T cell-dependent B cell activation in the model of Lupus

We strive to decipher the underlying mechanisms of Systemic lupus erythematosus. We are particularly interested in the role that peripheral helper T cells might play in disease severity.

Systemic lupus erythematosus (SLE) is an autoimmune inflammatory disease which can affect virtually any part of the body. Most often it targets the skin, the kidneys and the joints. Its prevalence in the general population is 20 to 150 cases per 100,000 inhabitants and it affects mainly women. The underlying causes are diverse, with a small genetic component and a variety of external factors: such as medication, tobacco consumption, viral infections or UV exposure. There is a strong need for a better understanding of human SLE pathogenesis, as only a few drugs are effective and new treatments are lacking.
Tertiary lymphoid structures (TLS) are ectopic lymphoid formations that form within non-lymphoid tissue. These structures support the proliferation and differentiation of (auto)-reactive B cells, and perpetuate in situ inflammatory processes. TLS develop in the affected tissues of many inflammatory disorders including rheumatoid arthritis, Sjogren Syndrome, and in the kidneys of SLE patients with lupus nephritis (LN) and lupusprone mice.
Although of significant importance, the signals/cells involved in TLS establishment and maturation remain unknown particularly in AID patients. Our results indicate that peripheral helper T cells (Tph) which secrete IL21 and IFN-gamma correlate to disease severity, and infiltrate inflammatory tissues in SLE patients. Our goal is to delineate the signals involved in Tph differentiation/maturation, and to evaluate whether their specific targeting impacts disease severity in mouse models of SLE.

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