Autoimmune diseases

1. What is the primary cause of autoimmune diseases?
   A. Overactive immune response to pathogens
   B. Breakdown of self-tolerance
   C. Excessive production of cytokines
   D. Genetic mutations in immune cells
   

1. Answer: B. Breakdown of self-tolerance
   Explanation: Autoimmune diseases occur when the immune system loses its ability to distinguish between self and non-self, leading to attacks on the body's own tissues.

1. Which mechanism explains the development of rheumatic fever after a streptococcal infection?
   A. Polyclonal lymphocyte activation
   B. Molecular mimicry
   C. Release of sequestered antigens
   D. Failure of apoptosis
   

1. Answer: B. Molecular mimicry
   Explanation: Rheumatic fever occurs due to molecular mimicry, where streptococcal antigens resemble heart tissue, leading to cross-reactive immune responses.

What is the role of regulatory T cells (Tregs) in preventing autoimmune diseases?
A. They produce autoantibodies
B. They suppress self-reactive lymphocytes
C. They activate B cells
D. They promote inflammation

Answer: B. They suppress self-reactive lymphocytes
Explanation: Regulatory T cells (Tregs) play a key role in maintaining peripheral tolerance by suppressing self-reactive lymphocytes

1. Which type of hypersensitivity reaction is involved in systemic lupus erythematosus (SLE)?
   A. Type I
   B. Type II
   C. Type III
   D. Type IV
   

1. Answer: C. Type III
   Explanation: SLE involves Type III hypersensitivity, where immune complexes deposit in tissues, causing inflammation and damage.

What is the primary target of autoantibodies in Hashimoto's thyroiditis?
A. Pancreatic beta cells
B. Thyroid peroxidase and thyroglobulin
C. Joint synovium
D. Nuclear antigens

Answer: B. Thyroid peroxidase and thyroglobulin
Explanation: In Hashimoto's thyroiditis, autoantibodies target thyroid peroxidase and thyroglobulin, leading to hypothyroidism

1. Which genetic factor is most commonly associated with autoimmune diseases?
   A. HLA genes
   B. BRCA genes
   C. p53 gene
   D. CFTR gene
   

1. Answer: A. HLA genes
   Explanation: HLA genes, especially HLA-DR and HLA-DQ, are strongly associated with susceptibility to autoimmune diseases.

1. What is the primary mechanism of tissue damage in Type 1 Diabetes Mellitus?
   A. Immune complex deposition
   B. Autoantibody-mediated cell destruction
   C. Molecular mimicry
   D. Polyclonal lymphocyte activation
   

1. Answer: B. Autoantibody-mediated cell destruction
   Explanation: In Type 1 Diabetes Mellitus, autoantibodies destroy pancreatic beta cells, leading to insulin deficiency.

1. Which of the following is a systemic autoimmune disease?
   A. Hashimoto's thyroiditis
   B. Type 1 Diabetes Mellitus
   C. Systemic lupus erythematosus (SLE)
   D. Graves' disease
   

1. Answer: C. Systemic lupus erythematosus (SLE)
   Explanation: SLE is a systemic autoimmune disease that affects multiple organs, including the skin, kidneys, and joints.

1. Which of the following is an example of an organ-specific autoimmune disease?
   A. Systemic lupus erythematosus (SLE)
   B. Rheumatoid arthritis
   C. Hashimoto's thyroiditis
   D. Multiple sclerosis
   

1. Answer: C. Hashimoto's thyroiditis
   Explanation: Hashimoto's thyroiditis is an organ-specific autoimmune disease where autoantibodies target the thyroid gland.

1. What is the role of molecular mimicry in autoimmune diseases?
   A. It causes non-specific activation of lymphocytes
   B. It leads to the release of sequestered antigens
   C. It triggers cross-reactive immune responses
   D. It promotes immune complex deposition
   

1. Answer: C. It triggers cross-reactive immune responses
   Explanation: Molecular mimicry occurs when microbial antigens resemble self-antigens, leading to cross-reactive immune responses that attack the body's own tissues.

1. Regarding self-tolerance:
   A. Central tolerance occurs in the thymus and bone marrow.
   B. Peripheral tolerance involves the suppression of self-reactive lymphocytes by Tregs.
   C. Breakdown of self-tolerance leads to autoimmune diseases.
   D. Central tolerance is sufficient to prevent all autoimmune reactions.
   E. Peripheral tolerance mechanisms include anergy, deletion, and suppression.

1. A. Central tolerance occurs in the thymus and bone marrow. (True)
   B. Peripheral tolerance involves the suppression of self-reactive lymphocytes by Tregs. (True)
   C. Breakdown of self-tolerance leads to autoimmune diseases. (True)
   D. Central tolerance is sufficient to prevent all autoimmune reactions. (False)
   E. Peripheral tolerance mechanisms include anergy, deletion, and suppression. (True)

   Explanation:

   • Central tolerance occurs in the thymus (T cells) and bone marrow (B cells).

   • Peripheral tolerance involves mechanisms like anergy, deletion, and suppression by Tregs.

   • Breakdown of self-tolerance leads to autoimmune diseases.

   • Central tolerance is not perfect, and peripheral tolerance is needed to prevent autoimmune reactions.

1. Regarding autoimmune diseases:
   A. Autoimmune diseases can be organ-specific or systemic.
   B. Type 1 Diabetes Mellitus is an example of a systemic autoimmune disease.
   C. Hashimoto's thyroiditis is an organ-specific autoimmune disease.
   D. Systemic lupus erythematosus (SLE) is a systemic autoimmune disease.
   E. Autoimmune diseases are always caused by genetic mutations.

1. A. Autoimmune diseases can be organ-specific or systemic. (True)
   B. Type 1 Diabetes Mellitus is an example of a systemic autoimmune disease. (False)
   C. Hashimoto's thyroiditis is an organ-specific autoimmune disease. (True)
   D. Systemic lupus erythematosus (SLE) is a systemic autoimmune disease. (True)
   E. Autoimmune diseases are always caused by genetic mutations. (False)

   Explanation:

   • Autoimmune diseases can be organ-specific (e.g., Hashimoto's thyroiditis) or systemic (e.g., SLE).

   • Type 1 Diabetes Mellitus is an organ-specific autoimmune disease targeting pancreatic beta cells.

   • Autoimmune diseases are influenced by both genetic and environmental factors, not just genetic mutations.

1. Regarding molecular mimicry:
   A. Molecular mimicry involves microbial antigens resembling self-antigens.
   B. Rheumatic fever is an example of molecular mimicry.
   C. Molecular mimicry leads to cross-reactive immune responses.
   D. Molecular mimicry is the only mechanism of autoimmune disease development.
   E. Molecular mimicry can occur after viral infections.

1. A. Molecular mimicry involves microbial antigens resembling self-antigens. (True)
   B. Rheumatic fever is an example of molecular mimicry. (True)
   C. Molecular mimicry leads to cross-reactive immune responses. (True)
   D. Molecular mimicry is the only mechanism of autoimmune disease development. (False)
   E. Molecular mimicry can occur after viral infections. (True)

   Explanation:

   • Molecular mimicry occurs when microbial antigens resemble self-antigens, leading to cross-reactive immune responses.

   • Rheumatic fever is caused by molecular mimicry between streptococcal antigens and heart tissue.

   • Molecular mimicry is one of several mechanisms of autoimmune disease development.

1. Regarding systemic lupus erythematosus (SLE):
   A. SLE is a multisystem autoimmune disease.
   B. SLE is characterized by autoantibodies against nuclear antigens.
   C. SLE primarily affects the thyroid gland. (False)
   D. SLE involves Type III hypersensitivity reactions.
   E. SLE is more common in males than females.

1. A. SLE is a multisystem autoimmune disease. (True)
   B. SLE is characterized by autoantibodies against nuclear antigens. (True)
   C. SLE primarily affects the thyroid gland. (False)
   D. SLE involves Type III hypersensitivity reactions. (True)
   E. SLE is more common in males than females. (False)

   Explanation:

   • SLE is a systemic autoimmune disease affecting multiple organs, including the skin, kidneys, and joints.

   • SLE is characterized by autoantibodies against nuclear antigens (e.g., DNA, histones).

   • SLE involves Type III hypersensitivity reactions due to immune complex deposition.

   • SLE is more common in females than males.

1. Regarding Hashimoto's thyroiditis:
   A. Hashimoto's thyroiditis is an organ-specific autoimmune disease.
   B. Autoantibodies in Hashimoto's target thyroid peroxidase and thyroglobulin.
   C. Hashimoto's thyroiditis leads to hyperthyroidism.
   D. Hashimoto's thyroiditis involves Type II hypersensitivity reactions.
   E. Hashimoto's thyroiditis is caused by molecular mimicry.

1. A. Hashimoto's thyroiditis is an organ-specific autoimmune disease. (True)
   B. Autoantibodies in Hashimoto's target thyroid peroxidase and thyroglobulin. (True)
   C. Hashimoto's thyroiditis leads to hyperthyroidism. (False)
   D. Hashimoto's thyroiditis involves Type II hypersensitivity reactions. (True)
   E. Hashimoto's thyroiditis is caused by molecular mimicry. (False)

   Explanation:

   • Hashimoto's thyroiditis is an organ-specific autoimmune disease targeting the thyroid gland.

   • Autoantibodies in Hashimoto's target thyroid peroxidase and thyroglobulin, leading to hypothyroidism.

   • Hashimoto's involves Type II hypersensitivity reactions, where autoantibodies cause cell damage.

   • Hashimoto's is not primarily caused by molecular mimicry.

1. What is the difference between central and peripheral tolerance?
   

1. Answer:

   • Central Tolerance: Occurs in the thymus (T cells) and bone marrow (B cells), where self-reactive lymphocytes are deleted during maturation.

   • Peripheral Tolerance: Occurs in peripheral tissues and involves mechanisms like anergy, deletion, and suppression by regulatory T cells (Tregs) to prevent autoimmune reactions.
     Explanation: Central tolerance eliminates self-reactive lymphocytes during development, while peripheral tolerance prevents autoimmune reactions in mature lymphocytes.

1. What is molecular mimicry, and how does it contribute to autoimmune diseases?
   

1. Answer: Molecular mimicry occurs when microbial antigens resemble self-antigens, leading to cross-reactive immune responses that attack the body's own tissues.
   Explanation: Molecular mimicry is a key mechanism in autoimmune diseases like rheumatic fever, where streptococcal antigens resemble heart tissue.

1. What are the primary mechanisms of tissue damage in autoimmune diseases?
   

1. Answer: Tissue damage in autoimmune diseases is primarily caused by:

   • Type II Hypersensitivity: Autoantibodies bind to cell surface antigens, leading to cell destruction.

   • Type III Hypersensitivity: Immune complexes deposit in tissues, causing inflammation and damage.
     Explanation: Autoimmune diseases often involve Type II and Type III hypersensitivity reactions, leading to tissue damage and organ dysfunction.

1. What are the clinical features of systemic lupus erythematosus (SLE)?
   

1. Answer: SLE is a multisystem autoimmune disease that can affect the skin, kidneys, joints, and serosal membranes. Clinical features include inflammation, tissue damage, and the presence of autoantibodies against nuclear antigens (e.g., DNA, histones).
   Explanation: SLE involves widespread tissue damage due to immune complex deposition and autoantibody-mediated inflammation.