Role of Regulatory T Cells and Inhibitory Molecules in the Development of Immune Exhaustion During Human Immunodeficiency Virus Type 1 Infection.
Medellín, Colombia. In Viral Immunol, Jan 2016
One of the key hallmarks of chronic human immunodeficiency virus type 1 (HIV-1) infection is the persistent immune activation triggered since early stages of the infection, followed by the development of an exhaustion phenomena, which leads to the inability of immune cells to respond appropriately to the virus and other pathogens, constituting the acquired immunodeficiency syndrome (AIDS); this exhausting state is characterized by a loss of effector functions of immune cells such as proliferation, production of cytokine, as well as cytotoxic potential and it has been attributable to an increased response of regulatory T cells and recently also to the expression in different cell populations of inhibitory molecules, such as programmed death receptor-1 (PD-1), cytotoxic T lymphocyte antigen-4 (CTLA-4), T cell immunoglobulin-3 (Tim-3), and lymphocyte activation gene-3 (LAG-3).
[Progress of molecular genetics research on rheumatoid arthritis].
Nanchong, China. In Zhonghua Yi Xue Yi Chuan Xue Za Zhi, Oct 2015
In addition to genes from human leukocyte antigen (HLA) region, such as HLA-DRB, genes from non-HLA region, such as TIM-3, PTPN22, TRAF1/C5, STAT4, CCR5, PADI4 and FCGR2A may also contribute to its susceptibility.
CEACAM1 regulates TIM-3-mediated tolerance and exhaustion.
Boston, United States. In Nature, Feb 2015
T-cell immunoglobulin domain and mucin domain-3 (TIM-3, also known as HAVCR2) is an activation-induced inhibitory molecule involved in tolerance and shown to induce T-cell exhaustion in chronic viral infection and cancers.
Protective HIV-specific CD8+ T cells evade Treg cell suppression.
Seattle, United States. In Nat Med, 2011
This differential sensitivity of HIV-specific CD8(+) T cells to T(reg) cell-mediated suppression correlates with their expression of the inhibitory receptor T cell immunoglobulin domain and mucin domain 3 (Tim-3) after stimulation with their cognate epitopes.