We have located links that may give you full text access.
JOURNAL ARTICLE
RESEARCH SUPPORT, NON-U.S. GOV'T
REVIEW
The role of innate immunity in autoimmune tissue injury.
Current Opinion in Rheumatology 2008 September
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.
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.
Full text links
Trending Papers
A Personalized Approach to the Management of Congestion in Acute Heart Failure.Heart International 2023
Potential Mechanisms of the Protective Effects of the Cardiometabolic Drugs Type-2 Sodium-Glucose Transporter Inhibitors and Glucagon-like Peptide-1 Receptor Agonists in Heart Failure.International Journal of Molecular Sciences 2024 Februrary 21
The Effect of Albumin Administration in Critically Ill Patients: A Retrospective Single-Center Analysis.Critical Care Medicine 2024 Februrary 8
Get seemless 1-tap access through your institution/university
For the best experience, use the Read mobile app
All material on this website is protected by copyright, Copyright © 1994-2024 by WebMD LLC.
This website also contains material copyrighted by 3rd parties.
By using this service, you agree to our terms of use and privacy policy.
Your Privacy Choices
You can now claim free CME credits for this literature searchClaim now
Get seemless 1-tap access through your institution/university
For the best experience, use the Read mobile app