What Is An Autoimmune Disease

GENERAL MICROBIOLOGY AND
IMMUNOLOGY ASSIGNMENT 1.
Q1. Discuss autoimmunity using at least two autoimmune
diseases in your discussion.
16TH APRIL, 2019.
Name of Student & ID #: Lecturer:

MBILI BISHOP-005-610 Mr. H.C. NKAMBA
What is autoimmune and autoimmune disease?
Autoimmune reactions reflect an imbalance between effector and regulatory
immune responses, typically develop through stages of initiation and propagation,
and often show phases of resolution (indicated by clinical remissions) and
exacerbations (indicated by symptomatic flares). The fundamental underlying
mechanism of autoimmunity is defective elimination and/or control of self-reactive
lymphocytes.
An autoimmune disease is a condition in which the immune system mistakenly

attacks its own body.
The immune system normally guards against germs like bacteria and viruses.
When it senses these foreign invaders, it sends out an army of fighter cells to attack
them. Normally, the immune system can tell the difference between foreign cells
and your own cells.
In an autoimmune disease, the immune system mistakes part of your body, like
your joints or skin, as foreign. It releases proteins called autoantibodies that attack
healthy cells. Some autoimmune diseases target only one organ. Type 1 diabetes
damages the pancreas. Other diseases, like systemic lupus erythematosus (SLE),
affect the whole body.
Why does the immune system attack the body?
Doctors don’t know exactly what causes the immune-system misfire. Yet some
people are more likely to get an autoimmune disease than others. According to
a 2014 study, women get autoimmune diseases at a rate of about 2 to 1 compared
to men — 6.4 percent of women vs. 2.7 percent of men. Often the disease starts
during a woman’s childbearing years (ages 15 to 44).
Some autoimmune diseases are more common in certain ethnic groups. For
example, lupus affects more African-American and Hispanic people than
Caucasians. Certain autoimmune diseases, like multiple sclerosis and lupus, run in
families. Not every family member will necessarily have the same disease, but they
inherit a susceptibility to an autoimmune condition.
Because the incidence of autoimmune diseases is rising, researchers suspect

environmental factors like infections and exposure to chemicals or solvents might
also be involved.
A “Western diet” is another suspected risk factor for developing an autoimmune

disease. Eating high-fat, high-sugar, and highly processed foods is thought to be
linked to inflammation, which might set off an immune response. However, this
hasn’t been proven.
A 2015 study focused on another theory called the hygiene hypothesis. Because of
vaccines and antiseptics, children today aren’t exposed to as many germs as they
were in the past. The lack of exposure could make their immune system prone to
overreact to harmless substance. In this article, diabetes type 1 and systemic
lupus erythematosus are used to explain autoimmune diseases in details.
Autoimmune type 1 diabetes is characterized by selective destruction of insulin-
secreting beta cells in the pancreas of genetically susceptible individuals. The
mechanisms underlying the development of type 1 diabetes are not fully
understood. However, a widely accepted point is that type 1 diabetes is caused by a
combination of genetic and environmental factors. Although most type 1 diabetes
patients do not have a family history, genetic susceptibility does play a vital role in
beta cell autoimmunity and destruction. Human leukocyte antigen (HLA) regions
are the strongest genetic determinants, which can contribute 40-50 % of the genetic
risk to type 1 diabetes. Other genes, including INS also contribute to disease risk.
The mechanisms of the susceptible genes in type 1 diabetes may relate to their
respective roles in antigen presentation, beta cell autoimmunity, immune tolerance,
and autoreactive T cell response. Environmental susceptibility factors also
contribute to the risk of developing type 1 diabetes. From an epigenetic standpoint,
the pathologic mechanisms involved in the development of type 1 diabetes may
include DNA methylation, histone modification, microRNA, and molecular
mimicry. These mechanisms may act through regulating of gene expression,
thereby affecting the immune system response toward islet beta cells. One of the
characteristics of type 1 diabetes is the recognition of islet autoantigens by
autoreactive CD4(+) and CD8(+) T cells and autoantibodies. Autoantibodies
against islet autoantigens are involved in autoantigen processing and presentation
by HLA molecules. This review will mainly focus on the molecular mechanism by
which genetic, epigenetic, and environmental factors contribute to the risk of type
1 diabetes.
Systemic lupus erythematosus (SLE, or lupus) is a systemic autoimmune disease
with multiorgan inflammation. SLE is characterized by production of pathogenic
autoantibodies directed against nucleic acids and their binding proteins, reflecting a
global loss of self-tolerance . The loss of tolerance with subsequent immune
dysregulation is a consequence of genetic factors, in the setting of environmental
triggers and stochastic events, with recent studies implicating over 30 genetic loci
in disease pathogenesis .
Aberrant innate immune responses play a significant role in the pathogenesis of
SLE, contributing both to tissue injury via release of inflammatory cytokines as
well as to aberrant activation of autoreactive T and B cells, with the latter leading
to pathogenic autoantibody production and resultant end-organ injury.
Autoantigenic nucleic acids and their binding proteins are required for self-antigen
specific activation of autoreactive lymphocytes. Autoantigens complexed with
their cognate autoantibodies also directly contribute to activation of innate immune
cells via Fc receptor (FcR)-mediated uptake of complexes (or in the case of
autoreactive B cells, initial engagement of the B cell antigen receptor by
autoantigens per se), with the nucleic acid component of these complexes upon
endosomal trafficking engaging intracellular Toll-like receptors (TLRs) with
subsequent innate and B cell activation.
Mechanism of autoantibody production and tissue injury in lupus: A

paradigm
Self-antigen dependent activation of autoreactive B cells and CD4 T cells in
secondary lymphoid organs, leads to production of pathogenic autoantibodies that,
along with inflammatory cytokines, promotes tissue injury in lupus. Antigen-
presenting dendritic cells are necessary for adaptive immune cell activation, and
contribute to inflammatory cytokine production. Autoantibodies in complexes with
autoantibodies contribute to innate immune cell activation and cytokine
production. Genetic predisposition is a requisite for aberrant immune system
activation, in the setting of environmental and stochastic events. Abbreviations:
DC, dendritic cells; pDC, plasmacytoid dendritic cells.
CONCLUSSION
Solving the enigma of human autoimmunity will require translating the vast
amount of knowledge that has accumulated from animal models for the clinic.
Several challenges inherent in this translation to the clinic have become apparent.
First, there needs to be a renewed emphasis on studying possible defects in
autoantigen-specific T and B cells in humans. Analyses of bulk lymphocyte
populations are unlikely to reveal defects that largely affect cells of only a few
specificities. This may be especially true in organ-specific autoimmune diseases.
Studying antigen-specific lymphocytes will require new technologies that can be
readily applied to humans. Second, the definitions of biological aberrations need to
be complemented by analysis of molecular pathways.
REFFERENCES
1. ^ Arthur M. Silverstein: Autoimmunity: A History of the Early Struggle for Recognition,

in: Ian R. Mackay, Noel R Rose: The Autoimmune Diseases (chapter 2), Academic Press,
2013.
2. ^ Poletaev AB, Churilov LP, Stroev YI, Agapov MM (2012). "Immunophysiology versus
immunopathology: Natural autoimmunity in human health and
disease". Pathophysiology. 19 (3): 221-
31. doi:10.1016/j.pathophys.2012.07.003. PMID 22884694.Autoimmunity might aid in
the recognition of neoplastic cells by CD8+ T cells, and thus reduce the incidence
of cancer.
3. ^ Stefanova I.; Dorfman J. R.; Germain R. N. (2002). "Self-recognition promotes the
foreign antigen sensitivity of naive T lymphocytes". Nature. 420 (6914): 429–
434. doi:10.1038/nature01146. PMID 12459785.
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GENERAL MICROBIOLOGY AND

16TH APRIL, 2019.

Name of Student & ID #: Lecturer:

An autoimmune disease is a condition in which the immune system mistakenly

Why does the immune system attack the body?

Because the incidence of autoimmune diseases is rising, researchers suspect

A “Western diet” is another suspected risk factor for developing an autoimmune

Mechanism of autoantibody production and tissue injury in lupus: A

1. ^ Arthur M. Silverstein: Autoimmunity: A History of the Early Struggle for Recognition,

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