title: Increased Toll-like receptor-2 expression on nonclassic CD16+ monocytes from patients with inflammatory stage of Eales' disease.
abstract: OBJECTIVE
  To identify the distribution, differential Toll-like receptor (TLR) expression, and functional contribution of monocyte subpopulations in the inflammatory stage of Eales' disease (ED).
  
  
  METHODS
  Peripheral blood mononuclear cells were isolated from nine patients during the inflammatory stage of ED and nine age- and sex-matched healthy controls. The expression of CD14, CD16, TLR-2, and TLR-4 on monocytes was measured by flow cytometry. The CD14⁺, CD16⁻, and CD16⁺ monocyte populations were sorted on the basis of magnetic-activated cell-sorting methodology, and levels of cytokines were measured by ELISA.
  
  
  RESULTS
  In ED patients, the number of circulating monocytes was significantly expanded compared with that in controls (P = 0.01), with a marked increase in the nonclassic CD16⁺ subset, which showed an activated phenotype in patients that correlated with levels of serum proinflammatory cytokines and clinical progression. A higher expression of cell surface TLR-2 (P = 0.02), but not TLR-4, was found in monocytes of patients with ED. Furthermore, TLR-2 was expressed at higher levels on CD16⁺ monocytes than on CD16⁻ monocytes in patients, whereas no significant variation was found in TLR-4 expression on different monocyte subsets. Peptidoglycan-induced TNF-α expression correlated with TLR-2 expression in monocytes isolated from controls (r = 0.85, P = 0.0061), but not in monocytes isolated from ED patients (r = 0.553, P = 0.1328).
  
  
  CONCLUSIONS
  These results indicate that in the pathogenesis of ED, TLR activation and increased numbers of nonclassic CD16⁺ monocytes are crucial regulators, along with the secretion of proinflammatory cytokines that perpetuate the inflammatory process in the retina.
authors.affiliation: Department of Biochemistry, Dr.B. C. Roy Post Graduate Institute of Basic Medical Education and Research (IPGME&R), Kolkata, India.
authors.forename: Aditi
authors.initials: A
authors.lastname: Sen
authors.forename: Imran Hussain
authors.initials: IH
authors.lastname: Chowdhury
authors.forename: Debanjan
authors.initials: D
authors.lastname: Mukhopadhyay
authors.forename: Suman Kalyan
authors.initials: SK
authors.lastname: Paine
authors.forename: Amrita
authors.initials: A
authors.lastname: Mukherjee
authors.forename: Lakshmi Kanta
authors.initials: LK
authors.lastname: Mondal
authors.forename: Mitali
authors.initials: M
authors.lastname: Chatterjee
authors.forename: Basudev
authors.initials: B
authors.lastname: Bhattacharya
mesh_terms: D000328:Adult; D001799:Blood Sedimentation; D002097:C-Reactive Protein / Q000378:metabolism; D018929:Cell Culture Techniques; D002469:Cell Separation; D016207:Cytokines / Q000378:metabolism; D004797:Enzyme-Linked Immunosorbent Assay; D005260:Female; D005434:Flow Cytometry; D005451:Fluorescein Angiography; D058851:GPI-Linked Proteins / Q000378:metabolism; D006801:Humans; D018950:Lipopolysaccharide Receptors / Q000378:metabolism; D008297:Male; D009000:Monocytes / Q000378:metabolism*; D009389:Neovascularization, Pathologic / Q000378:metabolism*; D034741:RNA, Small Interfering / Q000494:pharmacology; D017452:Receptors, IgG / Q000378:metabolism*; D031300:Retinal Vasculitis / Q000378:metabolism*; D051195:Toll-Like Receptor 2 / Q000037:antagonists & inhibitors / Q000378:metabolism*
chemical_list: D016207:Cytokines; C428200:FCGR3B protein, human; D058851:GPI-Linked Proteins; D018950:Lipopolysaccharide Receptors; D034741:RNA, Small Interfering; D017452:Receptors, IgG; D051195:Toll-Like Receptor 2; D002097:C-Reactive Protein