Abstract
The fact that TNF receptor family members are involved in the control of diverse gene products that effect both pro-inflammatory and homeostatic functions related to immune protection offers multiple targets for clinical intervention in a range of disease contexts. The stunning success of anti-TNF-alpha therapy in the treatment of the inflammatory disease rheumatoid arthritis perhaps best illustrates the vast potential of antagonism of TNF family members in clinical medicine [1]. The involvement of other family members, such as CD40, in many other immune regulated diseases will also no doubt lead to similar success stories. In contrast to the pro-inflammatory pathways controlled by TNF-alpha, our lab has begun to determine whether antagonism of the “homeostatic” pathways in secondary and “ectopic” or tertiary lymphoid tissues that are under the control of the TNF receptor family member lymphotoxin-beta receptor (LTBR) might represent a useful target in the treatment of certain diseases such as Sjogren’s syndrome where frank inflammation is not the primary pathogenic impetus.
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Fava, R.A., Browning, J.L., Gatumu, M., Skarstein, K., Bolstad, AI. (2011). LTBR-Pathway in Sjogren’s Syndrome: CXCL13 Levels and B-cell-Enriched Ectopic Lymphoid Aggregates in NOD Mouse Lacrimal Glands Are Dependent on LTBR. In: Wallach, D., Kovalenko, A., Feldmann, M. (eds) Advances in TNF Family Research. Advances in Experimental Medicine and Biology, vol 691. Springer, New York, NY. https://doi.org/10.1007/978-1-4419-6612-4_39
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