Abstract

Systemic lupus erythematosus (SLE) is an autoimmune disease characterized by immune system hyperactivity and autoantibody production that can affect almost any organ system. TREM like transcript-1 (TLT-1) is a membrane receptor found in platelets α-granules with activating properties. We have demonstrated that activated platelets release a soluble isoform of TLT-1 (sTLT-1) which is not found in the plasma of healthy individuals. Moreover, evaluation of patients suffering from inflammatory diseases, such as sepsis, reveals a significant increase of plasma sTLT-1 levels. It is not known if TLT-1 plays a role in auto immune diseases such as Lupus. In the present study we evaluate the potential that TLT-1 may play a role in the etiology of SLE. We assessed the plasma of 46 SLE patients and compared to 28 healthy controls by ELISA. Our results showed that SLE patients had a significant decrease in plasma sTLT-1 levels compared to healthy controls (9.0 [7.2] vs. 18.6 [22.3] ng/ml, p=0.008). A negative correlation was observed between TLT-1 levels and LupusPRO [lupus symptoms (r = -0.388, p = 0.055). Based on this data; we hypothesize that SLE patients produce autoantibodies against TLT-1 in serum which might correlate with clinical aspects of the disease . To address this question; TLT-1 antibodies levels in serum were measured by ELISA. Our data suggests that a sub-population of SLE patients have TLT-1 autoantibodies. This data was further confirmed by confocal microscopy. Using human embryonal kidney cells (HEKt) stably transfected with TLT-1, we evaluated the serum of SLE patients for the presence of TLT-1 autoantibodies using immunofluorescence. Our data confirms that a sub-population of SLE patients with active disease is expressing antibodies against TLT-1. These findings suggest a possible role for TLT-1 during the pathogenesis of SLE and targets new treatment possibilities for lupus patients.

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