SS-A (Ro) and SS-B (LA) antibodies found in Sjogren syndrome are targeted against:
Ans: C (Ribonucleoproteins) Ref: Robbins and Cotran, 'Pathologic Basis of Disease 8th Edition, Elsevier, 2011. Page 221-3.Explanation:SJOGREN SYNDROMEIt is a immune-mediated destruction of the lacrimal and salivary glands characterized by dry eyes (keratoconjunctivitis sicca) and dry mouth (xerostomia), resulting from immune-mediated destruction of the lacrimal and salivary glands.It occurs as an isolated disorder (primary form), also known as the sicca syndrome, or more often in association with another autoimmune disease (secondary form).Associated with Rheumatoid Arthritis (Most common SLE. polymyositis, systemic sclerosis, vasculitis, or thyroiditis.The ductal epithelial cells of the exocrine glands are the primary target for auto- antibodies.There is also systemic B-cell hyperactivity, as evidenced by the presence of ANAs and RF (even in the absence of associated RA).Most patients with primary Sjogren syndrome have autoantibodies to the RNP antigens SS- A (Ro) and SS-B (La) (These are also present in SLE).Other secretory glands, including those in the nasopharynx, upper airway, and vagina, may also be involved.Involved tissue", show an intense lymphocyte (primarily activated CD4+ T cells) and plasmacell infiltrate.There is associated destruction of the native architecture.Lacrimal gland destruction results in a lack of tears, leading to drying of the corneal epithelium, with subsequent inflammation, erosion, and ulceration (keratoconjunctivitis sicca).Similar changes may occur in the oral mucosa as a result of loss of salivary gland output, giving rise to mucosal atrophy, with inflammatory Assuring and ulceration (xerostomia).Dryness and crusting of the nose may lead to ulcerations and even perforation of the nasal septum.When the respiratory passages are involved, secondary laryngitis, bronchitis, and pneumonitis may appear.Approximately 25% of the patients (especially those with anti-SS-A antibodies) develop extraglandular disease affecting the CNS. skin, kidneys and muscles.Renal lesions take the form of mild interstitial nephritis associated with tubular transport defects; unlike in SLE. glomerulonephritis is rare.Approximately 90% of Sjogren syndrome cases occur in women between the ages of 35 and 45 years.Extraglandular manifestations include synovitis, pulmonary fibrosis and peripheral neuropathy.Notably, there is a 40-fold increased risk of developing a non-Hodgkin B-cell lymphoma, arising in the setting of the initial robust polyclonal B-cell proliferation.
DNA topoisomerase 1
Histones
Ribonucleoproteins
Native DNA