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HTLV‐1 decreases Th2 type of immune response in patients with strongyloidiasis

Porto, Aurélia F. ; Neva, Franklin A. ; Bittencourt, Helito ; Lisboa, Waldir ; Thompson, Robert ; Alcântara, Luís ; Carvalho, Edgar M.

Parasite Immunology, September 2001, Vol.23(9), pp.503-507 [Periódico revisado por pares]

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  • Título:
    HTLV‐1 decreases Th2 type of immune response in patients with strongyloidiasis
  • Autor: Porto, Aurélia F. ; Neva, Franklin A. ; Bittencourt, Helito ; Lisboa, Waldir ; Thompson, Robert ; Alcântara, Luís ; Carvalho, Edgar M.
  • Assuntos: Htlv‐1 ; Strongyloidiasis ; Ige ; S. Stercoralis
  • É parte de: Parasite Immunology, September 2001, Vol.23(9), pp.503-507
  • Descrição: Eosinophils, immunoglobilin (Ig)E and cytokines have important roles in defence mechanisms against helminths. In this study, the influence of HTLV‐1 infection, characterized by a Th1 type of immune response, was evaluated on the cytokine pattern and parasitic specific IgE response in patients with strongyloidiasis. Patients were divided into four groups: strongyloidiasis without HTLV‐1 infection, strongyloidiasis with HTLV‐1, HTLV‐1 without strongyloidiasis and controls without either helminth infection or HTLV‐1. The cytokine profile was determined in supernatants of mononuclear cells stimulated with crude antigen and the parasite specific IgE was measured by ELISA. Patients coinfected with HTLV‐1 had higher levels of interfron (IFN)‐γ and interleukin (IL)‐10 ( < 0·05) and lower levels of IL‐5 and IgE ( < 0·05) than patients with strongyloidiasis without HTLV‐1. There was an inverse relationship between IFN‐γ and IL‐5 ( = 0·01;  = − 0·37) and between IFN‐γ and parasite specific IgE ( = 0·01;  = − 0·39), and a direct relationship between IFN‐γ and IL‐10 ( = 0·04;  = 0·35). These data show that coinfection with HTLV‐1 decreases IL‐5 and IgE responses in patients with strongyloidiasis consistent with a relative switch from Th2 to Th1 response. Immunological responses such as these are important in the control of this helminthic infection.

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