Can Lupus Flares be Associated with Tuberculosis Infection?

Ribeiro, Francinne Machado; Szyper‐Kravitz, Martine; Klumb, Evandro Mendes; Lannes, G.; Ribeiro, Fontes; Albuquerque, Elise M.; Shoenfeld, Yehuda

doi:10.1007/s12016-009-8149-7

Cited by 37 publications

(33 citation statements)

References 36 publications

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“…NOD2-deficient mice have impaired resistance to mycobacterium tuberculosis infection through defective innate and adaptive immunity [67]. Our group also reported a higher prevalence of mycobacterial tuberculosis infection in patients with SLE [68], and there are several reports suggesting that mycobacterium tuberculosis infection precipitates SLE in patients from endemic areas [69]. Whether decreased NOD2 expression may contribute towards the induction and reactivation of chronic inflammation by mycobacterial infection in patients with SLE deserves further study.…”

Section: Discussionmentioning

confidence: 52%

Down-Regulated NOD2 by Immunosuppressants in Peripheral Blood Cells in Patients with SLE Reduces the Muramyl Dipeptide-Induced IL-10 Production

Wong

et al. 2011

PLoS ONE

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BackgroundPattern recognition receptors (PRRs) such as Toll-like receptors are aberrantly expressed of peripheral blood mononuclear cells (PBMCs) in systemic lupus erythematosus (SLE) patients, for playing immunopathological roles.Methodology/Principal FindingsWe investigated the expression and function of the PRR nucleotide-binding oligomerization domain (NOD2) in SLE. NOD2 expression in T, B lymphocytes, monocytes, myeloid dendritic cells (mDCs) and plasmacytoid dendritic cells (pDCs) was assessed in SLE patients and healthy controls (HCs) using flow cytometric analysis. Ex vivo production of cytokines from PBMCs upon NOD2 agonist muramyl dipeptide (MDP) stimulation was assessed using Cytometric Bead Array. Over-expression of NOD2 in monocytes was observed in immunosuppressant naïve SLE patients, and was positively associated with longer disease duration. Immunosuppressive therapy was an independent explanatory variable for downregulating NOD2 expression in CD8+ T, monocytes, mDCs and pDCs. Ex vivo basal productions of cytokines (IL-6, IL-8 and IL-10) were significantly increased in immunosuppressant naïve patients and patients with active disease despite immunosuppressants compared with HCs. Upon MDP stimulaiton, relative induction (%) of cytokines (IL-1β) from PBMC was significantly increased in immunosuppressant naïve patients with inactive disease, and patients with active disease despite immunosuppressant treatment compared with HCs. Immunosuppressant usage was associated with a decreased basal production and MDP induced relative induction (%) of IL-10 in patients with inactive disease compared with immunosuppressant naïve patients and HCs.Conclusions/SignificanceBacterial exposure may increase the NOD2 expression in monocytes in immunosuppressant naïve SLE patients which can subsequently lead to aberrant activation of PBMCs to produce proinflammatory cytokines, implicating the innate immune response for extracellular pathogens in the immunopathological mechanisms in SLE. Immunosuppressant therapy may downregulate NOD2 expression in CD8+ T lymphocytes, monocytes, and DCs in SLE patients which subsequently IL-10 reduction, contributing towards the regulation of immunopathological mechanisms of SLE, at the expense of increasing risk of bacterial infection.

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Section: Discussionmentioning

confidence: 52%

Down-Regulated NOD2 by Immunosuppressants in Peripheral Blood Cells in Patients with SLE Reduces the Muramyl Dipeptide-Induced IL-10 Production

Wong

et al. 2011

PLoS ONE

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“…Interestingly, HsP60 and HsP65 have been demonstrated as autoantigenic in atherogenesis and are present in the sera of many autoimmune diseases like RA, ankylosing spondylitis and SLE. 76 Multiple autoimmune diseases (vitiligo, idiopathic thrombocytopenic purpura, thyroiditis and myasthenia gravis) occurring in the same patient have been described following TB infection. In this specific case the haplotypes related to multiple autoimmune diseases, like HLA-A1, B8, and DR3, are not present, raising the possibility of a mycobacterial trigger.…”

Section: Mycobacteria and Autoimmune Diseasesmentioning

confidence: 99%

“…75 Nevertheless in some patients, MT infection was diagnosed in the presence of persistent, active SLE. 76,77 One mechanism suggested is molecular mimicry based on the concept that chronic infections may act as a trigger for immune hyperactivity. 78 The evidence of antigen resemblance between mycobacterial cell wall glycolipids and DNA could corroborate this hypothesis.…”

Section: Mycobacteria and Autoimmune Diseasesmentioning

confidence: 99%

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Mycobacteria and autoimmunity

Ribeiro

Goldenberg

2015

Lupus

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Mycobacterial infections can cause a variety of different manifestations. The increasing incidence of these infections worldwide brought another medical dilemma: immunological manifestations characterized by the presence of many autoantibodies and concomitant presence of autoimmune diseases. The burden of tuberculosis reactivation that emerged with immunosuppressive therapy worsened with the growing use of biological disease-modifying antirheumatic drugs (DMARDs). This review will address the relationship between the immune system and mycobacteria.

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“…25 Antibodies against TB may carry a common anti-DNA idiotype; 26 while proteins from M. tuberculosis like heat-shock protein 60 and 65 may act as super-antigens in autoimmunity development. 27 Given the protean clinical manifestation of miliary TB, a high index of clinical suspicion is essential, particularly in situations of rapid organ decompensation and extra-pulmonary involvement. 10 Certain hematologic and biochemical abnormalities may be found in miliary TB, namely normocytic normochromic anemia, pancytopenia, deranged liver function tests, hyponatremia, elevated ESR, sterile pyuria, and less commonly, hypercalcemia and disseminated intravascular coagulopathy, which should raise concern for possible TB infection.…”

Section: Discussionmentioning

confidence: 99%

Disseminated tuberculosis masquerading as a presentation of systemic lupus erythematosus

Fong

Wijaya

et al. 2017

Int J of Rheum Dis

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Tuberculosis (TB) infection is the endemic in Asia-Pacific region. Miliary TB is a disseminated form which may present similarly as autoimmune conditions. Here we describe a 17-year-old girl who had miliary TB with manifestations mimicking new-onset systemic lupus erythematosus (SLE) including oral ulcers, serositis, cytopenia, proteinuria and raised autoantibody titers. Complex associations between SLE and TB are highlighted. High index of clinical suspicion for TB infection is needed upon presentations resembling immune diseases like SLE.

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Can Lupus Flares be Associated with Tuberculosis Infection?

Cited by 37 publications

References 36 publications

Down-Regulated NOD2 by Immunosuppressants in Peripheral Blood Cells in Patients with SLE Reduces the Muramyl Dipeptide-Induced IL-10 Production

Down-Regulated NOD2 by Immunosuppressants in Peripheral Blood Cells in Patients with SLE Reduces the Muramyl Dipeptide-Induced IL-10 Production

Mycobacteria and autoimmunity

Disseminated tuberculosis masquerading as a presentation of systemic lupus erythematosus

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