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Dysfunctions in the migratory phenotype and properties of circulating immature transitional B cells during HIV-1 infection.

Dysfunctions in the migratory phenotype and properties of circulating immature transitional B cells during HIV-1 infection.
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Amu S, Fievez V, Nozza S, Lopalco L, Chiodi F,


Amu S, Fievez V, Nozza S, Lopalco L, Chiodi F, (click to view)

Amu S, Fievez V, Nozza S, Lopalco L, Chiodi F,

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AIDS (London, England) 30(14) 2169-77 doi 10.1097/QAD.0000000000001182

Abstract
OBJECTIVE
The frequency of immature transitional B cells is increased in blood of HIV-1-infected individuals. We investigated whether HIV-1 infection affects expression and function of chemokine receptors important for egress of immature transitional B cells from bone marrow and migration to lymphoid organs.

DESIGN
This is a cross-sectional study analysing the migratory phenotype and function of immature transitional B cells in HIV-1-infected individuals, in relation to antiretroviral treatment and age.

METHODS
Frequency of blood immature transitional B cells and their phenotypic characteristics, including chemokine receptors and a maturation marker, were determined by immunostainings. Migratory capacities were studied in a migration assay.

RESULTS
The increased frequency of immature transitional B cells in untreated HIV-1 infection was normalized in patients receiving antiretroviral treatment; in our cohorts, age did not have an impact on the frequency of circulating immature transitional B cells. Immature transitional B cells from nontreated patients expressed low levels of CD21 molecule. We found an elevated frequency of CXCR3 and CXCR4 expressing immature transitional B cells in treated and nontreated patients. CXCR4 receptor was unresponsive to CXCL12 ligand in in-vitro migration and internalization assays. In addition, CXCR5 expression was downregulated on immature transitional B cells from infected patients, and these cells migrated poorly in response to CXCR5 ligand.

CONCLUSION
Circulating immature transitional B cells from HIV-1-infected patients are not fully mature, probably due to premature egress from bone marrow; these cells showed a phenotype which could impair entry into secondary lymphoid organs. Changes in migratory capacity of immature transitional B cells may affect B-cell maturation during HIV-1 infection.

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