JAKs inhibitors were widely applied in the treatment of immunodeficiency diseases, inflammation and cancers.
Therefore immunodeficiency and chronic inflammation are proposed to be major risk factors, besides smoking, involved in the lung cancer pathogenesis.
Although the cause of this disorder has not been definitely established, chronic low-grade inflammation, immunodeficiency state and autoimmunity are the proposed pathogenetic mechanisms.
Inflammation, immunodeficiency, peripheral neuropathy and ischemia from peripheral vascular disease, and subsequent infection are underlying factors that contribute to unhealed chronic wounds in diabetic foot ulcers [ 8].
Although the cause of CD is unknown; chronic low-grade inflammation, immunodeficiency state and autoimmunity have been proposed as likely pathogenic mechanisms Numerous autoimmune diseases are associated with CD including Sjögren syndrome and rheumatoid arthritis.
We were unable to garner any evidence on immunodeficiency or auto-inflammation in the three probands from two families in our study, although they both have clear signs of amylopectinosis (glycogen storage disease type IV), which was the very reason they were referred to us.
Cuchet-Lourenco, D. et al. Biallelic RIPK1 mutations in humans cause severe immunodeficiency, arthritis, and intestinal inflammation.
However, the same mechanisms can backfire upon immune evasion of invading pathogens or under physiological stress and instead result in severe disorders, such as immunodeficiency, chronic infection and inflammation, autoimmune diseases, allergy, degenerative diseases, and cancer.
Increased vulnerability among the populations in healthcare institutions is likely to be multifactorial and may include the following: nutritional status, immunodeficiency or senescence, chronic inflammation, and microbiome alterations.
Patients with mutations in HOIL1 (RBCK1) present with amylopectinosis-associated myopathy with or without hyper-inflammation and immunodeficiency.
DOI: http://dx.doi.org/10.7554/eLife.04494.005 The ability of HOIL-1 KO mice to effectively control chronic herpesvirus infection allowed us to test the hypothesis that persistent virus infection might alter two phenotypes, hyper-inflammation and immunodeficiency, in which HOIL-1 KO mice appear to differ from some reported patients with bi-allelic mutations in RBCK1 (HOIL1) (Boisson et al., 2012).
