Memory CD4+ T cell induce innate responses independently of pathogen (Nat Med, 2010, 16:558-564)

報告日期: 2010/09/21
報告時間: 16:00/16:50
報告學生: 呂佳馨
講評老師: 黎煥耀

Full Text:

Memory CD4+ T cells induce innate responses independently of pathogen

Strutt et al. Nature medicine 16, 558-564, 2010

Speaker: Chia-Hsing Leu              

Commentator: Dr. Huan-Yao Lei        

Time: 16:00~16:50, Sep. 21, 2010

Room: 601



The immune system can recognize microbes directly through pattern recognition receptors (PRRs), which respond to conserved microbial molecules or motifs called pathogen-associated molecular patterns (PAMPs). PRRs rapidly activate intracellular signaling pathway which facilitates the production of inflammatory mediators in innate immunity. Cells principally expressing PRRs include antigen-presenting cells (APCs), which ingest and digest pathogens. APCs also trigger the adaptive immune response and begin the immunological memory. Whether adaptive immune cells regulate innate inflammation is largely unknown. In this study, the authors measured innate immunity-related cytokines and chemokines after influenza A virus challenge of naïve mice or mice primed with influenza A virus. They found that memory CD4+ T cells could enhance early expression of innate immunity-related cytokines and chemokines in the lung during influenza virus infection. After transfer of TH1, TH2, TH17 or TH0 memory cells to naïve mice followed by infection with influenza A virus, the authors found TH1 or TH17 memory cells recognized antigens by major histocompatibility complex (MHC)-II+ APCs, leading to increased chemokine production and viral control in the initial phase of infection. This protective response is independent of the interferon-γ (IFN-γ), tumor necrosis-α (TNF-α) and PAMP-recognition pathways. Collectively, this study demonstrates that memory CD4+ T cells induce innate inflammatory response independently of pathogen recognition pathway. This may help explain why memory CD4+ T cells have been implicated in several autoimmune diseases.



1. Powell, T.J. et al. (2007) Priming with cold-adapted influenza A does not prevent infection but elicits long-lived protection against supralethal challenge with heterosubtypic virus. J. Immunol. 178, 1030-1038.