Abstract
Erythema Nodosum Leprosum (ENL) is an immune reaction in leprosy that aggravates the patient´s clinical condition. ENL presents systemic symptoms of an acute infectious syndrome with high leukocytosis and intense malaise clinically similar to sepsis. The treatment of ENL patients requires immunosuppression and thus needs to be early and efficient to prevent both disabilities and permanent nerve damage. Some patients experience multiple episodes of ENL and prolonged use of immunosuppressive drugs may lead to serious adverse effects. Thalidomide treatment is extremely effective at ameliorating ENL symptoms. Several mechanisms have been proposed to explain the efficacy of thalidomide in ENL, including the inhibition of TNF production. Given its teratogenicity, thalidomide is prohibitive for women of childbearing age. A rational search for molecular targets during ENL episodes is essential to better understand the disease mechanisms involved, which may also lead to the discovery of new drugs and diagnostic tests. Previous studies have demonstrated that IFN-γ and GM-CSF, involved in the induction of CD64 expression, increase during ENL. The aim of the present study was to investigate CD64 expression during ENL and whether thalidomide treatment modulated its expression. Leprosy patients were allocated to one of five groups: (1) Lepromatous leprosy, (2) Borderline leprosy, (3) Reversal reaction, (4) ENL, and (5) ENL 7 days after thalidomide treatment. The present study demonstrated that CD64 mRNA and protein were expressed in ENL lesions and that thalidomide treatment reduced CD64 expression and neutrophil infiltrates—a hallmark of ENL. We also showed that ENL blood neutrophils exclusively expressed CD64 on the cell surface and that thalidomide diminished overall expression. Patient classification based on clinical symptoms found that severe ENL presented high levels of neutrophil CD64. Collectively, these data revealed that ENL neutrophils express CD64, presumably contributing to the immunopathogenesis of the disease.
Highlights
Leprosy, the leading infectious cause of disability, is a chronic infectious disease caused by Mycobacterium leprae
Reactions are classified into type 1 and type 2 according to the etiopathogenesis
The current study investigated whether or not CD64 is expressed during Erythema Nodosum Leprosum (ENL)
Summary
The leading infectious cause of disability, is a chronic infectious disease caused by Mycobacterium leprae. The disease is characterized by skin lesions and peripheral nerve impairment reflecting the preference of the bacteria for macrophages and Schwann cells. Leprosy is manifested by a spectrum of clinical and histopathological presentations that are directly related to the immune status of the patient. One pole of the disease, known as polar tuberculoid leprosy (TT), is characterized by an efficient specific cellular immune response. The absence of an immune response with no apparent resistance to M. leprae characterizes lepromatous leprosy (LL) at the opposite pole. Most affected individuals show intermediate clinical and immunological patterns, commonly referred to as borderline tuberculoid (BT), borderline borderline (BB), and borderline lepromatous (BL) [2,3]
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