Low CD1c+myeloid dendritic cell counts correlated with a high risk of rapid disease progression during early HIV-1 infection

2Citations
Citations of this article
28Readers
Mendeley users who have this article in their library.

This article is free to access.

Abstract

Background: During early HIV-1 infection (EHI), the interaction between the immune response and the virus determines disease progression. Although CD1c+myeloid dendritic cells (mDCs) can trigger the immune response, the relationship between CD1c+mDC alteration and disease progression has not yet been defined. Methods: EHI changes in CD1c+mDC counts, surface marker (CD40, CD86, CD83) expression, and IL-12 secretion were assessed by flow cytometry in 29 patients. Results: When compared with the normal controls, patients with EHI displayed significantly lower CD1c+mDC counts and IL-12 secretion and increased surface markers. CD1c+mDC counts were positively correlated with CD4+ T cell counts and inversely associated with viral loads. IL-12 secretion was only positively associated with CD4+ T cell counts. Rapid progressors had lower counts, CD86 expression, and IL-12 secretion of CD1c+mDCs comparing with typical progressors. Kaplan-Meier analysis and Cox regression models suggested patients with low CD1c+mDC counts (<10 cells/μL) had a 4-fold higher risk of rapid disease progression than those with high CD1c+mDC counts. However, no relationship was found between surface markers or IL-12 secretion and disease progression. Conclusions: During EHI, patients with low CD1c+mDC counts were more likely to experience rapid disease progression than those with high CD1c+mDC counts.

Cite

CITATION STYLE

APA

Diao, Y., Geng, W., Fan, X., Cui, H., Sun, H., Jiang, Y., … Shang, H. (2015). Low CD1c+myeloid dendritic cell counts correlated with a high risk of rapid disease progression during early HIV-1 infection. BMC Infectious Diseases, 15(1). https://doi.org/10.1186/s12879-015-1092-8

Register to see more suggestions

Mendeley helps you to discover research relevant for your work.

Already have an account?

Save time finding and organizing research with Mendeley

Sign up for free