We describe a Chinese American family with a hereditary syndrome consisting of retinopathy, nephropathy, and stroke, affecting 11 members spanning three generations. Ophthalmologic evaluations revealed macular edema with capillary dropout and perifoveal microangiopathic telangiectases. Several members had renal abnormalities with proteinuria and hematuria. Initial manifestations were visual impairment and renal dysfunction; neurologic deficits occurred in the third or fourth decade of life. Symptoms included migraine-like headache, psychiatric disturbance, dysarthria, hemiparesis, and apraxia. Neuroimaging consistently demonstrated contrast-enhancing subcortical lesions with surrounding edema. Ultrastructural studies showed distinctive multilaminated vascular basement membranes in the brain and in other tissues, including the kidney, stomach, appendix, omentum, and skin. Genetic analysis ruled out linkage to the CADASIL locus on chromosome 19. Distinct from CADASIL, hereditary endotheliopathy with retinopathy, nephropathy, and stroke (HERNS) is an autosomal dominant multi-infarct syndrome with systemic involvement.
In order to investigate the role of Th17 cytokines in the pathogenesis of psoriasis, reverse transcriptase-polymerase chain reaction (RT-PCR) was used to detect the expression of IL-17, IL-23 (p19/p40), and IL-6 in skin lesions and non-lesions of the patients with psoriasis and skin tissues of normal subjects. The results showed that the mRNA expression levels of IL-17, IL-23p19, IL-23p40 and IL-6 in psoriasis lesion were significantly higher than those of non-lesions (1.231 +/- 0.843 vs 1.003 +/- 0.044, 1.166 +/- 0.142 vs 0.765 +/- 0.133, 1.125 +/- 0.104 vs 0.730 +/- 0.103, 1.186 +/- 0.222 vs 0.976 +/- 0.122, respectively, all P < 0.05). Meanwhile, The expression levels of IL-17 mRNA, IL-23p19 mRNA, IL-23p40 mRNA and IL-6 mRNA were higher in non-lesions than those in normal skin tissues (1.003 +/- 0.044 vs 0.620 +/- 0.104, 0.765 +/- 0.133 vs 0.584 +/- 0.078, 0.730 +/- 0.103 vs 0.000 +/- 0.000, 0.976 +/- 0.122 vs 0.656 +/- 0.121, respectively, all P < 0.05). The overexpression of Th17 cytokines in the skin lesions of patients with psoriasis may indicate that Th17 cytokines play a very important role in the immunopathogenesis of psoriasis.
The lung is the primary site of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2)-induced immunopathology whereby the virus enters the host cells by binding to angiotensin-converting enzyme 2 (ACE2). Sophisticated regeneration and repair programs exist in the lungs to replenish injured cell populations.
This study examined the correlation of the expression of interleukin-36 (IL-36), a novel member of interleukin-1 (IL-1) family, with p38 mitogen-activated protein kinase (p38 MAPK) and nuclear factor-kappa B (NF-κB) pathways in psoriasis vulgaris skin lesions. The expression levels of IL-36α, IL-36β, IL-36Γ, phosphorylated p38 MAPK, and NF-κBp65 were detected in the skin tissues of 38 psoriasis patients and 17 healthy control subjects by real-time quantitative reverse transcription polymerase chain reaction (qRT-PCR) and Western blotting. The cytokine expression levels were compared between the psoriasis group and the control group. A correlation analysis between cytokine proteins was performed in the psoriasis group. Results showed that the expression levels of IL-36a, IL-36β, IL-36Γ, phosphorylated p38 MAPK and NF-κBp65 in the psoriasis group were significantly higher than those in the control group (P<0.001). In the psoriasis group, the IL-36 cytokine expression was positively correlated with phosphorylated p38 MAPK and NF-κBp65 expression (P<0.05). A significant positive correlation was also found between the phosphorylated p38 MAPK and NF-κBp65 expression (P<0.01). It was concluded that the increased IL-36 expression is correlated with p38 MAPK and NF-κB pathways in psoriasis vulgaris skin lesions. All the three factors may be jointly involved in the pathogenesis and local inflammatory response of psoriasis.
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