Association between Takayasu arteritis and latent or active Mycobacterium tuberculosis infection: a systematic review

Pedreira, Ana Luisa Souza; Santiago, Mittermayer Barreto

doi:10.1007/s10067-019-04818-5

Cited by 28 publications

(16 citation statements)

References 40 publications

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“…In particular, the administration of tumor necrosis factor-α (TNF-α) inhibitors, often chosen to treat patients with recurrent or refractory TAK (discussed below), would be expected to increase the risk of TB development by up to 25-fold [18]. However, systematic and careful reviews of the literature indicate that the risk is not higher in TAK patients than in patients with other rheumatic diseases treated with TNF-α inhibitors [19,20]. These observations are considered proof of concept that the relationship between TAK and TB is epiphenomenal rather than causal, although the clinical picture of TB arteritis should be considered in the differential diagnosis of TAK.…”

Section: Introductionmentioning

confidence: 99%

“…Activated CD8 and γδ T cells as well as natural killer (NK) cells release IFN-γ, perforin, and granzyme-B, which promote the apoptosis and necrosis of smooth muscle cells, with consequent injury to the intimal layer. NK cells and γδ T cells are also able to trigger a strong cytotoxic response against vascular EC mediated by natural killer group 2 member D/major histocompatibility class I-related chain A (NKG2D-MICA) interactions [19] 1 3…”

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Takayasu arteritis: a cohort of Italian patients and recent pathogenetic and therapeutic advances

et al. 2020

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Takayasu arteritis (TAK) is a rare granulomatous vasculitis of unknown etiology that mainly affects the aorta and its major branches. The aim is to describe the clinical features, diagnostic procedures, pathogenesis, and management of TAK in a longitudinal cohort of patients recruited within a single region of southern Italy. The cohort included 43 patients who were diagnosed with TAK and followed up according to a standard protocol, in a collaboration between four university tertiary referral centers and a regional hospital. Clinical and imaging classification criteria were those established by the American College of Rheumatology. Thirty-five patients (81.4%) were female, and the mean age at disease onset was 32.6 (range 16–54) years. Angiographic assessment of the vascular involvement allowed disease classification in five different types. Clinical features ranged from constitutional symptoms in the early inflammatory stage of the disease to cardiovascular ischemic symptoms in the late, chronic stage. Noninvasive imaging techniques were employed to assess the extent and severity of the arterial wall damage and to monitor the clinical course and response to therapy. Medical treatment, based on pathogenetic insights into the roles of humoral and cell-mediated immune mechanisms, included glucocorticoids mostly combined with steroid-sparing immunosuppressive agents and, in patients with relapsing/refractory disease, biologic drugs. Significant clinical and angiographic differences have been detected in TAK patients from different geographic areas. Patients with life-threatening cardiovascular and neurologic manifestations as well as sight-threatening ophthalmologic signs and symptoms should be promptly diagnosed, properly treated, and closely followed up to avoid potentially severe consequences.

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Section: Introductionmentioning

confidence: 99%

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Takayasu arteritis: a cohort of Italian patients and recent pathogenetic and therapeutic advances

et al. 2020

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“…Thus, our patient developed a Takayasu disease associated with latent tuberculosis. To date, although studies show a high prevalence of TB in patients with TA, there is no evidence of a causal relationship between these 2 diseases [ 15 , 16 ]. Furthermore, the association tuberculosis and systemic disease has been rarely reported in the African literature despite the endemicity of tuberculosis in our region (high prevalence of tuberculosis in Gabon according to WHO) and the underlying systemic diseases [ 17 ].…”

Section: Discussionmentioning

confidence: 99%

Takayasu Arteritis Associated with Latent Tuberculosis Infection: A 39-Year-Old Woman Is the First Case in Gabon

et al. 2020

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“…Recent studies have con rmed that patients with TAK have a higher proportion of TB infection [10,11] . The M.TB antigen, HSP65, was identi ed in TAK artery tissue and the sites of increased HSP65 expression also displayed γ-δT cell in ltration, which suggested that HSP65 could be directly recognized by these cytotoxic cells [15,23] .…”

Section: Discussionmentioning

confidence: 99%

“…The prevalence of TAK is signi cantly higher in countries and regions where tuberculosis (TB) is prevalent. Moreover, several studies have explored the potential role of M.TB infection in the pathogenesis of TAK [9,10,11] . The 65 kDa heat shock protein (HSP65) is a small molecular antigen derived from M.TB, which has been reported to be associated with a variety of autoimmune diseases [12,13,14] , including TAK.…”

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confidence: 99%

Therapeutic value of curcumin on the initiation and development of inflammation in Takayasu’s arteritis mediated by HSP65-induced CCL2 overexpression

Wang

Kong

et al. 2020

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Background Takayasu’s arteritis (TAK) is a chronic inflammatory disease characterized by macrophage infiltration. During the active stage, aorta adventitial fibroblasts (AAFs) proliferate excessively and produce numerous pro-inflammatory factors in the adventitia, the primary target of TAK therapy. Although the monocyte chemokine, CCL2, may contribute to macrophage infiltration in TAK arteries, whether there is an associated relationship with HSP65 remains unknown. Moreover, there are no reports of the activation of AAFs to produce inflammatory factors involvement in TAK pathogenesis. TAK treatment is associated with several challenges and contradictions. Curcumin is a traditional Chinese medicine with anti-inflammatory effects; however, its effectiveness for TAK and the underlying mechanism remains unclear. Methods We first verified high HSP65 expression in the aortic adventitia of TAK patients by IHC. mRNA-seq was used to profile differentially expressed genes (DEGs) between AAFs stimulated by HSP65 with or without pretreatment with curcumin, and untreated AAFs. The key chemokine, CCL2, screened by mRNA-seq was detected in the adventitia of the TAK aorta, and its correlation with HSP65 expression was analyzed by double-labelled immunofluorescence. We subsequently explored how HSP65 affected the production of inflammatory factors by AAFs at a cellular level and the related signaling pathway. We explored whether curcumin could hinder this process and verified the effect of curcumin on the level of serum CCL2 in patients with TAK. Results HSP65 was highly expressed in the adventitia of TAK arteries. The DEG analysis showed a key role of CCL2. The expression of CCL2 in the adventitia of TAK arteries was significantly higher than that of healthy subjects, and was correlated with HSP65. HSP65 facilitated the production of CCL2, IL-6, and IL-1β by AAFs via activation of the TLR4-JAK2/AKT/STAT3 pathway, among which the change in CCL2 was the greatest. Curcumin treatment reversed HSP65-induced CCL2 upregulation in vitro, which was more obvious than that of MTX and tofacitinib. Finally, curcumin significantly downregulated the level of serum CCL2 in TAK patients. Conclusion HSP65 initiates and promotes TAK inflammation by upregulating CCL2 in AAFs through the JAK2/AKT/STAT3 pathway, whereas curcumin could reverse this process and slow the initiation and development of TAK.

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Association between Takayasu arteritis and latent or active Mycobacterium tuberculosis infection: a systematic review

Cited by 28 publications

References 40 publications

Takayasu arteritis: a cohort of Italian patients and recent pathogenetic and therapeutic advances

Takayasu arteritis: a cohort of Italian patients and recent pathogenetic and therapeutic advances

Takayasu Arteritis Associated with Latent Tuberculosis Infection: A 39-Year-Old Woman Is the First Case in Gabon

Therapeutic value of curcumin on the initiation and development of inflammation in Takayasu’s arteritis mediated by HSP65-induced CCL2 overexpression

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