Question

What are the trade-offs in the process of creating a system that can distinguish between self and non-self? How do you think the system balances the need to maximize recognition of potential threats with the danger of autoimmunity? Give an example of a way the immune system might prevent autoimmune responses, and a way a microbe might exploit that system.

Answer 1

In immune system, the term “self-” refers to the cells or molecules belonging to one’s own body, which are recognized. The term “Non-self” refers to the foreign molecules or cells. Each cell contains surface markers, based on which the self and non-self-cells or antigens are identified.

The immune system uses a complex array of protective mechanisms to control and usually eliminate these organisms and toxins. A general feature of the immune system is that these mechanisms rely on detecting structural features of the pathogen or toxin that mark it as distinct from host cells. Such host-pathogen or host-toxin discrimination is essential to permit the host to eliminate the threat without damaging its own tissues.

The innate immune system includes membrane bound receptors and cytoplasmic proteins that bind to molecular patterns expressed on the surfaces of invading microbes. Some aspects of the innate host defenses are always active regardless of the physiological demand(such as the mucociliary blanket overlying many epithelia), and others are activated after interactions of host cells or host proteins with chemical structures that are characteristic of invading microbes but that are absent from host cells.

Unlike the germ-line-encoded recognition molecules of the innate immune response, the antigen-specific receptors of the adaptive response are encoded by genes that are assembled when encountered by germ-line gene elements to form intact T cell receptor (TCR) and immunoglobulin (B cell antigen receptor; Ig) genes. The assembly of antigen receptors from a collection of a few hundred germ-line-encoded gene elements permits the formation of millions of different antigen receptors, each with potentially unique specificity for a different antigen.

HOW PATHOGENS EVADE BODY'S DEFENCE MECHANISM BY EXPLOITING ITS MECHANISM OF PROTECTING OWN CELLS?

A way in which an infectious agent can evade immune surveillance is by altering its antigens; this is particularly important for extracellular pathogens, against which the principal defense is the production of antibody against their surface structures. There are three ways in which antigenic variation can occur.

First, many infectious agents exist in a wide variety of antigenic types. There are, for example, 84 known types of Streptococcus pneumoniae, an important cause of bacterial pneumonia. Each type differs from the others in the structure of its polysaccharide capsule.

second, more dynamic mechanism of antigenic variation is seen in the influenza virus. At any one time, a single virus type is responsible for most infections throughout the world. The human population gradually develops protective immunity to this virus type, chiefly by directing neutralizing antibody against the major surface protein of the influenza virus, its hemagglutinin.

third mechanism of antigenic variation involves programmed rearrangements in the DNA of the pathogen. The most striking example occurs in African trypanosomes, where changes in the major surface antigen occur repeatedly within a single infected host.

Some viruses, however, can enter a state known as latency in which the virus is not being replicated. In the latent state, the virus does not cause disease but, because there are no viral peptides to flag its presence, the virus cannot be eliminated. Such latent infections can be reactivated and this results in recurrent illness.