Among the many genes that increase the risk of autoimmune conditions, the risk allele encoding the W620 variant of protein tyrosine phosphatase N22 (PTPN22) is shared between multiple rheumatic diseases, suggesting that it plays a fundamental role in the development of immune dysfunction.
Polymorphisms of the cluster of differentiation 40 (CD40) gene have recently been identified to be associated with the risk to several immune diseases.
CD4+CD25+ T regulatory cells (Tregs) play an important role in regulating immune responses, and in influencing human immune diseases such as HIV infection.
Confirmation of the roles of CTLA4 and PTPN22 as general immune function modulators with a nonlinear dose-response effect on autoimmunity, and confirmation of the role of IL2RA, which may act via a regulatory T cell subset on immune disease risk.
Confirmation of the roles of CTLA4 and PTPN22 as general immune function modulators with a nonlinear dose-response effect on autoimmunity, and confirmation of the role of IL2RA, which may act via a regulatory T cell subset on immune disease risk.
Although TNIP1 and the TNF-α/NF-κB axis play key roles in immune diseases and inflammatory responses, their relationship and role in glioma remain unknown.
Although several genetic associations have been identified between CCR6 polymorphisms and immune system disorders (e.g., rheumatoid arthritis and Crohn's disease), the pharmacological effects of naturally occurring missense mutations in this receptor have yet to be characterized.
Recent investigations show that the CTLA4, CD28, and ICOS genes are located on chromosome 2q33 and their polymorphisms confer susceptibility to infectious and immune diseases through deregulation of T-cell stimulation.
Further study will be of interest to test whether CCR3-C218S variation or any of the CCR4 variations has a significant role in rendering susceptibility to immunological diseases or resistance to HIV infection.