human hematopoietic tissue requires the chemokine CXCL12 and its receptor CXCR4
We previously demonstrated that a1PI deficiency attends HIV-1 disease
In HIV-1 uninfected individuals, CD4+ lymphocytes were correlated with the combined factors a1PI, HLE is located on the cell surface (HLECS)+ lymphocytes, and CXCR4+ lymphocytes (r2 = 0.91, p < 0.001, n = 30), but not CXCL12
Summary
Adult stem cell migration through human hematopoietic tissue requires the chemokine CXCL12 and its receptor CXCR4. Human leukocyte elastase (HLE) plays a key role. When HLE is located on the cell surface (HLECS), it acts not as a proteinase, but as a receptor for a1proteinase inhibitor (a1PI, a1antitrypsin). Binding of a1PI to HLECS forms a motogenic complex. We previously demonstrated that a1PI deficiency attends HIV-1 disease. We investigate the mechanism and therapeutically address the a1PI deficiency of HIV-1 infection
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