TNFα Inhibition in MRL/lpr Mice Ameliorates Pulmonary but not Renal Disease
| Autor: | Nahmah A. Kim, Xin Cheng, Kathleen E. Sullivan, Ramachandran Murali, Lashon Ussin |
|---|---|
| Rok vydání: | 2002 |
| Předmět: |
Lung Diseases
Mice Inbred MRL lpr Systemic disease medicine.medical_treatment Immunology Antibodies Nephropathy Pathogenesis Mice medicine Animals Immunology and Allergy Autoimmune disease Lupus erythematosus Systemic lupus erythematosus Tumor Necrosis Factor-alpha business.industry DNA medicine.disease Connective tissue disease Lymphocyte Subsets Cytokine Female Kidney Diseases business Spleen |
| Zdroj: | Journal of Autoimmunity. 19:215-222 |
| ISSN: | 0896-8411 |
| DOI: | 10.1006/jaut.2002.0617 |
| Popis: | TNFalpha inhibition has a clearly beneficial effect in a number of arthritides and in Crohn's disease. The exact mechanism of action is uncertain with studies showing inhibition of chemokines, inhibition of adhesion molecule expression, and improved T-cell function. Unlike most therapeutic interventions for autoimmune disease, TNFalpha inhibition appears to act on specific pathologic processes. It is not known how wide-spread these TNFalpha-mediated pathologic processes are. Efforts to expand the use of TNFalpha inhibition have had notable successes but have been disappointing in other disorders. We hypothesized that TNFalpha-mediated pathologic processes might play a significant role in the end-organ effects seen in SLE. We modeled SLE by using MRL/lpr mice and treated with two types of TNFalpha inhibitor. Pulmonary disease was significantly improved in the treated groups compared to controls. In contrast, renal disease was unaffected suggesting that in lupus, where multiple organs are affected, different pathologic processes may be mediating the end-organ damage. This has important implications for designing therapeutics for SLE. |
| Databáze: | OpenAIRE |
| Externí odkaz: |
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