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Interleucina 17

Estrutura cristalográfica de IL-17F dimérica

A interleukine 17 (IL-17 ou IL-17A) é uma citocina da família das citocinas IL-17. IL-17A foi originalmente identificada como um transcrito de um determinado hibridoma de célula T hybridome de roedor.[1] A IL-17A age nos tecidos através de um receptor constituído pelas subunidades  IL-17RA e IL-17RC, induzindo a secreção de quimiocinas como a interleucina 8, que permitem o recrutamento de neutrófilos.[2]

Família de citocinas IL-17

A família de citocinas IL-17  compreende seis membros: IL-17A, IL-17B, IL-17C, IL-17D, IL-17E e IL-17F. Essas citocinas possuem em comum a presença de resíduos de cisteína particulares. A-17F possui a maior homologia em resíduos de aminoácidos com IL-17A (50 %) enquanto a IL-17E possui a menor homologia (16 %).[3] A IL-17A e a IL-17F são produzidas por uma subpopulação de linfócitos T auxiliares denominados linfócitos Th17 (por analogia com os linfócitos Th1 e Th2.)[4][5]

Há 5 receptores de IL-17 identificados até hoje, denomindados de IL-17RA a IL-17RE.[6]

Papel da l'IL-17A

A IL-17A parece possuir um papel importante no curso de infecções por bactérias extracelulares como Klebsiella pneumoniae ou leveduras como Candida albicans.[7] De forma lógica, anomalias no receptor para essa citocina estão relacionadas a maior susceptibilidade à essas infecções.[8] No homem, diversas mutações genéticas levam à defeitos na produção ou transdução de sinal por IL-17A. Essas mutações são associadas com candidoses cutaneomucosas e,  em menor grau, a infecções por Staphylococcus aureus.[9] Um papel da IL-17A já foi demonstrado também em modelos murinos experimentais de diversas patologias auto-imunes a (esclerose múltipla, artrite reumatóide, psoríase) e nas doenças crônicas inflamatórias intestinais.

Alvo terapêutico

Diversos estudos clinícos baseados na utilização de anticorpos monoclonais bloqueadores dessa citocina, tanto diretamente (como o ixekizumab) ou através do receptorr (como o brodalumab),foram realizados ou estão em curso.[10][11]

Notas e referências

  1. ↑ (em inglês) Rouvier E, Luciani MF, Mattéi MG, Denizot F, Golstein P CTLA-8, cloned from an activated T cell, bearing AU-rich messenger RNA instability sequences, and homologous to a herpesvirus saimiri gene.
  2. ↑ (em inglês) Fossiez F, Djossou O, Chomarat P, et. al.
  3. ↑ (em inglês) Iwakura Y, Ishigame H, Saijo S, Nakae S.
  4. ↑ (em inglês) Harrington LE, Hatton RD, Mangan PR, Turner H, Murphy TL, Murphy KM, Weaver CT.
  5. ↑ (em inglês)Park H, Li Z, Yang XO, Chang SH, Nurieva R, Wang YH, Wang Y, Hood L, Zhu Z, Tian Q, Dong C.
  6. ↑ Gaffen SL, Recent advances in the IL-17 cytokine family, Curr Opin Immunol, 2011;23:613-619
  7. ↑ (em inglês)Conti HR, Gaffen SL.
  8. ↑ Ye P, Rodriguez FH, Kanaly S et al.
  9. ↑ (em inglês)Puel A, Cypowyj S, Bustamante J, et. al.
  10. ↑ (em inglês)http://clinicaltrials.gov/ct2/results?term=IL-17
  11. ↑ (em inglês)van den Berg WB, Miossec P.

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