Macrophage and TGF-β immunohistochemical expression in Jorge Lobo's disease

Xavier, Marília Brasil; Libonati, Rosana Maria Feio; Unger, Deborah Aben Athar; Oliveira, Clivia Maria Moraes de; Corbett, Carlos Eduardo Pereira; Brito, Arival Cardoso de; Quaresma, Juarez Antônio Simões

doi:10.1016/j.humpath.2007.06.016

Cited by 30 publications

(17 citation statements)

References 25 publications

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“…The early lesions have been described as wart-like, and as the disease progresses they become more keloidal in appearance [Lupi et al 2005]. The lesions may remain localized, or they can be disseminated by the lymphatics to several areas of the body [Lupi et al 2005;Xavier et al 2008]. Superinfection can occur in ulcerated lesions.…”

Section: Discussionmentioning

confidence: 99%

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Jorge Lobo’s disease: a case of keloidal blastomycosis (lobomycosis) in a nonendemic area

Arju

Kothadia²,

Kaminski

et al. 2014

Therapeutic Advances in Infection

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Section: Discussionmentioning

confidence: 99%

“…It has also been found in high quantities in other acute and chronic disease processes, such as chronic hepatitis, leprosy, and yellow fever [Xavier et al 2008]. The high expression of TGF-b causing macrophage suppression may in part be responsible for the difficult clearance of the disease once it infiltrates the skin [Xavier et al 2008].…”

Section: Discussionmentioning

confidence: 99%

Jorge Lobo’s disease: a case of keloidal blastomycosis (lobomycosis) in a nonendemic area

Arju

Kothadia²,

Kaminski

et al. 2014

Therapeutic Advances in Infection

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“…31 In humans, the slow incubation period and development of lesions may be attributed to the suppression of macrophagic activity through the cytokine TGFβ that inhibits nitric oxide and γ-interferon expression, impacting cell mediated immunity, leading to an antigen-specific cell mediated immune deficiency and inducing fibrosis. 32,33 Langerhan's cells may be implicated in modulating the local immune system to evade antigen presentation by those cells. 33 However, neutrophil function and complement system activity are normal as L. loboi may activate the alternative pathway of the complement system.…”

Section: Discussionmentioning

confidence: 99%

Lobomycosis: A case from Southeastern Europe and review of the literature

Papadavid¹,

Dalamaga²,

Kapniari³

et al. 2012

J Dermatol Case Rep

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Background: Lobomycosis, also known as Jorge Lobo's disease, represents a rare chronic subcutaneous mycosis caused by the fungus Lacazia loboi, an organism that is found within lesions but has not been cultured to date. The natural reservoir of L. loboi is unknown but it is believed to be aquatic, or associated with soil and vegetation. More than 550 human cases have been reported, especially in patients with a history of travel or residence in endemic areas (Central and South America, particularly Brazil) or in communities along rivers. Main observations:We describe a 64-year-old Greek female farmer living in a coastal region, who presented with an erythematous plaque on her left inner thigh resembling a keloid. The diagnosis was based on the triad: 1) absence of fungal growth in cultures, 2) positive direct microscopic examination of the lesion and 3) histopathology, all consistent with lobomycosis. Particularly, skin biopsy showed deep cutaneous fungal infection with granulomatous reaction. Fungal cells were found inside giant cells. The fungi were thick-walled with some budding, isolated or in short chains. Dermal fibrosis was present. Our patient had a medical history of common variable immunodeficiency but no history of travel to South or Central America. She probably acquired this rare infection by injury during her agricultural works. Conclusion:Our case represents probably the first documented case of human lobomycosis in Southeastern Europe. This case is unusual due to the rarity of lobomycosis in Mediterranean countries, particularly in Southeastern Europe. (J Dermatol Case Rep. 2012; 6(3): 65-69)

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“…Vilani-Moreno et al [6] characterized the inflammatory infiltrate in lacaziosis lesions and showed a predominance of macrophages followed by, in decreasing order of frequency, CD3 + , CD4 + , and CD8 + T cells; CD57 + natural killer cells; CD79 + plasma cells; and CD20 + B lymphocytes. Xavier et al [7] characterized the presence of CD68 cells and intense staining for transforming growth factor β (TGF-β) that is a strong inhibitor of the microbicidal activity of macrophages and induces fibrosis in keloid-like lesions [8]. The pathogenesis of the disease has been investigated in cases of lesions limited and localized in different regions of the body.…”

Section: Introductionmentioning

confidence: 99%