CD134 expression on CD4+ T cells is associated with nephritis and disease activity in patients with systemic lupus erythematosus, Clinical and Experimental Immunology, Volume 145, Number 2, August 2006, Pages 235-242(8), S. Patschan,S. Dolff, A. Kribben, et. al.

The immune system is triggered to promote inflammation by a complicated series of signals that pass between and among the various types of white blood cells. When white blood cells signal to each other with multiple signals at the same time, the proteins that are involved in these signals are called co-stimulation proteins. Co-stimulation signals are involved in the activation of T-cells. One co-stimulation protein, CD134, may be a marker for lupus kidney disease.
T-cells, a group of white blood cells, are involved in stimulating and suppressing the immune response. The proteins on the surface of T cells help to distinguish the different types of T cells that perform various tasks. T-cells that have a protein named CD4 on their surface promote the immune response, helping the immune system to recognize foreign substances that enter the body, and targeting them for destruction.

When CD4 T cells interact with another kind of white blood cell called the B cells, the B cells may be induced to stimulate the production of disease-fighting proteins called antibodies. Too many antibodies of the type that can cause inflammation in the organs of a person’s own body are a hallmark of lupus.

T cells and B cells trigger antibody production by interacting in complicated ways using co-stimulatory proteins that interlock with each other, almost as if two centipedes were shaking hands. Some of these co-stimulatory signals have been associated with autoimmune diseases, including lupus. In some cases there may be a reduced threshold for T-cell activation after triggering by co-stimulatory interactions.

In this study, a German research group looked at a number of co-stimulatory markers on CD4 T-cells in blood samples obtained from 28 patients with lupus and 11 healthy individuals. Of the 28 lupus patients, 11 had kidney inflammation, the other 17 did not. The study found increased co-stimulatory proteins called CD80, CD86, and CD134 on CD4 T-cells of patients with kidney involvement and also in those with increased overall disease activity.
The researchers suggested that increased co-stimulatory molecules such as CD134 might cause increased production of antibodies that have the potential to target kidney cells. Another possibility is that a co-stimulatory molecule on a white blood cell might interact directly with kidney cells leading to an inflammatory response. Increased CD80 or CD86 might cause enhancement of one white blood cell in the absence of signals from another.
Some early clinical trials have been performed with treatments that can block interactions between some of the co-stimulatory molecules. With this study, the researchers may have identified new strategic approaches to achieving this end. However, the potential for this kind of treatment to ameliorate lupus remains to be proven