Infective dermatitis has similar immunological features to human T lymphotropic virus-type 1-associated myelopathy/tropical spastic paraparesis.
Human T lymphotropic virus-type 1 (HTLV-1) is the causal agent of the HTLV-1-associated myelopathy/tropical spastic paraparesis (HAM/TSP), adult T cell leukaemia/lymphoma and infective dermatitis associated with HTLV-1 (IDH). Over-production of proinflammatory cytokines and an increase in HTLV-1 proviral load are features of HAM/TSP, but the immunological basis of IDH has not been established. In addition to severe cutaneous manifestations, the importance of IDH relies on the observation that up to 30% of children with IDH develop HAM/TSP in childhood and adolescence. In this study we determined the immune response in patients with IDH measuring interleukin (IL)-4, IL-5, IL-10, interferon (IFN)-gamma and tumour necrosis factor (TNF)-alpha levels as well as the HTLV-1 proviral load. Additionally, regulatory cytokines and anti-cytokines were added to cultures to evaluate the ability of these molecules to down-modulate TNF-alpha and IFN-gamma synthesis. HTLV-1 carriers and patients with HAM/TSP served as controls. TNF-alpha and IFN-gamma levels were higher in IDH than in HTLV-1 carriers. There was no difference in IFN-gamma and TNF-alpha concentrations in IDH and HAM/TSP patients. There was a tendency for higher IL-4 mRNA expression and immunoglobulin E (IgE) levels in IDH than in HTLV-1 carriers, but the difference did not reach statistical significance. The HTLV-1 proviral load was significantly higher in IDH patients than in HTLV-1 carriers. IDH is characterized by an exaggerated Th1 immune response and high HTLV-1 proviral load. The similarities between the immunological response in patients with IDH and HAM/TSP and the high proviral load observed in IDH provide support that IDH is a risk factor for development of HAM/TSP.
Serviço de Imunologia, Hospital Universitário Professor Edgard Santos, Universidade Federal da Bahia, Salvador, Bahia, Brazil.
M C F
MC
Nascimento
J
J
Primo
A
A
Bittencourt
I
I
Siqueira
M
M
de Fátima Oliveira
R
R
Meyer
A
A
Schriefer
S B
SB
Santos
E M
EM
Carvalho
D002353:Carrier State / Q000276:immunology; D002478:Cells, Cultured; D003430:Cross-Sectional Studies; D016207:Cytokines / Q000096:biosynthesis* / Q000276:immunology; D015536:Down-Regulation / Q000276:immunology; D015870:Gene Expression; D015368:Human T-lymphotropic virus 1 / Q000302:isolation & purification; D006801:Humans; D007073:Immunoglobulin E / Q000097:blood; D007371:Interferon-gamma / Q000096:biosynthesis; D016753:Interleukin-10 / Q000097:blood; D015847:Interleukin-4 / Q000096:biosynthesis / Q000235:genetics; D015493:Paraparesis, Tropical Spastic / Q000276:immunology*; D011533:Proviruses / Q000302:isolation & purification; D012333:RNA, Messenger / Q000235:genetics; D017193:Skin Diseases, Viral / Q000276:immunology*; D014409:Tumor Necrosis Factor-alpha / Q000097:blood; D019562:Viral Load
D016207:Cytokines; D012333:RNA, Messenger; D014409:Tumor Necrosis Factor-alpha; D016753:Interleukin-10; D015847:Interleukin-4; D007073:Immunoglobulin E; D007371:Interferon-gamma