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Mucosa-associated lymphoid tissue (MALT) lymphoma of the larynx is a rare but well-documented entity which may arise from chronic inflammatory process. Supraglottic left regions are predominant due to unknown reason.We present the case of a 62-year-old man with a dry cough, stridor and developing exertional dyspnea. This subglottic almost circumferential MALT lymphoma showed a temporary distinct disappearance after cortisone administration during the diagnostic process. Bronchoscopy confirmed the diagnosis of a primary MALT lymphoma of the larynx. The patient received chemotherapy according to CHOP scheme plus rituximab. A reliable post-treatment care period of 15 months showed no sign of recurrence.MALT lymphoma of the larynx are believed to arise from preexisting or acquired lymphoid tissue of the upper airway. Acquired lymphoid tissue is documented in the supraglottic region and may be associated with a chronic inflammatory process. However, in subglottic cases it is unclear whether the chronic inflammation arises from a local or systemic process.

Acute glomerulonephritis can lead to chronic glomerulonephritis or resolve without permanent damage to the kidneys. Differential gene expression was studied in a model of acute and chronic glomerulonephritis to identify factors influencing the course of glomerulonephritis towards healing or chronification. One of the differentially expressed genes was identified as SCL, encoding selenocysteine lyase. Its expression was higher in acute glomerulonephritis and lower in chronic glomerulonephritis. The transcriptional regulation of SCL was studied in vitro in rat mesangial cells (MC). SCL RNA expression increased eight-fold compared to the baseline after stimulation with interleukin-1β (IL-1β) for three hours. Luciferase expression and gel shift experiments revealed an enhancer element between bp −152 and −298 of the SCL 5’-regulatory region, with protein binding to an AP-1 binding site that may be involved in the regulation of SCL-RNA in vivo in an endogenous feedback mechanism to the inflammatory reaction in acute glomerulonephritis, leading to resolution of this disease.