Limfocyty Th22, Th17.1, Tc17, Tfh i NKTfh w patogenezie stwardnienia rozsianego
 
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Katedra i Zakład Immunologii Klinicznej, Uniwersytet Medyczny w Lublinie
AUTOR DO KORESPONDENCJI
Michał Konrad Zarobkiewicz   

Katedra i Zakład Immunologii Klinicznej, Uniwersytet Medyczny w Lublinie, ul. Chodźki 4a, 20-093 Lublin
 
Ann. Acad. Med. Siles. 2019;73:19–24
 
SŁOWA KLUCZOWE
DZIEDZINY
STRESZCZENIE
Stwardnienie rozsiane (multiple sclerosis – MS) jest najczęstszą chorobą zapalno-demielinizacyjną. Chorobowość wynosi od około 2/100 000 w okolicach równika do około 100/100 000 w Europie i Ameryce Północnej. Pomimo znacznego postępu medycyny, jaki dokonał się w ostatnich dziesięcioleciach, schorzenie to cały czas pozostaje nieuleczalne. Jedyną możliwością jest walka o spowolnienie nieuchronnego postępu choroby, który w końcu doprowadzi do niepełnosprawności pacjenta. Z tego względu ważne jest dokładne poznanie immunopatogenezy MS. Prowadzone dotychczas badania skupiały się na klasycznych subpopulacjach komórek T. W niniejszym artykule przyjrzymy się stanowi badań i dostępnej wiedzy na temat udziału „nowych” subpopulacji komórek T, tj. limfocytów Th22, Th17.1, Tc17, Tfh, NKTfh, w patogenezie MS.
 
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