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Understanding of Systemic Lupus Erythematosus
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Baylor Institute for Immunology Research
3434 Live Oak St.
Dallas, Texas 75204

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Understanding Systemic Lupus Erythematosus (SLE)
Investigators: Virginia Pascual, Jacques Banchereau, A. Karolina Palucka

SLE is a prototype systemic autoimmune disease characterized by flares of high morbidity for which we have no predictors. Current treatment is symptomatic and based on non-specific immune suppression by glucocorticoids and chemotherapy. Thus, SLE is an unmet medical need particularly in children. Until recently SLE has been viewed mainly as a B cell disease resulting from altered T/B cell interactions. The recognition of the fundamental role of dendritic cells (DCs) in the control of tolerance and immunity led to the hypothesis that SLE may be driven through unabated DC activation.

BIIR scientists made fundamental progresses in understanding of SLE that may lead to novel therapeutic modalities.

First, it was shown that monocytes from SLE blood include cells that act as dendritic cells. These cells are being generated in response to circulating Interferon alpha (IFN-alpha). Second, we found that IFN-alpha is a powerful inducer of plasma cell differentiation and survival possibly explaining the hypergammaglobulinemia observed in SLE patients. Third, we have confirmed the role of IFN using oligonucleotide microarrays and shown that SLE can be distinguished by overexpression of granulopoiesis-related and interferon-induced genes. Repeated IV infusion of glucocorticoids at high dose, the standard treatment of disease flares, shuts down the interferon signature. Thus, SLE may be controlled by targeting IFN-alpha and targeting IFN-alpha may benefit all SLE patients. Accordingly, a program has been launched to generate anti-IFN antibody for therapy. This novel therapeutic approach might bring to SLE patients the relief that anti-TNF therapy brought to patients with arthritis.