The change of Th17/Treg cells and IL-10/IL-17 in Chinese children with Henoch–Schonlein purpura

Li, Bowen; Ren, Qian; Ling, Jizu; Tao, Zhongbin; Xiong, Yijun; Li, Yuning

doi:10.1097/md.0000000000013991

Cited by 10 publications

(9 citation statements)

References 37 publications

(37 reference statements)

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“…Although this patient did not show symptoms of tuberculosis at first, the CT scan, PPD test, and IGRAs provided deterministic evidence for our conjecture. Multiple studies suggesting that[ 20 21 22 23 24 25 26 27 28 29 30 31 32 ] the pathogenetic mechanisms of tuberculosis infection could lead to vascular damage through inflammatory mediators further support our diagnosis. However, the pathophysiology of this rare disease is still poorly understood.…”

Section: Discussionmentioning

confidence: 88%

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Pulmonary tuberculosis presenting as henoch–schönlein purpura

Wang

et al. 2020

Medicine

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Introduction: Henoch–Schönlein purpura (HSP) is an extremely rare condition in patients with pulmonary tuberculosis, with only a few reported cases. Compared to patients with typical clinical symptoms, it is difficult to make a definitive diagnosis when HSP presents as an initial manifestation in pulmonary tuberculosis patients. Herein, a case of pulmonary tuberculosis that showed HSP at first was reported, and the related literatures were reviewed. Patient Concerns: A 24-year-old man presented with palpable purpura on the extremities, accompanied by abdominal pain, bloody stools, and knee pain. Diagnoses: The patient was diagnosed with pulmonary tuberculosis based on the results of interferon gamma release assays, purified protein derivative test, and computed tomography. Interventions: The patient was treated with vitamin C and chlorpheniramine for 2 weeks, and the above-mentioned symptoms were relieved. However, 3 weeks later, the purpura recurred with high-grade fever and chest pain during the inspiratory phase. The patient was then treated with anti-tuberculosis drugs, and the purpura as well as the high fever disappeared. Outcomes: The patient recovered well and remained free of symptoms during the follow-up examination. Conclusion: Pulmonary tuberculosis presenting with HSP as an initial manifestation is not common. Therefore, it is difficult to clinically diagnose and treat this disease. When an adult patient shows HSP, it is important to consider the possibility of tuberculosis to avoid misdiagnosis and delayed treatment.

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Section: Discussionmentioning

confidence: 88%

“… [29] IL-10/IL-17 and Th17/Treg cells also play important roles in the pathogenesis of childhood HSP. [ 30 31 32 ] To summarize, these theories further suggest that tuberculosis might be an aggravating factor for HSP.…”

Section: Discussionmentioning

confidence: 99%

Pulmonary tuberculosis presenting as henoch–schönlein purpura

Wang

et al. 2020

Medicine

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“…Since the importance of the different cytokines in the development of autoimmune diseases, it has been proposed that the relationship established between them may indicate a trend in the development of the pathology, the relationship between IL-10 and IL-17A would indicate a limitation in the inflammatory phenomenon [39]. At the same time, the ratio of IL-23 and IL-17A would show the possibility of increased inflammation [28,40]. In order to explore these relationships, both balances were evaluated (Figure 3).…”

Section: Discussionmentioning

confidence: 99%

Anti-Aminoacyl Transfer-RNA-Synthetases (Anti-tRNA) Autoantibodies Associated with Interstitial Lung Disease: Pulmonary Disease Progression has a Persistent Elevation of the Th17 Cytokine Profile

Ramos-Martı́nez

Falfán-Valencia

Pérez-Rubio

et al. 2020

JCM

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Anti-tRNA autoantibodies are associated with interstitial lung disease (ILD), in at least two clinical scenarios: the anti-synthetase syndrome (ASSD) and interstitial pneumonia with autoimmune features (IPAF). Under pathological conditions, cytokines indicate the participating elements and the course of inflammatory phenomena. We aimed to quantify serum concentrations of different inflammatory cytokines profiles in patients with anti-tRNA associated ILD (anti-tRNA-ILD) and estimate the association between these and ILD improvement and progression. Serum levels of 18 cytokines from baseline and after six months of treatment of ILD patients’ positives to anti-tRNA were included in the current study. At six months, patients were classified as with or without ILD progression. A total of 39 patients were included (10 anti-Jo1, eight anti-PL7, 11 anti-PL12, and 10 anti-Ej). Three patients (7.6%) had ILD progression (progressors patients, PP) and showed statistically higher levels in IL-4, IL-10, IL-17A, IL-22, GM-CSF, IL-1β, IL-6, IL-12, IL-18, and TNF-α, compared to patients without disease progression (no progressors patients, NPP). IL-17A, IL-1β, and IL-6 (T-helper-lymphocyte (Th)17 inflammatory cytokine profile) were elevated and had a high discriminatory capacity in distinguishing ILD PP of those NPP at follow-up. Overall, there is an association between the cytokines of the Th17 inflammatory profile and the ASSD progression.

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“…Target organs include skin, kidneys, gastrointestinal tract, and joints. Like most systemic vasculitides, HSP patients have lower numbers and weak suppressive function of Treg cells (126)(127)(128)(129). As a reflection of a shift in the balance between proinflammatory effector T cells and suppressive Treg cells, the Th17/Treg ratio has been positively correlated with the erythrocyte sedimentation rate, kidney lesions, and multiorgan involvement (126).…”

Section: Henoch-schoenlein Purpura (Iga Vasculitis)mentioning

confidence: 99%

Regulatory T Cells in Autoimmune Vasculitis

et al. 2022

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Blood vessels are indispensable for host survival and are protected from inappropriate inflammation by immune privilege. This protection is lost in patients with autoimmune vasculitides, a heterogeneous group of diseases causing damage to arteries, arterioles, and capillaries. Vasculitis leads to vascular wall destruction and/or luminal occlusion, resulting in hemorrhage and tissue ischemia. Failure in the quantity and quality of immunosuppressive regulatory T cells (Treg) has been implicated in the breakdown of the vascular immune privilege. Emerging data suggest that Treg deficiencies are disease-specific, affecting distinct pathways in distinct vasculitides. Mechanistic studies have identified faulty CD8+ Tregs in Giant Cell Arteritis (GCA), a vasculitis of the aorta and the large aortic branch vessels. Specifically, aberrant signaling through the NOTCH4 receptor expressed on CD8+ Treg cells leads to rerouting of intracellular vesicle trafficking and failure in the release of immunosuppressive exosomes, ultimately boosting inflammatory attack to medium and large arteries. In Kawasaki’s disease, a medium vessel vasculitis targeting the coronary arteries, aberrant expression of miR-155 and dysregulated STAT5 signaling have been implicated in undermining CD4+ Treg function. Explorations of mechanisms leading to insufficient immunosuppression and uncontrolled vascular inflammation hold the promise to discover novel therapeutic interventions that could potentially restore the immune privilege of blood vessels and pave the way for urgently needed innovations in vasculitis management.

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The change of Th17/Treg cells and IL-10/IL-17 in Chinese children with Henoch–Schonlein purpura

Cited by 10 publications

References 37 publications

Pulmonary tuberculosis presenting as henoch–schönlein purpura

Pulmonary tuberculosis presenting as henoch–schönlein purpura

Anti-Aminoacyl Transfer-RNA-Synthetases (Anti-tRNA) Autoantibodies Associated with Interstitial Lung Disease: Pulmonary Disease Progression has a Persistent Elevation of the Th17 Cytokine Profile

Regulatory T Cells in Autoimmune Vasculitis

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