The Failure Of An Individuals Immune System Biology Essay

Published: Last Edited:

This essay has been submitted by a student. This is not an example of the work written by our professional essay writers.

Antigen identification, including self-recognition, requires pre existing T cells and B cells that assume antigen receptors complementary to the antigen, be it a foreign or a self-antigen; this is the basic principle of the clonal selection theory of acquired immunity (SAGE Publications).

The process on how autoimmune diseases develop, range from a combination of genetic predisposition, sex, age and environmental factors (Iorio and Lennon, 2012). The most challenging aspect of autoimmunity is identifying the proceedings that underwrite the initiation of the response (Kalvakolanu, 2011). External factors such as chemicals, medications and microbes, present as extrinsic factors that trigger commencement of an autoimmune response. Although they are not the sole contribution to development of disease, they appear as a reoccurring factor in many studies which have been conducted to demonstrate attributable risk to autoimmune disease (Van Eden, 2006). There are many types of autoimmune diseases such as systemic lupus erythematous (SLE), Type I Diabetes (T1D), Scleroderma, Rheumatoid Arthritis (RA) to name a few. When the immune system responds to invaders, it generates antibodies that are used to eliminate the threat however when the system fails to effectively create these antibodies, the malfunction can cause the construction of autoantibodies (Sherwood, 2010).

Autoantibodies are immune proteins that misguidedly target and damage specific tissues or organs of the body. Autoantibodies can be produced by the body's immune system when it fails to discriminate between "self" and "non-self" proteins (Carr, 2005). When the body creates these immune proteins, it can cause inflammation and damage to the target organs, which results in the development of an autoimmune disease (Herkel and Lohse, 2008). Although many studies have been conducted to establish the causation of this malfunction, it is still unclear why the body initiates this mechanism.

Autoantibodies are a vital serological feature of autoimmune diseases and can play a key role in the diagnosis or prognosis. Selected autoantibody types are of particular diagnostic assessment, in that they are favorably disease-specific, particularly those that are a component of the disease process, such as autoantibodies to the acetylcholine receptor in myasthenia gravis (Herkel and Lohse, 2008). Other antibodies are pathognomonic for a particular disease without having evident pathogenic effects, such as antimitochondrial antibodies in primary biliary cirrhosis (Perl, 2004). A specific indication to disease pathogenesis is offered by antibodies to transglutaminase in celiac disease: the disease causing antigen is gliadin, in fact primarily deaminated gliadin, which is recognized by specific T cells. Transglutaminase is the enzyme responsible for deamination of gliadin, and therefore directly related to the key antigen, without itself being the key target antigen of the inflammatory condition (Perl, 2004). Voluminous amounts of autoantibodies associated with autoimmune diseases are directed towards posttranslational protein modifications or enzymes, and it may well be, that the pathogenic key event may not be the autoimmune recognition of the modified proteins, but aberrant ligand binding or modification (Herkel and Lohse, 2008).

Several mechanisms can alter self-constituents so they appear foreign to the immune system. New antigenic determinants can be attached to self-proteins, or the shape of a self antigen can shift for many reasons so that previously unresponsive helper T cells are stimulated and can cooperate with preexisting B cells to secrete autoantibodies (Weetman, 2004). Alteration of the shape of a self-protein has been shown to occur in experimental animals such as mice, and is the most plausible explanation for the production of the rheumatoid factors that are characteristic of rheumatoid arthritis. Infectious organisms also can modify self antigens, which may clarify why viral infection of specialized cells-such as those in the pancreas that secrete insulin or those in the thyroid gland that make thyroid hormones-often leads the maturity of autoantibodies against the cells themselves and against their hormonal products (Herkel and Lohse, 2008).

Intracellular antigens and antigens located on tissues that are not in contact with the circulation normally are segregated effectively from the immune system. Thus, they may be considered foreign when introduced into the circulation as a result of tissue destruction initiated by trauma or infection (Weetman, 2004).

Cross-reaction with foreign antigens is also an important area of interest. This is a process that occurs when an infectious agent harvests antigens so similar to those on normal tissue cells that the antibodies stimulated to react against the foreign antigen also recognize the similar self antigen; hence, the two antigens are said to be cross-reactive. Autoantibodies stimulated by external antigens in this way can result in severe harm (Van Eden, 2006).

Activation of auto reactive T cells is crucial for the induction of autoimmunity (Carr, 2005). Resting auto reactive T cells are part of the normal immune repertoire and therefore do not induce disease (Carr, 2005). Numerous mechanisms may be accountable for the initiation of auto reactive T cells in autoimmune diseases. These include cross-reactive microbial peptides (molecular mimicry), viral or bacterial super antigens, release of auto antigen during inflammation, or bystander activation (Cunningham and Fujinami, 2000). With the complexity of human autoimmune diseases, it is questionable that a single mechanism may be operative during growing stages of disease pathogenesis (Sherwood, 2010). The key concept that must be noted is that activation of auto reactive T cells is necessary, but not sufficient, for the advancement of clinical disease. A principal locus in many autoimmune diseases is the MHC on human chromosome 6 (Henderson et al., 1998). Also important is the induction of a sufficient degree of clonal expansion and a functional phenotype (i.e. cytokine profile) that renders the T cells Pathogenic (Henderson et al., 1998). Access to the target organ as well as the levels of expression of MHC class II and co-stimulatory molecules in the target organ may limit the progression of autoimmunity.

CARR, D. J. J. 2005. Interferon Methods and Protocols, United States of America, Humanapress.

CUNNINGHAM, M. W. & FUJINAMI, R. S. 2000. Molecular Mimicry, Microbes, and Autoimmunity, United States of America, ASM Press.

HENDERSON, B., POOLE, S. & WILSON, M. 1998. Bacteria-Cytokine Interactions in Health and Disease, London, Portland Press Ltd.

HERKEL, J. & LOHSE, A. W. 2008. Significance of autoantibodies. Hepatology, 47, 786-788.

IORIO, R. & LENNON, V. A. 2012. Neural antigen-specific autoimmune disorders. Immunological Reviews, 248, 104-121.

KALVAKOLANU, D. V. 2011. An Introduction to the Special Issue on "Cytokines and Autoimmune Diseases". Journal of Interferon & Cytokine Research, 31, 693-694.

NA 2001. Autoimmune Diseases. New England Journal of Medicine, 345, 1707-1708.

PERL, A. 2004. Autoimmunity Methods and Protocols, United States of America, Humanapress.

SAGE PUBLICATIONS, I. Disease. Encyclopedia of Health Services Research. SAGE Publications, Inc, Thousand Oaks, SAGE Publications, Inc.

SHERWOOD, L. 2010. Human Physiology: From Cells to Systems, USA, Yolanda Cossio.

VAN EDEN, W. 2006. Immunoregulation of Autoimmune Diseases. Human Immunology, 67, 446-453.

WEETMAN, A. P. 2004. Cellular immune responses in autoimmune thyroid disease. Clinical Endocrinology, 61, 405-413.