Function:
Phospholipids are a class of lipids that are a major component of all cell membranes. They play a role in the formation of lipid bilayers. Most phospholipids contain a diglyceride, a phosphate group, and a simple organic molecule such as choline.
Antibodies Appear:
- Antiphospholipid Syndrome[1, 4]
- NIDDM [7]
- Systemic Lupus Erythematosus [3, 6]
Known Cross-Reactions:
- Anti-ribosomal P protein antibodies [1]
- DNA [2]
- Cardiolipin [2]
Clinical Significance:
Antibodies against phospholipids may have an important role in mediating platelet destruction in autoimmune disorders. Anti-phospholipid antibodies (anti-PL) have been shown to bind to the membrane of activated platelets; thus it has been postulated that this may result in increased destruction of platelets by the reticuloendothelial system. [3]
Anti-PL have been demonstrated in patients with autoimmune thrombocytopenia (AITP) and Systemic lupus erythematosus (SLE). [3]
Anti-PL are directed against a diverse group of phospholipids and phospholipid-binding proteins; among these, anti-cardiolipin (anti-CL), anti-beta-2-glycoprotein I (b2-GP-I) and anti-prothrombin antibodies seem to be the most relevant from the clinical viewpoint. [1]
Anti-PL have been found in moderate and severe noninsulin-dependent diabetes mellitus patients, and thus may suggest that autoimmune nerve destruction may be involved in diabetic neuropathy in NIDDM patients. [7]
Anti-phospholipid antibody syndrome may appear as a stand-alone syndrome or associated with major connective tissue disease such as SLE and may manifest in a number of neurological conditions. [1]
Widespread thrombosis and infarction of placentas obtained from women with antiphospholipid syndrome (APS) was actually reported both in first and second trimester abortions. [4] There is evidence from in vitro studies that anti-PL may induce pro-coagulant state at the placental level, thus playing a pathogenic role of thrombotic events in anti-PL-associated pregnancy. [4]
It can be concluded that impaired endothelial fibrinolysis is a potential prothrombotic mechanism in subjects with antiphospholipid antibodies. [5]
References:
1. Caponi, et al. Antibodies directed against ribosomal P proteins cross-react with phospholipids. Clin exp Immunol, 2007; 150:140–143.
2. Koike, et al. Antibodies cross-reactive with DNA and cardiolipin in patients with systemic lupus erythematosus. Clin exp Immunol, 1982; 50:298-302.
3. Lipp, et al. Antibodies against platelet glycoproteins and antiphospholipid antibodies in autoimmune thrombocytopenia. Eur J Haemotol, 1998; 60:283-288.
4. Meroni, et al. Anti-phospholipid antibody mediated fetal loss: still an open question from a pathogenic point of view. Lupus, 2010; 19:453-456.
5. Patterson, et al. The influence of anti-endothelial/antiphospholipid antibodies on fibrin formation and lysis on endothelial cells. Br J Haematol, 2006; 133:323–330.
6. Petri. Update on anti-phospholipid antibodies in SLE: the Hopkins’ Lupus Cohort. Lupus, 2010; 19:419-423.
7. Shigeta, et al. Serum Autoantibodies Against Sulfatide and Phospholipid in NIDDM Patients With Diabetic Neuropathy. Diabetes Care, 1997; 20(12): 1896-1899.
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Antibodies against phospholipids may have an important role in mediating platelet destruction in autoimmune disorders. Anti-phospholipid antibodies (anti-PL) have been shown to bind to the membrane of activated platelets; thus it has been postulated that this may result in increased destruction of platelets by the reticuloendothelial system. [3]
Anti-PL have been demonstrated in patients with autoimmune thrombocytopenia (AITP) and Systemic lupus erythematosus (SLE). [3]
Anti-PL are directed against a diverse group of phospholipids and phospholipid-binding proteins; among these, anti-cardiolipin (anti-CL), anti-beta-2-glycoprotein I (b2-GP-I) and anti-prothrombin antibodies seem to be the most relevant from the clinical viewpoint. [1]
Anti-PL have been found in moderate and severe noninsulin-dependent diabetes mellitus patients, and thus may suggest that autoimmune nerve destruction may be involved in diabetic neuropathy in NIDDM patients. [7]
Anti-phospholipid antibody syndrome may appear as a stand-alone syndrome or associated with major connective tissue disease such as SLE and may manifest in a number of neurological conditions. [1]
Widespread thrombosis and infarction of placentas obtained from women with antiphospholipid syndrome (APS) was actually reported both in first and second trimester abortions. [4] There is evidence from in vitro studies that anti-PL may induce pro-coagulant state at the placental level, thus playing a pathogenic role of thrombotic events in anti-PL-associated pregnancy. [4]
It can be concluded that impaired endothelial fibrinolysis is a potential prothrombotic mechanism in subjects with antiphospholipid antibodies. [5]
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21-Hydroxylase (Adrenal Cortex), Alpha + Beta Tubulin IgG+IgA, Alpha + Beta Tubulin IgM, Alpha-Myosin, Arthritic Peptide, ASCA + ANCA, Asialoganglioside IgG+IgA, Asialoganglioside IgM, Cerebellar IgG+IgA, Cerebellar IgM, Collagen Complex, Cytochrome P450 (Hepatocyte), Fibulin, Glutamic Acid Decarboxylase 65 (GAD 65), Glutamic Acid Decarboxylase Autoantibody, IA-2 Autoantibody, Insulin + Islet Cell Antigen, Intrinsic Factor, Myelin Basic Protein IgG + IgA, Myelin Basic Protein IgM, Myocardial Peptide, Osteocyte, Ovary/Testis, Parietal Cell + ATPase, Phospholipid, Platelet Glycoprotein, Synapsin IgG+IgA, Synapsin IgM, Thyroglobulin, Thyroglobulin IgG, Thyroid Peroxidase (TPO), Thyroid Peroxidase IgG, Tropomyosin