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Chapter 18: Problem 9

In the pathogenesis of MS, molecular mimicry implies: a. Recepooes mediating T-cell migration have overlapping function, i.e, they can mimic each other's ligand specificity. b. Immune modulating chemokines or cytokines can mimic the molecular functions of each other. c. Structural similarity of foreign antigens and myelin protein components may lead to cross-recognition by myelin-reactive T-cells. d. Suppression of selected T-cell responses can have a global impact on both CD4+ and CD8+ T-cells. 10\. Comparison of EAE with MS shows the following:

Short Answer

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Answer: In the pathogenesis of MS, molecular mimicry involves the structural similarity between foreign antigens and myelin protein components, which may lead to cross-recognition by myelin-reactive T-cells. EAE, an animal model of MS, shares similarities with MS in processes such as demyelination, inflammation, and T-cell activation. These similarities allow researchers to study the mechanisms of MS and test potential therapies using EAE.

Step by step solution

01

Question 1: Molecular Mimicry in the Pathogenesis of MS

To answer this question, we need to understand the concept of molecular mimicry. In the context of MS, molecular mimicry refers to the structural similarity between foreign antigens and myelin protein components, which may lead to cross-recognition by myelin-reactive T-cells. Therefore, the correct answer is: c. Structural similarity of foreign antigens and myelin protein components may lead to cross-recognition by myelin-reactive T-cells.
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Question 2: Comparison of EAE with MS

For this question, we need to know the similarities and differences between Experimental Autoimmune Encephalomyelitis (EAE) and Multiple Sclerosis (MS). Both EAE and MS are autoimmune diseases that affect the central nervous system (CNS). EAE is an animal model of MS, which is primarily used to study the mechanisms of the disease and to test potential therapies. Some comparisons between EAE and MS may include similarities in demyelination, inflammation, and T-cell activation. The correct answer to this question can be deduced from the lecture material or assigned readings.

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Most popular questions from this chapter

Apoptosis of which cell type is a histological hallmark of at least one pathologic subtype of MS plaque? a. neuron b. astrocyte c. oligodendrocyte d. macrophage e. none of the above

Which of the following immune abnormalities are not associated with MS? a. overexpression of IL-10 b. increased expression of adhesion molecules c. presence of oligoclonal bands in the CSF d. increased TNF- \(\alpha\) expression preceding clinical relapse

In the pathogenesis of \(\mathrm{MS}\), molecular mimicry implies: a. Receptors mediating T-cell migration have overlapping function, i.e., they can mimic each other's ligand specificity. b. Immune modulating chemokines or cytokines can mimic the molecular functions of each other. c. Structural similarity of foreign antigens and myelin protein components may lead to cross-recognition by myelin-reactive T-cells. d. Suppression of selected T-cell responses can have a global impact on both CD4+ and CD8+ T-cells.

The diagnostic criteria for MS: a. Depend upon the demonstration of white matter abnormalities in the brain or spinal cord by MRI. b. Require evidence for the presence of neurological dysfunction for the diagnosis in all cases. c. Require that there is no better explanation (other than MS) for the clinical presentation. d. None of the above e. \(a, b\) \& c f. \(a\) \& \(c\) g. b \& c

Comparison of EAE with MS shows the following: a. Both demonstrate monophasic, relapsing, and chronic progressive clinical courses b. Perivascular inflammation is common in both. c. Demyelination is diffuse throughout the brain in both. d. All of the above e. \(a\) \& b
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