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1.
Fig. 1

Fig. 1. From: The effect of ageing on macrophage Toll-like receptor-mediated responses in the fight against pathogens.

Toll-like receptor (TLR)-mediated signalling pathways and adaptor proteins. Ligation of TLR results in receptor dimerization and subsequent recruitment of Mal and myeloid differentiation factor 88 (MyD88), interleukin 1 receptor associated kinase (IRAK) and tumour necrosis factor receptor associated factor (TRAF)-6 molecules lead to activation of nuclear factor (NF)-kB and mitogen-activated protein kinase (MAPK) pathways. This results in transcriptional activation of proinflammatory genes including cytokines. A delayed response is also activated by TLR dimerization, probably activated after endosomal internalization of the TLR-4 homodimer. This involves recruitment of TRAM and TRIF resulting in a delayed NF-kB activation and transcription via interferon regulatory factor (IRF)3 activation of late genes such as interferon.

C R Dunston, et al. Clin Exp Immunol. 2010 September;161(3):407-416.
2.
Fig. 2

Fig. 2. From: The effect of ageing on macrophage Toll-like receptor-mediated responses in the fight against pathogens.

The role of macrophages in the response and removal of bacterial pathogens. Monocytes are first recruited to the site of infection and undergo differentiation to macrophages (1). Toll-like receptor (TLR)-mediated signalling events are initiated (2) leading to increased production of cytokines and reactive oxygen species (ROS) products (3). Phagocytes initiate phagocytosis (4) resulting in the killing and removal of the pathogen. In an aged immune system monocytes are recruited and differentiate into macrophages (5). Subsequent TLR-mediated signalling events are deficient (6) and this results in decreased bactericidal and phagocytic activity (7). More macrophages are recruited (8) and although each cell is less functional, their increased numbers lead to increased serum cytokines levels (9). The ineffective signalling cascades do not result in the killing and removal of the invading pathogen, thereby leading to chronic inflammation and susceptibility to infection.

C R Dunston, et al. Clin Exp Immunol. 2010 September;161(3):407-416.

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