Premium
The effect of systemic corticosteroid therapy on the expression of toll‐like receptor 2 and toll‐like receptor 4 in the cutaneous lesions of leprosy Type 1 reactions
Author(s) -
Walker S.L.,
Roberts C.H.,
Atkinson S.E.,
Khadge S.,
Macdonald M.,
Neupane K.D.,
Ranjit C.,
Sapkota B.R.,
Dhakal S.,
Hawksworth R.A.,
Mahat K.,
Ruchal S.,
Hamal S.,
Hagge D.A.,
Lockwood D.N.J.
Publication year - 2012
Publication title -
british journal of dermatology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.304
H-Index - 179
eISSN - 1365-2133
pISSN - 0007-0963
DOI - 10.1111/j.1365-2133.2012.10891.x
Subject(s) - tlr2 , immunology , tlr4 , toll like receptor , medicine , corticosteroid , leprosy , receptor , pathogenesis , innate immune system , inflammation , immune system
Summary Background Leprosy is complicated by immunological reactions which can occur before, during and after successful completion of multidrug therapy. Genetic studies have suggested that polymorphisms in toll‐like receptors (TLRs) may affect the susceptibility of an individual with leprosy to developing Type 1 reactions. Objectives To examine the gene and protein expression of TLRs in the cutaneous lesions of leprosy Type 1 reactions at the onset of reaction and during systemic corticosteroid therapy. Methods Patients who were being treated for leprosy type 1 reactions with corticosteroids as part of a randomized controlled trial of corticosteroid treatment had skin biopsies performed before, during and at the end of treatment. The gene and protein expression of TLR2 and TLR4 were measured. Results We have demonstrated that the gene hARP‐P0 is a suitable control gene for TLR gene expression studies in this population. The gene and protein expression of TLR2 and TLR4 were both reduced significantly during corticosteroid treatment. Conclusions This is the first study to examine the expression of TLR2 and TLR4 in vivo in individuals experiencing leprosy Type 1 reactions. The data support the possibility of an important role for TLR2 and TLR4 in the pathogenesis of this important complication of leprosy.