Limfocyty Th22, Th17.1, Tc17, Tfh i NKTfh w patogenezie stwardnienia rozsianego
 
Więcej
Ukryj
1
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.
 
REFERENCJE (44)
1.
Potemkowski A. Stwardnienie rozsiane w świecie i w Polsce – ocena epidemiologiczna. Aktual. Neurol. 2009; 9(2): 91–97.
 
2.
Leray E., Moreau T., Fromont A., Edan G. Epidemiology of multiple sclerosis. Rev. Neurol. (Paris) 2016; 172(1): 3–13, doi: 10.1016/j.neurol.2015.10.006.
 
3.
Mitosek-Szewczyk K., Kułakowska A., Bartosik-Psujek H., Hożejowski R., Drozdowski W., Stelmasiak Z. Quality of life in Polish patients with multiple sclerosis. Adv. Med. Sci. 2014; 59(1): 34–38, doi: 10.1016/j.advms.2013.07.002.
 
4.
Duhen T., Geiger R., Jarrossay D., Lanzavecchia A., Sallusto F. Production of interleukin 22 but not interleukin 17 by a subset of human skin-homing memory T cells. Nat. Immunol. 2009; 10(8): 857–863, doi: 10.1038/ni.1767.
 
5.
Trifari S., Kaplan C.D., Tran E.H., Crellin N.K., Spits H. Identification of a human helper T cell population that has abundant production of interleukin 22 and is distinct from TH-17, TH1 and TH2 cells. Nat. Immunol. 2009; 10(8): 864–871, doi: 10.1038/ni.1770.
 
6.
Fard N.A., Azizi G., Mirshafiey A. The Potential Role of T Helper Cell 22 and IL-22 in Immunopathogenesis of Multiple Sclerosis. Innov. Clin. Neurosci. 2016; 13(7–8): 30–36.
 
7.
Duarte J.H., Di Meglio P., Hirota K., Ahlfors H., Stockinger B. Differential Influences of the Aryl Hydrocarbon Receptor on Th17 Mediated Responses in vitro and in vivo. PLoS One 2013; 8(11): e79819, doi: 10.1371/journal.pone.0079819.
 
8.
Rutz S., Noubade R., Eidenschenk C., Ota N., Zeng W., Zheng Y., Hackney J., Ding J., Singh H., Ouyang W. Transcription factor c-Maf mediates the TGF-β-dependent suppression of IL-22 production in TH17 cells. Nat. Immunol. 2011; 12(12): 1238–1245, doi: 10.1038/ni.2134.
 
9.
Leung J.M., Davenport M., Wolff M.J., Wiens K.E., Abidi W.M., Poles M.A., Cho I., Ullman T., Mayer L., Loke P. IL-22-producing CD4+ cells are depleted in actively inflamed colitis tissue. Mucosal Immunol. 2014; 7(1): 124–133, doi: 10.1038/mi.2013.31.
 
10.
Kreymborg K., Etzensperger R., Dumoutier L., Haak S., Rebollo A., Buch T., Heppner F.L., Renauld J.C., Becher B. IL-22 is expressed by Th17 cells in an IL-23-dependent fashion, but not required for the development of autoimmune encephalomyelitis. J. Immunol. 2007; 179(12): 8098–8104.
 
11.
Rolla S., Bardina V., De Mercanti S., Quaglino P., De Palma R., Gned D., Brusa D., Durelli L., Novelli F., Clerico M. Th22 cells are expanded in multiple sclerosis and are resistant to IFN-β. J. Leukoc. Biol. 2014; 96(6): 1155–1164, doi: 10.1189/jlb.5A0813-463RR.
 
12.
Xu W., Li R., Dai Y., Wu A., Wang H., Cheng C., Qiu W., Lu Z., Zhong X., Shu Y., Kermode A.G., Hu X. IL-22 secreting CD4+ T cells in the patients with neuromyelitis optica and multiple sclerosis. J. Neuroimmunol. 2013; 261(1–2): 87–91, doi: 10.1016/j.jneuroim.2013.04.021.
 
13.
Álvarez-Sánchez N., Cruz-Chamorro I., Díaz-Sánchez M., Sarmiento-Soto H., Medrano-Campillo P., Martínez-López A., Lardone P.J., Guerrero J.M., Carrillo-Vico A. Melatonin reduces inflammatory response in peripheral T helper lymphocytes from relapsing-remitting multiple sclerosis patients. J. Pineal Res. 2017; 63(4): e12442, doi: 10.1111/jpi.12442.
 
14.
Annunziato F., Cosmi L., Santarlasci V., Maggi L., Liotta F., Mazzinghi B., Parente E., Filì L., Ferri S., Frosali F., Giudici F., Romagnani P., Parronchi P., Tonelli F., Maggi E., Romagnani S. Phenotypic and functional features of human Th17 cells. J. Exp. Med. 2007; 204(8): 1849–1861.
 
15.
Duhen T., Campbell D.J. IL-1β Promotes the Differentiation of Polyfunctional Human CCR6+CXCR3+ Th1/17 Cells That Are Specific for Pathogenic and Commensal Microbes. J. Immunol. 2014; 193(1): 120–129, doi: 10.4049/jimmunol.1302734.
 
16.
Ramesh R., Kozhaya L., McKevitt K., Djuretic I.M., Carlson T.J., Quintero M.A., McCauley J.L., Abreu M.T., Unutmaz D., Sundrud M.S. Pro-inflammatory human Th17 cells selectively express P-glycoprotein and are refractory to glucocorticoids. J. Exp. Med. 2014; 211(1): 89–104, doi: 10.1084/jem.20130301.
 
17.
Ramstein J., Broos C.E., Simpson L.J., Ansel K.M., Sun S.A., Ho M.E., Woodruff P.G., Bhakta N.R., Christian L., Nguyen C.P., Antalek B.J. i wsp. IFN-γ–Producing T-Helper 17.1 Cells Are Increased in Sarcoidosis and Are More Prevalent than T-Helper Type 1 Cells. Am. J. Respir. Crit. Care Med. 2016; 193(11): 1281–1291, doi: 10.1164/rccm.201507-1499OC.
 
18.
Hirota K., Duarte J.H., Veldhoen M., Hornsby E., Li Y., Cua D.J., Ahlfors H., Wilhelm C., Tolaini M., Menzel U., Garefalaki A., Potocnik A.J., Stockinger B. Fate mapping of IL-17-producing T cells in inflammatory responses. Nat. Immunol. 2011; 12(3): 255–263, doi: 10.1038/ni.1993.
 
19.
Lexberg M.H., Taubner A., Albrecht I., Lepenies I., Richter A., Kamradt T., Radbruch A., Chang H.D. IFN-γ and IL-12 synergize to convert in vivo generated Th17 into Th1/Th17 cells. Eur. J. Immunol. 2010; 40(11): 3017–3027, doi: 10.1002/eji.201040539.
 
20.
Nistala K., Adams S., Cambrook H., Ursu S., Olivito B., de Jager W., Evans J.G., Cimaz R., Bajaj-Elliott M., Wedderburn L.R. Th17 plasticity in human autoimmune arthritis is driven by the inflammatory environment. Proc. Natl. Acad. Sci. U.S.A. 2010; 107(33): 14751–14756, doi: 10.1073/pnas.1003852107.
 
21.
Cosmi L., Cimaz R., Maggi L., Santarlasci V., Capone M., Borriello F., Frosali F., Querci V., Simonini G., Barra G., Piccinni M.P., Liotta F., De Palma R., Maggi E., Romagnani S., Annunziato F. Evidence of the transient nature of the Th17 phenotype of CD4+CD161+ T cells in the synovial fluid of patients with juvenile idiopathic arthritis. Arthritis Rheum. 2011; 63(8): 2504–2515, doi: 10.1002/art.30332.
 
22.
Mazzoni A., Santarlasci V., Maggi L., Capone M., Rossi M.C., Querci V., De Palma R., Chang H.D., Thiel A., Cimaz R., Liotta F. i wsp. Demethylation of the RORC2 and IL17A in Human CD4 + T Lymphocytes Defines Th17 Origin of Nonclassic Th1 Cells. J. Immunol. 2015; 194(7): 3116–3126, doi: 10.4049/jimmunol.1401303.
 
23.
da Costa D.S., Hygino J., Ferreira T.B., Kasahara T.M., Barros P.O., Monteiro C., Oliveira A., Tavares F., Vasconcelos C.C., Alvarenga R., Bento C.A. Vitamin D modulates different IL-17-secreting T cell subsets in multiple sclerosis patients. J. Neuroimmunol. 2016; 299: 8–18, doi: 10.1016/j.jneuroim.2016.08.005.
 
24.
Fan X., Jin T., Zhao S., Liu C., Han J., Jiang X., Jiang Y. Circulating CCR7+ICOS+ Memory T Follicular Helper Cells in Patients with Multiple Sclerosis. PLoS One 2015; 10(7): e0134523, doi: 10.1371/journal.pone.0134523.
 
25.
Ma C.S., Deenick E.K. Human T follicular helper (Tfh) cells and disease. Immunol. Cell Biol. 2014; 92(1): 64–71, doi: 10.1038/icb.2013.55.
 
26.
Crotty S. Follicular Helper CD4 T Cells (T FH). Annu. Rev. Immunol. 2011; 29: 621–663, doi: 10.1146/annurev-immunol-031210-101400.
 
27.
Lee S.K., Rigby R.J., Zotos D., Tsai L.M., Kawamoto S., Marshall J.L., Ramiscal R.R., Chan T.D., Gatto D., Brink R., Yu D., Fagarasan S., Tarlinton D.M., Cunningham A.F., Vinuesa C.G. B cell priming for extrafollicular antibody responses requires Bcl-6 expression by T cells. J. Exp. Med. 2011; 208(7): 1377–1388, doi: 10.1084/jem.20102065.
 
28.
Odegard J.M., Marks B.R., DiPlacido L.D., Poholek A.C., Kono D.H., Dong C., Flavell R.A., Craft J. ICOS-dependent extrafollicular helper T cells elicit IgG production via IL-21 in systemic autoimmunity. J. Exp. Med. 2008; 205(12): 2873–2886, doi: 10.1084/jem.20080840.
 
29.
Zotos D., Coquet J.M., Zhang Y., Light A., D’Costa K., Kallies A., Corcoran L.M., Godfrey D.I., Toellner K.M., Smyth M.J., Nutt S.L., Tarlinton D.M. IL-21 regulates germinal center B cell differentiation and proliferation through a B cell-intrinsic mechanism. J. Exp. Med. 2010; 207(2): 365–378, doi: 10.1084/jem.20091777.
 
30.
Chang P.P., Barral P., Fitch J., Pratama A., Ma C.S., Kallies A., Hogan J.J., Cerundolo V., Tangye S.G., Bittman R., Nutt S.L., Brink R., Godfrey D.I., Batista F.D., Vinuesa C.G. Identification of Bcl-6-dependent follicular helper NKT cells that provide cognate help for B cell responses. Nat. Immunol. 2011; 13(1): 35–43, doi: 10.1038/ni.2166.
 
31.
King I.L., Fortier A., Tighe M., Dibble J., Watts G.F., Veerapen N., Haberman A.M., Besra G.S., Mohrs M., Brenner M.B., Leadbetter E.A. Invariant natural killer T cells direct B cell responses to cognate lipid antigen in an IL-21-dependent manner. Nat. Immunol. 2011; 13(1): 44–50, doi: 10.1038/ni.2172.
 
32.
Rampuria P., Lang M.L. CD1d-dependent expansion of NKT follicular helper cells in vivo and in vitro is a product of cellular proliferation and differentiation. Int. Immunol. 2015; 27(5): 253–263, doi: 10.1093/intimm/dxv007.
 
33.
Tellier J., Nutt S.L. The unique features of follicular T cell subsets. Cell. Mol. Life Sci. 2013; 70(24): 4771–4784, doi: 10.1007/s00018-013-1420-3.
 
34.
Christensen J.R., Börnsen L., Ratzer R., Piehl F., Khademi M., Olsson T., Sørensen P.S., Sellebjerg F. Systemic Inflammation in Progressive Multiple Sclerosis Involves Follicular T-Helper, Th17- and Activated B-Cells and Correlates with Progression. PLoS One 2013; 8(3): e57820, doi: 10.1371/journal.pone.0057820.
 
35.
Li Y.J., Zhang F., Qi Y., Chang G.Q., Fu Y., Su L., Shen Y., Sun N., Borazanci A., Yang C., Shi F.D., Yan Y. Association of circulating follicular helper T cells with disease course of NMO spectrum disorders. J. Neuroimmunol. 2015; 278: 239–246, doi: 10.1016/j.jneuroim.2014.11.011.
 
36.
Fraussen J., de Bock L., Somers V. B cells and antibodies in progressive multiple sclerosis: Contribution to neurodegeneration and progression. Autoimmun. Rev. 2016; 15(9): 896–899, doi: 10.1016/j.autrev.2016.07.008.
 
37.
Rivas J.R., Ireland S.J., Chkheidze R., Rounds W.H., Lim J., Johnson J., Ramirez D.M., Ligocki A.J., Chen D., Guzman A.A., Woodhall M. i wsp. Peripheral VH4+ plasmablasts demonstrate autoreactive B cell expansion toward brain antigens in early multiple sclerosis patients. Acta Neuropathol. 2017; 133(1): 43–60, doi: 10.1007/s00401-016-1627-0.
 
38.
Annibali V., Ristori G., Angelini D.F., Serafini B., Mechelli R., Cannoni S., Romano S., Paolillo A., Abderrahim H., Diamantini A., Borsellino G., Aloisi F., Battistini L., Salvetti M. CD161(high)CD8+T cells bear pathogenetic potential in multiple sclerosis. Brain 2011; 134(Pt 2): 542–554, doi: 10.1093/brain/awq354.
 
39.
Maggi L., Santarlasci V., Capone M., Peired A., Frosali F., Crome S.Q., Querci V., Fambrini M., Liotta F., Levings M.K., Maggi E., Cosmi L., Romagnani S., Annunziato F. CD161 is a marker of all human IL-17-producing T-cell subsets and is induced by RORC. Eur. J. Immunol. 2010; 40(8): 2174–2181, doi: 10.1002/eji.200940257.
 
40.
Chen H.W., Tsai J.P., Yao T.Y., Hsieh C.L., Chen I.H., Liu S.J. TGF-β and IL-21 cooperatively stimulate activated CD8(+) T cells to differentiate into Tc17 cells. Immunol. Lett. 2016; 174: 23–27, doi: 10.1016/j.imlet.2016.04.006.
 
41.
Huber M., Heink S., Pagenstecher A., Reinhard K., Ritter J., Visekruna A., Guralnik A., Bollig N., Jeltsch K., Heinemann C., Wittmann E. i wsp. IL-17A secretion by CD8+ T cells supports Th17-mediated autoimmune encephalomyelitis. J. Clin. Invest. 2013; 123(1): 247–260, doi: 10.1172/JCI63681.
 
42.
Tzartos J.S., Friese M.A., Craner M.J., Palace J., Newcombe J., Esiri M.M., Fugger L. Interleukin-17 Production in Central Nervous System-Infiltrating T Cells and Glial Cells Is Associated with Active Disease in Multiple Sclerosis. Am. J. Pathol. 2008; 172(1): 146–155.
 
43.
Nicol B., Salou M., Vogel I., Garcia A., Dugast E., Morille J., Kilens S., Charpentier E., Donnart A., Nedellec S., Jacq-Foucher M. i wsp. An intermediate level of CD161 expression defines a novel activated, inflammatory, and pathogenic subset of CD8+ T cells involved in multiple sclerosis. J. Autoimmun. 2018; 88: 61–74, doi: 10.1016/j.jaut.2017.10.005.
 
44.
Tajima M., Wakita D., Satoh T., Kitamura H., Nishimura T. IL-17/IFN-γ double producing CD8+ T (Tc17/IFN-γ) cells: A novel cytotoxic T-cell subset converted from Tc17 cells by IL-12. Int. Immunol. 2011; 23(12): 751–759, doi: 10.1093/intimm/dxr086.
 
eISSN:1734-025X
Journals System - logo
Scroll to top