@article{PAR00012304,
  title = {{I}mbalance of circulating monocyte subsets and {PD}-1 dysregulation in {Q} fever endocarditis : the role of {IL}-10 in {PD}-1 modulation},
  author = {{K}a, {M}. {B}. and {G}ondois-{R}ey, {F}. and {C}apo, {C}. and {T}extoris, {J}. and {M}illion, {M}. and {R}aoult, {D}idier and {O}live, {D}. and {M}ege, {J}. {L}.},
  editor = {},
  language = {{ENG}},
  abstract = {{Q} fever endocarditis, a severe complication of {Q} fever, is associated with a defective immune response, the mechanisms of which are poorly understood. {W}e hypothesized that {Q} fever immune deficiency is related to altered distribution and activation of circulating monocyte subsets. {M}onocyte subsets were analyzed by flow cytometry in peripheral blood mononuclear cells from patients with {Q} fever endocarditis and controls. {T}he proportion of classical monocytes ({CD}14(+){CD}16(-) monocytes) was similar in patients and controls. {I}n contrast, the patients with {Q} fever endocarditis exhibited a decrease in the non-classical and intermediate subsets of monocytes ({CD}16(+) monocytes). {T}he altered distribution of monocyte subsets in {Q} fever endocarditis was associated with changes in their activation profile. {I}ndeed, the expression of {HLA}-{DR}, a canonical activation molecule, and {PD}-1, a co-inhibitory molecule, was increased in intermediate monocytes. {T}his profile was not restricted to {CD}16(+) monocytes because {CD}4(+) {T} cells also overexpressed {PD}-1. {T}he mechanism leading to the overexpression of {PD}-1 did not require the {LPS} from {C}. burnetii but involved interleukin-10, an immunosuppressive cytokine. {I}ndeed, the incubation of control monocytes with interleukin-10 led to a higher expression of {PD}-1 and neutralizing interleukin-10 prevented {C}. burnetii-stimulated {PD}-1 expression. {T}aken together, these results show that the immune suppression of {Q} fever endocarditis involves a cross-talk between monocytes and {CD}4(+) {T} cells expressing {PD}-1. {T}he expression of {PD}-1 may be useful to assess chronic immune alterations in {Q} fever endocarditis.},
  keywords = {},
  booktitle = {},
  journal = {{P}los {O}ne},
  volume = {9},
  numero = {9},
  pages = {e107533},
  ISSN = {1932-6203},
  year = {2014},
  DOI = {10.1371/journal.pone.0107533},
  URL = {https://www.documentation.ird.fr/hor/{PAR}00012304},
}