| Title | The role of innate immunity in autoimmune tissue injury. | | Author(s) | Allam R, Anders HJ | | Institution | Medical Policlinic, University of Munich, Munich, Germany. | | Source | Curr Opin Rheumatol 2008 Sep; 20(5):538-44. | | Abstract | PURPOSE OF REVIEW: To discriminate the pathomechanims of autoimmunity from that of autoimmune tissue injury, for example, in systemic lupus erythematosus, with a special focus on the role of innate pathogen recognition receptors in lupus nephritis.
RECENT FINDINGS: Toll-like receptors mediate immune activation upon the recognition of pathogens in different extracellular and intracellular compartments. Systemic lupus erythematosus appears to be one of the conditions in which self-nucleic acid formats can activate innate viral nucleic acid recognition receptors like TLR-7 or TLR-9. This process can modulate the tolerance mechanisms by activating antigen-presenting cells in lymphoid organs. This mechanism does also occur at the tissue level in tissue macrophages, dendritic cells, B cells and nonimmune cells. For example, nonimmune renal cells express a limited set of functional Toll-like receptors that trigger local cytokine and chemokine release in lupus nephritis upon Toll-like receptor activation.
SUMMARY: In systemic lupus erythematosus, autoantibodies and expansion of autoreactive T cells indicate systemic autoimmunity, but organ damage involves additional mechanisms of inflammation and tissue remodelling. Targeting local release of proinflammatory cytokines, for example, by blocking Toll-like receptors or single cytokines, may enhance treatment efficacy in autoimmunity without increasing systemic immunosuppression. | | Language | eng | | Pub Type(s) | Journal Article
| | PubMed ID | 18698174 |
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