@article{fdi:010078824,
  title = {{A} receptor for the complement regulator factor {H} increases transmission of trypanosomes to tsetse flies},
  author = {{M}acleod, {O}.{J}.{S}. and {B}art, {J}ean-{M}athieu and {M}ac{G}regor, {P}. and {P}eacock, {L}. and {S}avill, {N}.{J}. and {H}ester, {S}. and {R}avel, {S}ophie and {S}unter, {J}.{D}. and {T}revor, {C}. and {R}ust, {S}. and {V}aughan, {T}.{J}. and {M}inter, {R}. and {M}ohammed, {S}. and {G}ibson, {W}. and {T}aylor, {M}.{C}. and {H}iggins, {M}.{K}. and {C}arrington, {M}.},
  editor = {},
  language = {{ENG}},
  abstract = {{P}ersistent pathogens have evolved to avoid elimination by the mammalian immune system including mechanisms to evade complement. {I}nfections with {A}frican trypanosomes can persist for years and cause human and animal disease throughout sub-{S}aharan {A}frica. {I}t is not known how trypanosomes limit the action of the alternative complement pathway. {H}ere we identify an {A}frican trypanosome receptor for mammalian factor {H}, a negative regulator of the alternative pathway. {S}tructural studies show how the receptor binds lig and, leaving inhibitory domains of factor {H} free to inactivate complement {C}3b deposited on the trypanosome surface. {R}eceptor expression is highest in developmental stages transmitted to thetsetsefly vector and those exposed to blood meals in the tsetse gut. {R}eceptor gene deletion reduced tsetse infection, identifying this receptor as a virulence factor for transmission. {T}his demonstrates how a pathogen evolved a molecular mechanism to increase transmission to an insect vector by exploitation of a mammalian complement regulator.},
  keywords = {{AFRIQUE} {SUBSAHARIENNE}},
  booktitle = {},
  journal = {{N}ature {C}ommunications},
  volume = {11},
  numero = {},
  pages = {art. 1326 [12 ]},
  ISSN = {2041-1723},
  year = {2020},
  DOI = {10.1038/s41467-020-15125-y},
  URL = {https://www.documentation.ird.fr/hor/fdi:010078824},
}