Important Autoimmune Disease | Immunology Notes and MCQs

 Important Autoimmune Disease

Type of Immune Response	Autoimmune Disease	Target of the Immune response
Antibody to receptors	Myasthenia gravis	Acetylcholine receptor
	Graves’s disease	TSH receptor
	Insulin resistant diabetes	Insulin receptor
	Lambert Eaton myasthenia	Calcium channel receptor
Antibody to cell components other than receptors	Sysytemic lupus erythematosus	ds DNA, histones
	Rheumatoid arthritis	IgG in Joints
	Rheumatic fever	Heart and Joint tissue
	Hemolytic anemia	RBC membrane
	Idiopathic thrombocytopenic	Platelet membranes
	Goodpastures’s syndrome	Basement membrane of Kidney and lung
	Pernicious anemia	Intrinsic factor and Parietal cells
	Hashimoto’s thyroiditis	Thyroglobulin
	Insulin independent diabetes mellitus	Islet cells
	Addison’s disease	Adrenal cortex
	Acute glomerulonephritis	Glomerular basement membrane
	Periarteritis nodosa	Small and medium sized arteries
	Guillain Barre syndrome	Myelin protein
Cell mediated (T cells and macrophages)	Allergic encephalomyelitis	Reaction to myelin protein causes brain demyelination

Hashimoto's thyroiditis: This disease frequently affects middle aged women due to production of autoantibodies due to sensitized TDTH cells specific for thyroid antigens. DTH response results in severe inflammatory reactions where the thyroid gland is infliltrated by lymphocytes, macrophages and plasma cells leading to the formation of lymphocytic follicles and germinal centers. As a result of inflammation, thyroid develops goiter. Autoantibodies are also produced against thyroid globulin and thyroid peroxidase,  both of which re involved in the uptake of iodine. Binding of autoantibodies to these protein products of thyroid severely impairs  iodine uptake resulting in hypothyroidism. 

Myasthenia gravis: The autoimmune disease is produced by antagonistic antibodies, which bring about negative reaction by blocking the receptor of a neurotransmitter that is acetylcholine. Acetylcholine receptors are abundant on skeletal muscles, and autoantibodies on binding to these receptors inhibit muscle action. Prolonged exposure of receptors to autoantibodies lead to complement mediated degradation of receptors, resulting in progressive weakening of skeletal muscle response. 

Rheumatoid Arthritis (RA): It is a systematic autoimmune disease most common among women and affects them between 40 to 60 years of age. Most common symptom is inflammation of joints and painful joints accompanied by other symptoms like cardiovascular, Hematologic, and respiratory system. Affected individuals produce autoantibodies called rheumatoid factors that are reactive in the Fc region of IgG. A classic rheumatoid factor is IgM antibody, which reacts with IgG to form IgM-IgG complex and deposits in the joints . These complexes activate complement reaction leading to Type III hypersensitivity reaction and chronic inflammation of the joints. 

In rheumatic fever, Group A Streptococci infection proceeds and protective antibodies are being generated . Normally these antibodies attack on Streptococcal antigen, but these antibodies "cross react" with heart muscle antigen against leading to damage and Rheumatic Fever

Asthma: It is conditional and paroxysmal difficulty in breathing with wheezing or whistling sound produced during respiration due to obstruction of smaller bronchioles. In some cases, air born or blood born allergen such as pollen, dust, fumes, insect product or viral antigen trigger an asthmatic attack (allergic asthma) in other case an asthmatic attack can be induced by exercise or cold, apparently independently of allergen stimulation (intrinsic asthma). Like hay fever, asthma is also triggered by degranulation of mast cell, which release the mediators in the lower respiratory tract. These results in contraction of bronchial smooth muscles, edema of airway. enhanced mucous secretion. And inflammation of bronchial passage. AIl these cause difficulties in breathing. The asthmatic response can be divided in to two types -Eariy and late response. The early response occurs within minutes of allergen exposure. The mediators involved here are histamine, Leukotriene (LTC4), and Prostaglandins D2. The late response occurs, hours after allergen exposure. The mediators involved are IL-4, IL-5, IL-6, IL-8, and TNF -alpha, eosinophil chemotactic factor (ECF). Neutrophil chemotactic factor (NCF) and platelet activating factor (PAF) causes bronchoconstriction and vasodilation. These mediators recruit inflammatory cells, including eosinophils and neutrophils into bronchial tissue. Leukotriens (SRS-A) cause prolonged constriction of smooth muscle. They are considered to be the cause of much antihistamine resistant asthma in humans.

Neutrophils and eosinophils are capable of causing significant tissue injury by releasing toxic enzymes and cytokines. The events lead to occlusion of bronchial lumen with mucous, proteins and cellular debris, sloughing off epithelial cells, thickening of basement membrane, oedema, and hypertrophy of bronchial smooth muscle.

MCQ on Autoimmune Disease:

1. Which among is a neuromuscular autoimmune disease?

(a)Myasthenia gravis (b)Rheumatoid arthritis (c) Pernicious anemia (d) Crohn's disease

Ans: (a)Myasthenia gravis

Learn more: MCQ on Immune Disorder