Question

How is immunity and Systemic lupus erythematosus related

Answer 1

Our immune system is an elaborate network of cells, tissues and organs that hepls to protect the body from invaders ( bacteria, viruses, fungal infections and parasites) .

Systemic lupus erythematosus ( SLE ) ia s severe , relapsing, remitting multisystem autoimmune disease. The name systemic lupus erythematosus implies that almost any organ or system with in the body might be affected and lupus is perhaps the classical multi symptom illness. Onset can occur at any age. Most typically present in young adult females.

The disease is charecterised by the production of 'self' ( auto) antibodies ( directed against nuclear self antigens) , inflammation and organ damage. The presence of antinuclear antibodies has been detected in the serum of a majority of patients before the onset of clinical disease symptoms and level of certain auto antibodies have been found to correlate with disease activity supporting a role for these antibodies in mediating disease pathology. It is thought that, these antibodies from antibody- nuclear antigen immune complexes, which deposit in tissues and trigger local inflammation , thereby contributing to tissue injury.

Increased apoptosis ( programmed cell death) and defective clearance of apoptotic material are charecteric of human SLE. Autoantigens typical of lupus cluster in surface blebs of apoptotic cells, increasing their immune exposure. Saturation of physiological processes to safely remove apoptotic debris amplifies autoantigen exposure.

NEUTROPHILS are the most abundant leukocyte in human blood and one of first immune subsets to respond to a microbial insult. Dysregulation in both their function and cell death has been reported in SLE. The Increased formation and decreased dismantling of neutrophil extracellular Traps ( NETs) is also thought to be a source of autoantigen exposure.

The innate immune system role in the development of SLE is supported by the observation that a majority of patients with SLE display an increased expression of type l interferon (lFN) - regulated genes. plasmacytoid dendritic cells ( pDC) are the main producers of type l IFNs in response to viral infections, in SLE , These cells are also induced to synthesize IFN via Troll like receptor ( TLR ) ligation by endogenous derived nucleic acids, a source of which may be Increased apoptosis and NETs. Type l IFN contributes to loss of tolerance and activation of autoreactive T and B cells with production of autoantibodies.

B LYMPHOCYTES are the cells of the immune system that make antibodies inappropriate activation and proliferation of autoreactive memory B cells in the periphery are also charecteric of SLE.

T LYMPHOCYTES are also thought to contribute to disease progression and pathology. T cells are reactive with several nuclear autoantigens have been isolated from peripheral blood of SLE patients. T-cells from SLE patients also display abnormal signalling and secrete cytokines that promote inflammation. Regulatory T cells have been shown to be low in SLE and their suppressive function impaired.

These all about relationships between immunity and systemic lupus erythematosus.