Biological agents: investigation into leprosy and other infectious diseases before indication

Antônio, Joäo Roberto; Soubhia, Rosa Maria Cordeiro; Paschoal, Vânia Del'Arco; Amarante, Carolina Forte; Travolo, Ana Regina Franchi

doi:10.1590/abd1806-4841.20132187

Cited by 12 publications

(10 citation statements)

References 8 publications

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“…Macrophages are the cell population that plays a central role in the interaction between the bacillus and host. Since macrophages are the main cells that exert microbicidal activity in leprosy, many studies have already described the role of these cells in the response to cytokines, including tumor necrosis factor-alpha (TNF-α) and interferon-gamma (IFN-γ) ( 35 , 36 ). In leprosy, both TNF-α and IFN-γ have been shown to bind to the cellular receptor of the macrophages, thereby changing the behavior of M0 macrophages, which undergo phenotypic modification to become M1 inflammatory macrophages.…”

Section: Immune Response In Leprosymentioning

confidence: 99%

Leprosy As a Complex Infection: Breakdown of the Th1 and Th2 Immune Paradigm in the Immunopathogenesis of the Disease

2017

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Leprosy is a chronic infectious disease whose evolution involves complex immune mechanisms of the host that influence the clinical presentation of the disease. For many years, the main interpretation of the host defense response was based on characterization of the established immune paradigm between T helper (Th) 1 and Th2 lymphocytes. However, with advances in the knowledge of immunology, new approaches have emerged along with the development of new immunological pathways that have changed the interpretation of the long-established paradigm of the polar forms of the disease, especially with the identification of new subtypes of T lymphocytes such as Th9, Th17, Th22, and Tregs. Thus, this review discusses the role of these new subtypes of T helper lymphocytes and how the development of the immune response of these cells modifies the pattern of the Th1/Th2 response in the immunopathogenesis of leprosy.

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Section: Immune Response In Leprosymentioning

confidence: 99%

Leprosy As a Complex Infection: Breakdown of the Th1 and Th2 Immune Paradigm in the Immunopathogenesis of the Disease

2017

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“…Adverse events in studies of sarcoidosis have included lymphoma, infusion reactions anaphylaxis, rash, sinusitis as well as numerous infections. Anti‐TNF‐α biologics cause a well‐documented increased risk for granulomatous infections including tuberculosis, leprosy and leishmaniasis . Curiously, some patients experienced worsening of sarcoidosis or the onset of new manifestations such uveitis or cutaneous sarcoidosis.…”

Section: Clinical Efficacy Of Anti‐tnf‐α Biologicsmentioning

confidence: 99%

TNF‐α: a treatment target or cause of sarcoidosis?

Amber

Bloom

Mrowietz³

et al. 2015

Acad Dermatol Venereol

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Sarcoidosis is a systemic granulomatous disease that affects numerous organs, commonly manifesting at the lungs and skin. While corticosteroids remain the first line of treatment, tumour necrosis factor alpha (TNF-α) inhibitors have been investigated as one potential steroid sparing treatment for sarcoidosis. TNF-α is one of many components involved in the formation of granulomas in sarcoidosis. While there have been larger scale studies of biologic TNF-α inhibition in systemic sarcoidosis, studies in cutaneous disease are limited. Paradoxically, in some patients treated with biologic TNF-α inhibitors for other diseases, treatment can induce the development of sarcoidosis. In the light of this complexity, we discuss the role of TNF-α in granuloma formation, the therapeutic role of TNF-α inhibition and immunologic abnormalities following treatment with these TNF-α inhibitors including drug-specific alterations involving interferon-γ, lymphotoxin-α, TNF receptor 2 (TNFR2) and T-regulatory cells.

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“…Anti-TNF agents cause death of cells expressing TNF and disrupting granulomas which lead to reactivation of granulomatous disease. Though attention has been focused more on TB, reactivation of leprosy has also been reported [ 3 ].…”

Section: Discussionmentioning

confidence: 99%

Leprosy Mimicking Common Rheumatologic Entities: A Trial for the Clinician in the Era of Biologics

Rath

Bhargava²,

Kundu

2014

Case Reports in Rheumatology

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Rheumatoid arthritis and seronegative spondyloarthritis, which make up the lion's share of cases attending a rheumatology clinic, are relatively easy to diagnose. However, when an entity of infective aetiology like leprosy known to be a great mimic of different autoimmune conditions presents with features similar to these, the possibility of it being diagnosed at the outset is very slim indeed. The ease with which the diagnosis of leprosy can be missed assumes sinister proportions as the use of disease modifying agents can have deleterious effects in these patients. In the era of increasing availability and use of biologic disease modifying agents, it is imperative not only to actively rule out the presence of leprosy but also to make it a part of the prebiologic screening of patients in whom biologics are being planned to be administered, especially in leprosy endemic areas.

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Biological agents: investigation into leprosy and other infectious diseases before indication

Cited by 12 publications

References 8 publications

Leprosy As a Complex Infection: Breakdown of the Th1 and Th2 Immune Paradigm in the Immunopathogenesis of the Disease

Leprosy As a Complex Infection: Breakdown of the Th1 and Th2 Immune Paradigm in the Immunopathogenesis of the Disease

TNF‐α: a treatment target or cause of sarcoidosis?

Leprosy Mimicking Common Rheumatologic Entities: A Trial for the Clinician in the Era of Biologics

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