Question

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.

Short answer

Answer: Molecular mimicry plays a role in the pathogenesis of Multiple Sclerosis due to the structural similarity of foreign antigens and myelin protein components, which may lead to cross-recognition by myelin-reactive T-cells and result in an attack on the host's own cells and tissues.

Step-by-step solution

Introduction to Molecular Mimicry

Molecular mimicry refers to the structural similarity between a foreign antigen and a host protein. This similarity may cause the immune system to mistakenly attack the host's own cells and tissues, resulting in autoimmune disorders like Multiple Sclerosis (MS).

Option A: Receptors mediating T-cell migration

This statement describes a situation where receptors on T-cells have overlapping function and can mimic each other's ligand specificity. However, this does not directly address the concept of molecular mimicry in the context of MS.

Option B: Immune modulating chemokines or cytokines

This statement refers to immune modulating chemokines or cytokines having similar molecular functions, but does not state anything about their structure. Therefore, this option does not describe molecular mimicry.

Option C: Structural similarity of foreign antigens and myelin protein components

This statement directly addresses the concept of molecular mimicry. Foreign antigens with structurally similar components to myelin protein may lead to cross-recognition by myelin-reactive T-cells, resulting in an attack on the host's own cells and tissues. This is the core idea of molecular mimicry in MS pathogenesis.

Option D: Suppression of selected T-cell responses

This statement talks about the impact of suppressing specific T-cell responses on both CD4+ and CD8+ T-cells. However, it does not address the concept of molecular mimicry.

Summary and Correct Answer

The correct answer is: c. Structural similarity of foreign antigens and myelin protein components may lead to cross-recognition by myelin-reactive T-cells. This option directly addresses the concept of molecular mimicry in the context of MS pathogenesis.

Key concepts

Understanding Autoimmune Disorders

Autoimmune disorders arise when the body's immune system mistakenly attacks its own tissues. Instead of defending against infections, the immune system becomes the perpetrator, leading to various health problems. One way this misdirection can occur is through a mechanism known as molecular mimicry.

Molecular mimicry occurs when parts of pathogens, such as bacteria or viruses, closely resemble the body's own cells or proteins. The immune system, while aiming to destroy these foreign invaders, can become confused and attack similar-looking self-tissues. Autoimmune disorders can affect nearly any part of the body, including the joints, skin, heart, and brain.

Common autoimmune diseases include rheumatoid arthritis, where joints are targeted; lupus, which can affect skin, kidneys, and other organs; and type 1 diabetes, where insulin-producing pancreatic cells are attacked. Each of these conditions demonstrates how a misdirected immune response can lead to chronic and often debilitating symptoms.

Multiple Sclerosis (MS) and the Immune System

Multiple Sclerosis (MS) is a chronic autoimmune disorder in which the immune system attacks the central nervous system (CNS), particularly the myelin sheath that surrounds nerves. Myelin is crucial as it serves as insulation and facilitates rapid signal transmission along the nerves.

MS is characterized by a wide range of symptoms, including muscle weakness, difficulty with coordination and balance, problems with vision, and cognitive impairment. In MS, myelin-reactive T-cells erroneously target and damage myelin, leading to communication problems between the brain and the rest of the body.

The precise cause of MS is unknown; however, it is thought to result from a combination of genetic susceptibility and environmental factors, such as viral infections. Following the theory of molecular mimicry, these environmental factors may introduce antigens that the immune system confuses with myelin, setting the stage for the misguided attack that is central to MS.

Role of Myelin-Reactive T-Cells in Autoimmunity

Myelin-reactive T-cells are a type of immune cell that plays a critical role in the pathogenesis of Multiple Sclerosis (MS). Under normal circumstances, T-cells are instrumental in protecting the body against pathogens. However, when these cells become autoreactive, they target the body's myelin as if it were an invading organism.

Myelin-reactive T-cells are activated when they encounter a foreign antigen that closely resembles myelin's molecular structure, a phenomenon described in molecular mimicry. Once activated, these T-cells cross the blood-brain barrier and cause inflammation and demyelination in the CNS.

These destructive processes can lead to the formation of scar tissue (sclerosis), interrupting nerve impulses and manifesting as the symptoms seen in MS. Targeting myelin-reactive T-cells is a focus in developing therapies for MS, aiming to reduce their harmful activity without compromising the body's overall immune defense.