A common form of dominant human IFNAR1 deficiency impairs IFN-α and -ω but not IFN-β-dependent immunity.

Autosomal recessive deficiency of the IFNAR1 or IFNAR2 chain of the human type I IFN receptor abolishes cellular responses to IFN-α, -β, and -ω, underlies severe viral diseases, and is globally very rare, except for IFNAR1 and IFNAR2 deficiency in Western Polynesia and the Arctic, respectively. We report 11 human IFNAR1 alleles, the products of which impair but do not abolish responses to IFN-α and -ω without affecting responses to IFN-β. Ten of these alleles are rare in all populations studied, but the remaining allele (P335del) is common in Southern China (minor allele frequency ≈2%).

Inhibiting DNA Sensing Pathway Controls Steroid Hyporesponsive Lung Inflammation.

DNA damage underlies the progression of asthma toward a severe, steroid hyporesponsive phenotype. The accumulation of double-stranded DNA within the cytosol triggers the activation of cytosolic DNA-sensing pathways, notably the Stimulator of Interferon Genes (STING) pathway. However, the precise role of STING in driving steroid hyporesponsiveness remains elusive and warrants further investigation.

Nirmatrelvir plus ritonavir reduces COVID-19 hospitalization and prevents long COVID in adult outpatients.

Nirmatrelvir plus ritonavir received Emergency Use Authorization for treating mild to moderate COVID-19 in high-risk patients. Its efficacy against the Omicron variant of SARS-CoV-2 remains uncertain. This retrospective cohort study assessed the effect of nirmatrelvir-ritonavir in preventing severe disease progression and long COVID symptoms after acute COVID-19 in non-hospitalized adults.

Elizabethkingia meningoseptica in Dubai, United Arab Emirates: A 7-year multicenter study.

Background: Elizabethkingia meningoseptica (E. meningoseptica) is a gram-negative bacillus. Widely distributed in nature, it poses a significant threat as a nosocomial pathogen, particularly affecting immunocompromised neonates and the elderly.

Calprotectin is regulated by IL-17A and induces steroid hyporesponsiveness in asthma.

Background: Calprotectin, a calcium-binding protein, plays a crucial role in inflammation and has been associated with various inflammatory diseases, including asthma. However, its regulation and impact on steroid hyporesponsiveness, especially in severe asthma, remain poorly understood.

Methods: This study investigated the regulation of calprotectin proteins (S100A8 and S100A9) by IL-17 and its role in steroid hyporesponsiveness using in vitro and in vivo models.