title: Antiretroviral Therapy Normalizes Autoantibody Profile of HIV Patients by Decreasing CD33⁺CD11b⁺HLA-DR⁺ Cells: A Cross-Sectional Study.
abstract: Autoimmune manifestations are common in human immunodeficiency virus (HIV) patients. However, the autoantibody spectrum associated with HIV infection and the impact of antiretroviral therapy (ART) remains to be determined. The plasma autoantibody spectrum for HIV patients was characterized by protein microarrays containing 83 autoantigens and confirmed by enzyme-linked immunosorbent assay (ELISA). Regulatory T cells (Tregs) and myeloid-derived suppressor cells (MDSCs) were analyzed by flow cytometry and their effects on autoantibodies production were determined by B cell ELISpot. Higher levels of autoantibody and higher prevalence of elevated autoantibodies were observed in ART-naive HIV patients compared to healthy subjects and HIV patients on ART. The highest frequency of CD33(+)CD11b(+)HLA-DR(+) cells was observed in ART-naive HIV patients and was associated with the quantity of elevated autoantibodies. In addition, CD33(+)CD11b(+)HLA-DR(+) cells other than Tregs or MDSCs boost the B cell response in a dose-dependent manner by in vitro assay. In summary, HIV infection leads to elevation of autoantibodies while ART suppresses the autoimmune manifestation by decreasing CD33(+)CD11b(+)HLA-DR(+) cells in vivo.The roles of CD33(+)CD11b(+)HLA-DR(+) cells on disease progression in HIV patients needs further assessment.
authors.affiliation: From the Oncology Bioinformatics Center, Minhang Hospital, Fudan University (ZM, LD); Shanghai, China; Department of Microbiology and Immunology and Center for AIDS Research, Indiana University School of Medicine, Indianapolis, Indiana, USA (ZM, DB, TA, NS, JL, QY); Zhejiang Provincial Key Laboratory for Technology and Application of Model Organisms, Wenzhou Medical University, University Park, Wenzhou, China (NH); Division of Infectious Diseases, Department of Medicine, Indiana University School of Medicine, Indianapolis, IN (MD, SG, QY); and Department of Surgery, Davis Heart and Lung Research Institute, Biomedical Sciences Graduate Program, Biophysics Graduate Program, The Ohio State University Wexner Medical Center, Columbus, OH, USA (RH).
authors.forename: Zhefeng
authors.initials: Z
authors.lastname: Meng
authors.forename: Ling
authors.initials: L
authors.lastname: Du
authors.forename: Ningjie
authors.initials: N
authors.lastname: Hu
authors.forename: Daniel
authors.initials: D
authors.lastname: Byrd
authors.forename: Tohti
authors.initials: T
authors.lastname: Amet
authors.forename: Mona
authors.initials: M
authors.lastname: Desai
authors.forename: Nicole
authors.initials: N
authors.lastname: Shepherd
authors.forename: Jie
authors.initials: J
authors.lastname: Lan
authors.forename: Renzhi
authors.initials: R
authors.lastname: Han
authors.forename: Qigui
authors.initials: Q
authors.lastname: Yu
mesh_terms: D044966:Anti-Retroviral Agents / Q000008:administration & dosage / Q000276:immunology; D001323:Autoantibodies / Q000097:blood*; D015551:Autoimmunity / Q000187:drug effects / Q000276:immunology; D039481:CD11b Antigen / Q000032:analysis; D018450:Disease Progression; D015658:HIV Infections / Q000188:drug therapy / Q000276:immunology; D006684:HLA-DR Antigens / Q000032:analysis; D006801:Humans; D011379:Prognosis; D063268:Sialic Acid Binding Ig-like Lectin 3 / Q000032:analysis; D050378:T-Lymphocytes, Regulatory / Q000276:immunology*
chemical_list: D044966:Anti-Retroviral Agents; D001323:Autoantibodies; D039481:CD11b Antigen; D006684:HLA-DR Antigens; D063268:Sialic Acid Binding Ig-like Lectin 3