Imunologia da esquizofrenia: evidências, perspectivas e desafios
DOI:
https://doi.org/10.25118/2236-918X-6-2-1Palavras-chave:
Sistema imune, esquizofrenia, tratamentoResumo
A etiopatogênese da esquizofrenia é complexa e envolve a interação entre fatores genéticos e ambientais. Alterações no sistema imune vêm sendo apontadas como possíveis participantes na fisiopatologia da esquizofrenia. Neste artigo, apresentamos uma revisão narrativa sobre as alterações imunes na fisiopatologia da esquizofrenia e o potencial de moléculas e/ou mecanismos do sistema imune serem biomarcadores e/ou alvos terapêuticos. Enquanto alguns estudos observam maior participação de citocinas da resposta imune do tipo células T auxiliares (Th1), interferon-gama (IFN-γ), interleucina 2 (IL-2) e fator de necrose tumoral-alfa (TNF-α), outros observam maior participação das citocinas IL-4, IL-6 e IL-10, pertencentes à reposta imune tipo Th2. A infecção pelo protozoário Toxoplasma gondii tem sido apontada como fator de risco para esquizofrenia, e uma possível explicação seria o desvio no metabolismo do triptofano, com consequente aumento de quinureninas, causado pela resposta inflamatória frente à presença do parasita. Ensaios clínicos têm sido realizados utilizando anti-inflamatórios como adjuvantes ao tratamento antipsicótico. Resultados promissores, como redução da sintomatologia vegativa e melhora cognitiva, foram observados. O uso de antiinflamatórios com consequente melhora clínica reforçam a ideia da participação de componentes imunes/inflamatórios na fisiopatologia da esquizofrenia.
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