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001-es BibID:	BIBFORM075028
035-os BibID:	(WoS)000441903500008 (Scopus)85050314318
Első szerző:	Fekete Rebeka
Cím:	Microglia control the spread of neurotropic virus infection via P2Y12 signalling and recruit monocytes through P2Y12-independent mechanisms / Rebeka Fekete, Csaba Cserép, Nikolett Lénárt, Krisztina Tóth, Barbara Orsolits, Bernadett Martinecz, Előd Méhes, Bálint Szabó, Valéria Németh, Balázs Gönci, Beáta Sperlágh, Zsolt Boldogkői, Ágnes Kittel, Mária Baranyi, Szilamér Ferenczi, Krisztina Kovács, Gergely Szalay, Balázs Rózsa, Connor Webb, Gabor G. Kovacs, Tibor Hortobágyi, Brian L. West, Zsuzsanna Környei, Ádám Dénes
Dátum:	2018
ISSN:	0001-6322
Megjegyzések:	Neurotropic herpesviruses can establish lifelong infection in humans and contribute to severe diseases including encephalitis and neurodegeneration. However, the mechanisms through which the brain's immune system recognizes and controls viral infections propagating across synaptically linked neuronal circuits have remained unclear. Using a well-established model of alphaherpesvirus infection that reaches the brain exclusively via retrograde transsynaptic spread from the periphery, and in vivo two-photon imaging combined with high resolution microscopy, we show that microglia are recruited to and isolate infected neurons within hours. Selective elimination of microglia results in a marked increase in the spread of infection and egress of viral particles into the brain parenchyma, which are associated with diverse neurological symptoms. Microglia recruitment and clearance of infected cells require cell-autonomous P2Y12 signalling in microglia, triggered by nucleotides released from affected neurons. In turn, we identify microglia as key contributors to monocyte recruitment into the inflamed brain, which process is largely independent of P2Y12. P2Y12-positive microglia are also recruited to infected neurons in the human brain during viral encephalitis and both microglial responses and leukocyte numbers correlate with the severity of infection. Thus, our data identify a key role for microglial P2Y12 in defence against neurotropic viruses, whilst P2Y12-independent actions of microglia may contribute to neuroinflammation by facilitating monocyte recruitment to the sites of infection.
Tárgyszavak:	Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban folyóiratcikk Microglia P2Y12 Neurotropic virus Transsynaptic spread Neuroinflammation
Megjelenés:	Acta Neuropathologica. - 136 : 3 (2018), p. 461-482. -
További szerzők:	Cserép Csaba Lénárt Nikolett Tóth Krisztina Orsolits Barbara Martinecz Bernadett Méhes Előd Szabó Bálint Németh Valéria Gönci Balázs Sperlágh Beáta Boldogkői Zsolt Kittel Ágnes Baranyi Mária Ferenczi Szilamér (1977-) (biológus) Kovács Krisztina Szalay Gergely Rózsa Balázs Webb, Connor Kovács Gábor Géza (1969-) (neurológus) Hortobágyi Tibor (1965-) (patológus) West, Brian L. Környei Zsuzsanna Dénes Ádám
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