Medical Health Encyclopedia

Other autoantibodies found in lupus patients include:

• Anti-Ro (SSA) and Anti-La (SSB). These autoantibodies may be involved in the sun-sensitive rashes sensitivity experienced by patients with SLE and are also found in association with neonatal lupus syndrome, in which a pregnant mothers' antibodies cross the placenta and cause inflammation in the developing child's skin or heart.
• Antiphospholipid antibodies. A quarter to a half of patients with SLE may have these antibodies. They attack blood clotting regulator proteins which stick to phospholipids, fatty compounds found in cell membranes throughout the body. Antiphospholipid antibodies increase the risks for blood clots and may be responsible for narrowing of and irregularities in blood vessels. Antiphospholipid antibodies are linked with miscarriages and other pregnancy complications, strokes, heart attacks and blood clots in almost any part of the body, including kidneys, legs, lungs, and eyes.

Cytokines. Most immune cells secrete or stimulate the production of powerful immune factors called cytokines. In small amounts, cytokines are indispensable for maintaining the balance of the body during immune responses, infections, injuries, tissue repair, blood clotting, clearing of debris from inflamed blood vessels, and other aspects of healing. If overproduced, however, they can cause serious damage, including dangerous levels of inflammation and cellular injury. Specific cytokines called interferons and interleukins play a critical role in SLE by regulating the secretion of autoantibodies by B cells. Researchers are currently interested in interferon alpha; some evidence suggests high levels of this cytokine may underlie the autoimmune response in SLE.

Text Continues Below

---

Complement. Another immune factor of high interest in SLE is the complement system. This is comprised of more than 30 proteins and is important for defending and regulating the immune response. Inherited deficiencies in certain complement components (C1q, C1r, C1s, C4, and C2) have long been associated with SLE. Deficiencies may contribute to SLE in the following manner:

• The complement system may protect against autoimmune disease by normalizing apoptosis, the natural process by which cells self-destruct. This self-destruction process is an important part of the normal way in which the body cleans out damaged or no longer useful cells. In healthy people, autoantibodies may also play a role in regulating apoptosis so that dangerous antigens are not left in the bloodstream long enough to trigger a more global (dysregulated) immune response.
• Complement components are also necessary for clearing molecular rubble called immune complexes. These are the end product of the battle between autoantibodies and antigens. In the absence of complement, this debris accumulates and is deposited in the kidneys, blood vessels, joints, and other sites where it can cause the immune system to produce inflammation and tissue damage.

Genetic Defects