Medical Health Encyclopedia

T cells can be further categorized as killer T-cells or helper T-cells. Killer T-cells directly attack antigens, such as viruses and tumor cells. Helper T-cells recognize antigens that are presented to them by special types of white blood cells (macrophages), and can stimulate B cells to mount various kinds of attacks on the antigen.

For reasons that are still not completely understood, both the T cells and B cells become overactive in lupus patients. In an immune response, it is normal for the antibody response to change over time, particularly if the first antibodies that are made do not eliminate the invading particles. Little by little, the types of antibodies being made undergo changes in an attempt to better recognize and fight an invader. In lupus, a complex interaction between activated immune cells and an impaired antigen-elimination process leads to a greater than normal range of what the antibodies recognize. Eventually, antibodies are made that recognize more of the body's own tissues in a stronger or more persistent manner than is healthy, and inflammatory responses are mounted in these tissues.

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Autoantibodies. In the majority of patients with SLE, antinuclear antibodies (ANA) are detectable. Important research published in 2003 found that such autoantibodies may be present in individuals up to 7 years prior to their developing symptoms of lupus. Some subtypes of ANA are found in lupus patients and only rarely in people without lupus. These include:

• Anti-ds DNA. An autoantibody called anti-double stranded DNA (anti-ds DNA) may play an important role in some lupus patients. A 2001 study suggested that some of these antibodies specifically recognize a protein in the kidney called alpha-actinin, which researchers suspect may also occur in other tissues that are affected by SLE, such as in the skin, joints, and brain. A subset of anti-DNA has also been found to target nerve-cell receptors in the brains of patients with SLE.
• Anti-Sm antibodies. This antibody is found most often in lupus patients of African descent and is almost never detected in people without lupus. Although it is not usually seen in lupus patients, it almost always indicates SLE when it is detected.