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Questions and Answers
What is the primary cause of type III hypersensitivity reactions?
What is the primary cause of type III hypersensitivity reactions?
- Antigen-mediated activation of mast cells
- Deficiency in factor I, C1, or C3
- Direct interaction between B cells and T cells
- Formation of immune complexes in the blood or tissues (correct)
Which statement accurately describes the pathophysiology of type III reactions?
Which statement accurately describes the pathophysiology of type III reactions?
- Type III reactions are characterized by direct cytotoxic effects of T cells on self-antigens.
- Immune complexes form and deposit in tissues, triggering chemotaxis of neutrophils and macrophages. (correct)
- Complement activation leads to direct destruction of antigens.
- The primary effector cells involved are natural killer (NK) cells.
What role do complement factors C3a and C5a play in type III hypersensitivity reactions?
What role do complement factors C3a and C5a play in type III hypersensitivity reactions?
- Activate B cells to produce antibodies against immune complexes
- Inhibit the production of pro-inflammatory cytokines
- Induce apoptosis of antigen-presenting cells
- Promote chemotaxis of immune cells to the site of immune complex deposition (correct)
Which factor deficiency can reduce clearance of immune complexes and increase susceptibility to type III reactions?
Which factor deficiency can reduce clearance of immune complexes and increase susceptibility to type III reactions?
In type III hypersensitivity, where do immune complexes deposit if they are not cleared from circulation?
In type III hypersensitivity, where do immune complexes deposit if they are not cleared from circulation?
What is the main consequence of complement activation in type III hypersensitivity reactions?
What is the main consequence of complement activation in type III hypersensitivity reactions?
What is the predominant T cell response in granulomatous hypersensitivity?
What is the predominant T cell response in granulomatous hypersensitivity?
Which cells are recruited to the site of chronic infection in granulomatous hypersensitivity?
Which cells are recruited to the site of chronic infection in granulomatous hypersensitivity?
What triggers airway macrophages to penetrate into the underlying tissue in granulomatous hypersensitivity?
What triggers airway macrophages to penetrate into the underlying tissue in granulomatous hypersensitivity?
Which cytokines are released by macrophages in granulomatous hypersensitivity to promote vasodilation and endothelial adhesion molecule expression?
Which cytokines are released by macrophages in granulomatous hypersensitivity to promote vasodilation and endothelial adhesion molecule expression?
What is a characteristic of immune complex deposition in Type III hypersensitivity reactions?
What is a characteristic of immune complex deposition in Type III hypersensitivity reactions?
How do T regulatory (Treg) cells aid in the resolution of the inflammatory response?
How do T regulatory (Treg) cells aid in the resolution of the inflammatory response?
What triggers the activation of phagocytes by binding to Fc receptors and complement receptors?
What triggers the activation of phagocytes by binding to Fc receptors and complement receptors?
Which factor may induce peptidyl arginine deiminases (PAD) activity to generate self-antigens for Rheumatoid Arthritis?
Which factor may induce peptidyl arginine deiminases (PAD) activity to generate self-antigens for Rheumatoid Arthritis?
In Rheumatoid Arthritis, what is the role of Rheumatoid Factor (RF)?
In Rheumatoid Arthritis, what is the role of Rheumatoid Factor (RF)?
What is the significance of HLA-DR4 in Rheumatoid Arthritis?
What is the significance of HLA-DR4 in Rheumatoid Arthritis?
Which disease is characterized by the formation of immune complexes that deposit in tissues, leading to type III hypersensitivity reactions?
Which disease is characterized by the formation of immune complexes that deposit in tissues, leading to type III hypersensitivity reactions?
In Systemic Lupus Erythematosus, what leads to chronic disease setting and eventual tissue destruction?
In Systemic Lupus Erythematosus, what leads to chronic disease setting and eventual tissue destruction?
What process in SLE results in the production of broad Ig responses against various self-antigens?
What process in SLE results in the production of broad Ig responses against various self-antigens?
What is the key factor that leads to T cell activation and epitope spreading in Systemic Lupus Erythematosus?
What is the key factor that leads to T cell activation and epitope spreading in Systemic Lupus Erythematosus?
Which cells are primarily involved in capturing haptenated proteins during the sensitization stage of Contact Hypersensitivity?
Which cells are primarily involved in capturing haptenated proteins during the sensitization stage of Contact Hypersensitivity?
What is the effect of Fas ligand engagement with Fas in Contact Hypersensitivity?
What is the effect of Fas ligand engagement with Fas in Contact Hypersensitivity?
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