Examination of immunological changes in transgender individuals undergoing gender-affirming testosterone treatment reveals sex hormone-regulated pathways in humans and explains sex-divergent responses...

The risk of life-threatening COVID-19 pneumonia increases sharply after 65 years of age, but other epidemiological risk factors, genetic or otherwise, are modest. Various rare monogenic inborn errors ...

During the 1999 West Nile virus outbreak, thousands of symptomless and symptomatic West Nile viral infections probably occurred, with fewer than 1% resulting in severe neurological disease.

Gervais et al. show that auto-Abs neutralizing type I IFNs and pre-existing infection underlie ∼40% of cases of West Nile virus (WNV) encephalitis. Blood a

COVID Human Genetic Effort is an international consortium aiming to discover inborn errors of immunity underlying severe forms of COVID-19 in previously healthy individuals

In 13 cohorts of individuals with WNV infection, the risk of WNV encephalitis is increased 20 to >>2,000 times by circulating auto-Abs neutralizing t

In 13 cohorts of individuals with WNV infection, the risk of WNV encephalitis is increased 20 to >>2,000 times by circulating auto-Abs neutralizing t

Here, Jensen and colleagues studied type I interferon (IFN-I) neutralizing autoAbs in people with HIV, and found that the prevalence does not significantly

Fulminant viral hepatitis (FVH) is a devastating condition caused by hepatotropic viruses. In 149 international FVH patients, auto-Abs neutralizing type I

Kilic et al. reported a child with a homozygous TBK1 mutation previously linked to autoinflammation, suggesting its role in recurrent severe viral infectio

USIDNET is a suite of resources for clinical immunologists. The registry of patient data utilizes data extraction from electronic health records to minimiz

A novel mutation in ORAI1 results in constitutive CRAC channel activation while abolishing stimulation-induced channel opening. The mutation is associated

We report the same ultra-rare pathogenic noncoding single-nucleotide variant in the promoter of WAS in four male patients from two unrelated kindreds with