When T cells cannot help.

摘要

Wiskott-Aldrich syndrome is caused by mutations in the WASP gene, which affects the function of most hematopoietic cells and leads to immunodeficiency, In this issue of Blood, Morales-Tirade and colleagues show that T helper cells lacking WASp have a selective deficiency in their memory response. The Wiskott-Aldrich syndrome protein (WASp) is a crucial regulator of actin polymerization. Its gene is located on the X chromosome and when mutated, it leads to thrombocytopenia, immunodeficiency, and eczema. WASp is expressed in hematopoietic cells and in its absence, migration, adhesion, activation, and antigen uptake malfunction. It has previously been shown that WASp plays a role in T-cell activation, being important for the regulation of the so-called immunologic synapse. This membrane structure, crucial for activation of T cells, is formed between T cells and antigen-presenting cells and is composed of clusters of T-cell receptor, adhesion molecules, and signaling molecules. It has also been suggested that WASp can regulate transcriptional activation in T cells independent of its role in actin polymerization.