Resumen de Regulación inmune durante la coinfección por el virus de la inmunodeficiencia humana y el Mycobacterium tuberculosis

César César Rueda, Paula Andrea Velilla Hernández, María Teresa Rugeles

• español

  Durante las infecciones crónicas la regulacióninmune constituye un mecanismo esencialpara controlar los procesos inflamatorios; sinembargo, la excesiva regulación impide el desarrollode una respuesta efectora adecuada.Las células T reguladoras, las células dendríticasy algunas moléculas inhibitorias, comoCTLA-4, PD-1, IL-10, TGF-? y dioxigenasa,participan en la modulación de la respuestainmune contra el virus de la inmunodeficienciahumana (VIH) y Mycobacterium tuberculosis.La mayoría de los hallazgos sustentan unefecto negativo de la regulación duranteambas infecciones, debido a que permiten lareplicación de los patógenos. La acumulaciónde células T reguladoras funcionales y la expresiónde estas moléculas se han asociadoa un mecanismo compensador, en respuestaa la hiperactivación celular y a una induccióndirecta por parte de los microorganismos.

• English

  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-? e IDO take part in the modulation of the immune response against the human immunodeficiency virus (HIV) andthe 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 theexpression 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 mechanismsthat further disturb the balance between the protective and pathogenic responses during co-infection, favoring the illness severity.