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Vol. 13. Issue 4.
Pages 268-282 (December 2009)
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Vol. 13. Issue 4.
Pages 268-282 (December 2009)
Open Access
Regulación inmune durante la coinfección por el virus de la inmunodeficiencia humana y el Mycobacterium tuberculosis
Immune regulation during Human Immunodeficiency Virus and Mycobacterium tuberculosis coinfection
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César Mauricio Rueda1,*, Paula Andrea Velilla1,*, María Teresa Rugeles
,1,
1 Grupo de Inmunovirología, Sede de Investigación Universitaria, Universidad de Antioquia, Medellín, Colombia
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Resumen

Durante las infecciones crónicas la regulación inmune constituye un mecanismo esencial para controlar los procesos inflamatorios; sin embargo, la excesiva regulación impide el desarrollo de una respuesta efectora adecuada. Las células T reguladoras, las células dendríticas y algunas moléculas inhibitorias, como CTLA-4, PD-1, IL-10, TGF-β y dioxigenasa, participan en la modulación de la respuesta inmune contra el virus de la inmunodeficiencia humana (VIH) y Mycobacterium tuberculosis.

La mayoría de los hallazgos sustentan un efecto negativo de la regulación durante ambas infecciones, debido a que permiten la replicación de los patógenos. La acumulación de células T reguladoras funcionales y la expresión de estas moléculas se han asociado a un mecanismo compensador, en respuesta a la hiperactivación celular y a una inducción directa por parte de los microorganismos.

En la coinfección, el VIH favorece la reactivación de M. tuberculosis y el desarrollo de formas extrapulmonares de la enfermedad.

La infección por M. tuberculosis facilita la entrada del virus a la célula blanco y su replicación. Asimismo, se evidencia un aumento del estado de hiperactivación inmune, junto a una menor respuesta efectora. Aunque la inmunopatogénesis durante la coinfección ha sido poco estudiada, es probable que el estado proinflamatorio y de hiperactivación, característico de ambas infecciones, facilita el desarrollo de mecanismos de regulación que alteren aún más el equilibrio de la respuesta protectora durante la coinfección y facilitan la gravedad de la enfermedad.

Palabras clave:
VIH
Mycobacterium tuberculosis
coinfección
regulación inmune
Abstract

During chronic infections, the immune regulation is an important mechanism to control inflammatory processes; however, the excessive regulation prevents the development of an appropriate effector immune response. The regulatory T cells (Treg), dendritic cells (DC) and some inhibitory molecules such as CTLA-4, PD-1, IL-10, TGF-β e IDO take part in the modulation of the immune response against the human immunodeficiency virus (HIV) and the Mycobacterium tuberculosis (M.tb).

Most of the evidence supports a negative effect of the immune regulation during both infections, due to the fact that they allow the active replication of the pathogens. The accumulation of functional Treg cells and the expression of these molecules have been associated with a compensating mechanism, in response to a cellular hyper-activation and to these microorganisms direct induction.

During the co-infection, the HIV favors the reactivation of M.tb and the development of extra-pulmonary TB forms. The M.tb infection promotes the entry of the virus into target cells and its replication. Likewise, an increase of the immune hyper-activation state has been reported along with low effector responses. Although the immune-pathogenesis during the co-infection has not been extensively studied, most likely the pro-inflammatory and immunological hyper-activation state, typical of both infections, promotes the development of immune regulatory mechanisms that further disturb the balance between the protective and pathogenic responses during co-infection, favoring the illness severity.

Key words:
HIV
Mycobacterium tuberculosis
co-infection
immune regulation
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Rueda C, Velilla P, Rugeles M. Regulación inmune de la infecciónde Mycobacterium tuberculosis durante la infección por el virus de inmunodeficiencia humana. Infectio. 2009 13 (4)

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