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Vol. 15. Núm. 4.
Páginas 259-267 (diciembre 2011)
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Vol. 15. Núm. 4.
Páginas 259-267 (diciembre 2011)
Open Access
Participación de las células Th17 en la patogenia de la infección por el virus de la inmunodeficiencia humana de tipo 1
Th17 cells involvement in the pathogenesis of the human immunodeficiency virus type 1
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3297
Wbeimar Aguilar-Jiménez, Wildeman Zapata, María Teresa Rugeles
Autor para correspondencia
mtrugel@udea.edu.co

Correspondencia: María Teresa Rugeles, Grupo Inmunovirología, Facultad de Medicina, Universidad de Antioquia, Calle 62 N° 52-59, Laboratorio 532, Medellín, Colombia. Teléfonos: (574) 219-6551 y (574) 219-6482.
Grupo Inmunovirología, Facultad de Medicina, Universidad de Antioquia, Medellín, Colombia
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Resumen

La infección por el VIH-1 se caracteriza por la eliminación de linfocitos T CD4+, particularmente en la mucosa gastrointestinal, que favorece la traslocación microbiana y la hiperactivación inmunitaria, principal mecanismo patogénico en esta infección.

Las células Th17 son una subpoblación proinflamatoria de linfocitos CD4+, que producen IL-17, IL-21 e IL-22, y son importantes en la respuesta antimicrobiana, principalmente en el sistema gastrointestinal, donde promueven la restauración de la mucosa. Aunque su eliminación se ha asociado con progresión de la infección por el VIH-1 y por el virus de la inmunodeficiencia de los simios, y han sido descritas como deletérea en autoinmunidad. Su papel en la patogenia de la infección por el VIH-1 no está claramente establecido.

Considerando su capacidad funcional, las células Th17 podrían tener un impacto dual, dependiendo de la fase de la infección en que se encuentre el individuo. Actualmente, hay más información que sugiere que estas células tienen un papel benéfico al promover la recuperación de la mucosa intestinal y disminuir la traslocación microbiana, así como la hiperactivación inmunitaria. Sin embargo, su papel patogénico, particularmente promoviendo la replicación viral mediante la producción de citocinas proinflamatorias, no debe descartarse.

En esta revisión, se presentan los datos científicos disponibles del efecto de las células Th17 en la patogenia de la infección por el VIH-1.

Palabras clave:
VIH-1
Th17
tejido linfoide asociado a mucosa gastrointestinal (GALT)
hiperactivación inmunológica
traslocación bacteriana
Abstract

HIV-1 infection is characterized by a gradual decrease of the immunological competence and a massive depletion of CD4+ T cells, particularly in gut-associated lymphoid tissue, which leads to microbial translocation, contributing to immune hyperactivation, the main pathogenic mechanism during HIV-1 infection.

Th17 cells are a proinflammatory CD4+ T cell subset, which produce IL-17, IL-21 and IL-22 and play a pivotal role in host defense, mainly in the gastrointestinal tissue, where they promote antimicrobial responses and gut mucosa restoration. Although Th17 depletion is a hallmark of the progression of the simian and human immunodeficiency viral infections and they have been involved in the pathogenic process in some autoimmune diseases, the role of these cells during HIV-1 infection is not completely understood.

Considering their functional potential, Th17 cells could have a dual role, depending on the stage of HIV infection a patient has reached. Currently, most evidence suggests that Th17 cells have a beneficial role by promoting gut mucosa recovery, preventing microbial translocation and decreasing immune hyperactivation. However, the pathogenic role of these cells, particularly, increasing viral replication through the production of inflammatory cytokines should not be ruled out.

In this review, scientific evidence regarding the role of Th17 on the pathogenesis of HIV infection is discussed.

Key words:
HIV-1
Th17
gut-associated lymphoid tissue (GALT)
immune hyperactivation
bacterial translocation
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