Expert Reviews in Molecular Medicine: http://www.expertreviews.org/
Accession information: Vol. 8; Issue 6; 24 March 2006 Abstract
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Possible pathways of immunopathological organ damage inside organ vessels

Tracey J. Lamb, Douglas E. Brown, Alexandre J. Potocnik and Jean Langhorne

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Figure 3. Possible pathways of immunopathological organ damage inside organ vessels. Macrophages can mediate damage to the endothelial barrier via several different mechanisms. (a) Parasites may sequester via a variety of adhesion molecules and receptors such as CD36. (b) The parasitised red blood cells (pRBCs) may also stick to the endothelium via attached platelets, and (c) might be in a rosetting format. (d) Macrophages recognise pRBCs via pattern-recognition receptors (PRRs) on their surface. Activation of macrophages results in amplification of the acute-phase reaction or respiratory burst. The respiratory burst (e) can cause lesions in the endothelium. In the case of cerebral malaria this can result in haemorrhaging. (f) Tumour necrosis factor a (TNF-a) secreted by activated macrophages up-regulates adhesion molecule expression on endothelial cells, amplifying sequestration; in addition, secretion of RANTES attracts additional macrophages and other lymphocytes from the blood stream (g), and can also activate the endothelial cells to become pro-inflammatory. Incoming CD8⁺ T cells cause damage via a perforin-dependent pathway (h), although the mechanism by which they become activated is unknown. Immune complexes are deposited on the endothelium (i), which will activate macrophages via Fc-receptors, again amplifying all of the responses described above. Abbreviations: CCR5, chemokine (CC motif) receptor 5 (receptor for RANTES); ICAM-1, intercellular adhesion molecule 1; LFA-1, lymphocyte-function associated antigen 1 (integrin b2; ligand for ICAM-1); RANTES, ‘chemokine regulated on activation, normal T cell expressed and secreted’.

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