A new peak in the ALPS

Apoptotic caspases belong to the protease enzyme family and are known to play an essential role in inflammation and programmed cell death. Here is the latest research.

A new peak in the ALPS

Abstract

References

Mutations in Fas associated with human lymphoproliferative syndrome and autoimmunity

Dominant interfering Fas gene mutations impair apoptosis in a human autoimmune lymphoproliferative syndrome

Fas gene mutations in the Canale-Smith syndrome, an inherited lymphoproliferative disorder associated with autoimmunity

Death receptors: signaling and modulation

Caspases: enemies within

Germline mutations in the extracellular domains of the 55 kDa TNF receptor, TNFR1, define a family of dominantly inherited autoinflammatory syndromes

Inherited human Caspase 10 mutations underlie defective lymphocyte and dendritic cell apoptosis in autoimmune lymphoproliferative syndrome type II

Citations

Chronic cholestatic diseases

Apoptosis in hematological disorders

New advances in the diagnosis and treatment of autoimmune lymphoproliferative syndrome

Perforin-dependent apoptosis functionally compensates Fas deficiency in activation-induced cell death of human T lymphocytes

FAS-L, IL-10, and double-negative CD4- CD8- TCR alpha/beta+ T cells are reliable markers of autoimmune lymphoproliferative syndrome (ALPS) associated with FAS loss of function

Autoimmune lymphoproliferative syndrome

Monogenic defects in lymphocyte apoptosis

Familial hemophagocytic lymphohistiocytosis: too little cell death can seriously damage your health

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