Up‐Regulation of Interleukin‐10 Expression in Dendritic Cells as an Important Role in The Immunomodulation By Strongyloides stercoralis

Abstract

Strongyloidiasis is a parasitic disease caused by Strongyloides stercoralis. Infection in the immunocompromised hosts such as organ transplants, SLE patients, or HIV and HIPV infected patients can cause severe strongyloidiasis. About 90% of patients with severe strongyloidiasis are dead. Infected patients have high levels of Th2, and Treg related cytokines, including IL‐4, IL‐5, IL‐9, IL‐10, IL‐13, and TGF‐β. These cytokines are then decreased to normal levels after the treatments. Parasites have several mechanisms to suppress or evade the host’s immune response, such as suppressing the expression of co‐stimulatory molecules on antigen presenting cells (APCs), stimulating apoptosis of APCs, or stimulating Th2 and Treg responses. Dendritic cells (DCs) play a crucial role in linking the innate and adaptive immune systems against pathogens by engulfing antigens and presenting to naïve T cells with appropriate cytokines. To understand the mechanisms of S. stercoralis to evade the host’s immune responses, we studied the alteration of antigen presentation process and cytokines productions by DCs stimulated with S. stercoralis. We treated murine dendritic cell line (DC2.4) with S. stercoralis L3s crude antigen and measured the expressions of genes related with antigen presentation and cytokine productions by quantitative real‐time PCR; including MHC‐II, CD40, CD80, TLR‐2, TLR‐4, IL‐6, IL‐10, TNF‐α, and TGF‐β. The results showed that the expression of TLR2 and CD40 were significantly increased after the stimulation by crude antigens for 1 hr and 3 hrs, respectively. Likewise, the significant up‐regulation of IL‐10 expression of dendritic cells was also detected. While the expression levels of IL‐6 were not changed, TNF‐α expression levels were significantly increased. Our result suggested that S. stercoralis modulate the host’s immune response through the induction of Treg response by IL‐10 production by dendritic cells, not by the suppression the expression of co‐stimulatory molecules on antigen presenting cells.Support or Funding Information1. The Ratchadaphiseksompotch Fund, Faculty of Medicine, Chulalongkorn University, grant number RA62/026 2. Overseas Academic Presentation Scholarship for Graduate Students from the Graduate School, Chulalongkorn University