title: Paradoxical role of CD16+CCR2+CCR5+ monocytes in tuberculosis: efficient APC in pleural effusion but also mark disease severity in blood.
abstract: The role of CD16(-) and CD16(+) Mo subsets in human TB remains unknown. Our aim was to characterize Mo subsets from TB patients and to assess whether the inflammatory milieu from TB pleurisy modulate their phenotype and recruitment. We found an expansion of peripheral CD16(+) Mo that correlated with disease severity and with TNF-α plasma levels. Circulating Mo from TB patients are activated, showing a higher CD14, CD16, and CD11b expression and Mtb binding than HS. Both subsets coexpressed CCR2/CCR5, showing a potential ability to migrate to the inflammatory site. In tuberculous PF, the CD16(+) subset was the main Mo/MΦ population, accumulation that can be favored by the induction of CD16 expression in CD16(-) Mo triggered by soluble factors found in this inflammatory milieu. CD16(+) Mo in PF were characterized by a high density of receptors for Mtb recognition (DC-SIGN, MR, CD11b) and for lipid-antigens presentation (CD1b), allowing them to induce a successful, specific T cell proliferation response. Hence, in tuberculous PF, CD16(+) Mo constitute the main APC population; whereas in PB, their predominance is associated with the severity of pulmonary TB, suggesting a paradoxical role of the CD16(+) Mo subset that depends on the cellular localization.
authors: Academia Nacional de Medicina, Pacheco de Melo 3081, 1425, Buenos Aires, Argentina. luciana_balboa@hotmail.com
authors: Luciana
authors: L
authors: Balboa
authors: María M
authors: MM
authors: Romero
authors: Juan I
authors: JI
authors: Basile
authors: Carmen A
authors: CA
authors: Sabio y García
authors: Pablo
authors: P
authors: Schierloh
authors: Noemí
authors: N
authors: Yokobori
authors: Laura
authors: L
authors: Geffner
authors: Rosa M
authors: RM
authors: Musella
authors: Jorge
authors: J
authors: Castagnino
authors: Eduardo
authors: E
authors: Abbate
authors: Silvia
authors: S
authors: de la Barrera
authors: María C
authors: MC
authors: Sasiain
authors: Mercedes
authors: M
authors: Alemán
mesh_terms: D000328:Adult; D000368:Aged; D000938:Antigen-Presenting Cells / Q000276:immunology / Q000378:metabolism; D002469:Cell Separation; D016207:Cytokines / Q000032:analysis / Q000097:blood; D004797:Enzyme-Linked Immunosorbent Assay; D005260:Female; D005434:Flow Cytometry; D058851:GPI-Linked Proteins / Q000032:analysis / Q000276:immunology / Q000378:metabolism; D006801:Humans; D008297:Male; D008875:Middle Aged; D009000:Monocytes / Q000276:immunology* / Q000378:metabolism; D010996:Pleural Effusion / Q000276:immunology / Q000378:metabolism; D054390:Receptors, CCR2 / Q000032:analysis* / Q000276:immunology / Q000378:metabolism; D019713:Receptors, CCR5 / Q000032:analysis* / Q000276:immunology / Q000378:metabolism; D017452:Receptors, IgG / Q000032:analysis* / Q000276:immunology / Q000378:metabolism; D014376:Tuberculosis / Q000276:immunology* / Q000378:metabolism; D014396:Tuberculosis, Pleural / Q000276:immunology* / Q000378:metabolism
chemical_list: C515334:CCR2 protein, human; D016207:Cytokines; C428200:FCGR3B protein, human; D058851:GPI-Linked Proteins; D054390:Receptors, CCR2; D019713:Receptors, CCR5; D017452:Receptors, IgG