Among the many diseases that are classified as an immune complex disease, Systemic Lupus Erythematosus (SLE) is the most common and often the most severe. SLE is characterized by the presence of multiple immune complexes, such as autoimmune antibodies, in the patient’s immune system. This leads to tissue damage and inflammation. A number of therapeutic approaches have been developed to combat this problem, including vaccines, immunotherapy, and autoimmune therapy. However, there is still much that we do not know about this disease.


Several different microbial diseases can cause immune complex-mediated vasculitis. These include lupus vasculitis, hepatitis B vasculitis, cryoglobulinemic vasculitis, and serum sickness.

Several different experimental systems have been used to examine the pathogenesis of immune complex-mediated vasculitis. One of the most frequently used assays is the solid-phase C1q binding assay. These studies have provided an initial glimpse into the pathogenic role of circulating immune complexes.

The pathogenesis of immune complex-mediated vasculitis involves the activation of the humoral inflammatory mediator systems in the vessel wall. These systems act in concert with leukocyte recruitment. The inflammatory events involved are largely governed by cytokines, which are involved in modulating the activity of nuclear factor-kB. Activated leukocytes are recruited to the vessel wall. They release inflammatory cytokines that trigger the activation of neutrophils. The inflammatory responses are largely dependent on the type of vessel affected. Some vasculitis has been associated with autoantibodies directed against capillary basement membrane collagen.

Clinical manifestations

Historically, the term immune complex disease has been used to describe a number of autoimmune diseases. These disorders all involve the deposition of immune complexes in the body. These complexes are formed by the binding of antibodies with antigens. These complexes may form directly in tissues or they may form in circulation, depending on the nature of the antigen. The severity of symptoms depends on the number of immune complexes present and the location of these complexes.

The immune complexes are deposited in the tissues and may precipitate in the joints, blood vessels, skin, glomerular basement membrane, and the brain’s choroid plexus. These complexes can activate the classical pathway and contribute to tissue damage. They also activate the complement system, leading to the release of proinflammatory cytokines.

An immune complex deposition is associated with several infectious diseases. In the case of the hepatitis B virus, the infection is accompanied by immune complex deposition early in the course of the disease.


Whether or not an immune complex has an effect on a particular patient is unclear, but it is known that circulating immune complexes are associated with a range of diseases. It has been hypothesized that circulating immune complexes may be a sign of chronic infections, malignancies and superinfections. In addition, the presence of immune complexes may be indicative of the importance of active viremia in patients with HIV infection.

Immune complexes are produced in response to a range of stimuli including foreign antigens, complement deposition and phagocytes. The production of these complexes is facilitated by turbulent blood flow. Other mechanisms such as opsonization and transport to phagocytes are also involved.

It is likely that an immune complex containing a small number of molecules has a small effect on a person’s health, but the production of a large number of molecules is also not uncommon in some diseases. The detection of the smallest circulating immune complexes may have prognostic implications, but it may not be the most appropriate diagnostic strategy for every case.

Therapeutic approaches based on the immune complex model for the cause of tissue damage in SLE

Several therapeutic approaches have been developed based on the immune complex model for the cause of tissue damage in SLE. However, these have been relatively disappointing. In contrast, recent studies have improved our understanding of the etiopathogenesis of SLE and have provided insight into putative biomarkers for disease onset and disease progression. These studies also provide the basis for future therapeutic approaches.

Recent studies have also identified aberrant levels of soluble mediators of the adaptive immune system in patients with SLE. These include autoantibodies, which circulate in the body and contribute to tissue damage. Specifically, autoantibodies are formed when the immune system fails to recognize self-antigens. They then send signals to other cells to remove the threat.

In addition, a number of studies have suggested that aberrant levels of cytokines are associated with the onset of SLE. Cytokines are produced by various types of T cells. These cells include tolerogenic and immunogenic types. Among the tolerogenic types, CD4+ T cells produce anti-inflammatory cytokines while CD8+ T cells contribute to inflammation.

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