Group 13 has created this presentation with the
aim of sensitising others about autoimmune
Autoimmune diseases are not as rare as the
name suggests, so it its important that we know
about the signs/symptoms, causes, diagnoses,
and treatment methods.
Do Learn and Enjoy!
Autoimmunity is an immune reaction against self-
antigens which evokes the production of humoral
mediated (autoantibodies), cell mediated (self reactive
T cells) or complement mediated immunity.
Autoimmunity can cause serious damage and loss of
function to self organs and tissues leading to
Organ specific autoimmune diseases affect tissues of
5 % to 7% adult affected.
Two third women.
More than 40 human diseases autoimmune
Hashimoto’s Thyroiditis- The body produces
autoantibodies and TDTH cells against thyroid antigens
leading to enlarged thyroid gland, goitre and
Pernicious Anaemia – Results from defective red blood cell
maturation due to inept B12 uptake. The body produces
autoantibodies against intrinsic factor which is needed for
B12 transport and uptake. Symptoms: loss of appetite,
• Autoimmune Haemolytic anaemia AHA. The body makes antibodies
(IgG/IgM) against a variety of RBC antigens which results in the
destruction or removal of blood cells.
• Drug Induced Haemolytic Anaemia. Occurs when a drug causes the
body’s immune system to react against its own red blood cells.
• Thrombocytopenic Purpura. It is a life-threatening disorder that
results from the destruction of platelets by autoantibodies. Phagocytes
in the liver and spleen endocytised antibody coated platelets.
Goodpasture Syndrome. A rare autoimmune disease of the
lungs and kidneys which involve the production of
autoantibodies against basal membrane of the alveoli and
glomeruli. Symptoms include kidney and pulmonary
damage, glomerulonephritis, pulmonary haemorrhage.
Insulin Dependent Diabetes Mellitus Type I Diabetes.
This disease is caused by a directed attack on the insulinproducing cell β-cells in the pancreas by antibody dependent
cytotoxicity, resulting in decreased production of insulin.
Graves’ Disease. This disease arises from the binding of
autoantibodies to the TSH (thyroid stimulating hormone)
receptors resulting in an overproduction of thyroxine.
Symptoms include bulging eyes, hyperthyroidism,
increased sweating, palpitation, heat intolerance.
• Myasthenia Gravis. A chronic autoimmune disease
resulting from faulty neuromuscular transmission. The
body produces autoantibodies (IgG isotype) which bind to
acetylcholine receptors in the neuromuscular junction
thereby blocking Ach which is needed to stimulate muscle
Systemic Lupus Erythematosus- Lupus is a conditioned
characterised by chronic inflammation of body tissues that
affects mainly women. The body produces autoantibodies
against a variety of antigens like RBC, mitochondrion,
lysosomes, and other common cell organelles.
The ratio of female to male patients is 10:1. It occurs more
frequently in Black and Hispanic women than Caucasian
Symptoms: erythrematosus skin rashes, glomerulinephritis,
Characteristic “butterfly” rash over the cheeks of a
young girl with lupus[From L. Steinman, 1993, Sci. Am. 269(3):80.]
Rheumatoid Arthritis RA. RA is a chronic inflammatory
disease affecting the synovial joints; mainly in middle aged
women. The inflamed synovial membrane is surrounded by
inflammatory cells which destroy the cartilage and bone of the
joints. Symptoms are: weight loss, fever, fatigue.
Multiple Sclerosis MS. This disease affects the central
nervous system. It characterised by the presence of
scleroses (scar tissue) in the white matter of neurons, as a
result of the response autoreactive T lymphocytes. Symptoms
include: motor weakness, paralysis in limbs, ataxia, urinary
dysfunction, mental aberration.
Sceleroderma- characterised by the deposition of excess collagen in the
connecting tissues which results in the thickening of the skin and gradual skin
The patient develops CREST syndrome - calcinosis (excess calcium
deposition), Reynauld’s phenomenon (abnormal blood flow in response to
stress or cold), eosophageal dysfunction (difficulty swallowing),
scelerodactyl (tightening scaly skin) and telangiectasia (red spots on skin).
Organs affected includes the skin, kidney, heart, lungs, GI tract, and joints.
Guillian Barre Syndrome. This disease commonly occurs after an
infectious disease or after vaccination. The disease arises from the
antibody-mediated and T-cell mediated damage against nerve tissues
Autoimmunity can be induced in animals in order to
carry out experiments and treatment trials with the
Animal models are used to clarify possible causes,
mechanisms and treatment of autoimmune diseases,
as some animals develop autoimmune diseases
which share significant features with that of their
• Obese strain chicken. The OS chicken has a thyroid
condition in which thyroid autoantibodies spontaneously
occur which results in gradual destruction of the thyroid
which resembles that of Hashimoto’s thyroiditis in human.
• Experiments on OS chicken have helped to elucidate the
roles of B lymphocytes and T lymphocytes in this
autoimmune disease; these were found to play significant
roles in the development of the disease.
• Non obese diabetic (NOD) mouse. NOD mouse shares key
features with human insulin-dependent diabetes mellitus
(IDDM). In both cases, the pancreatic β-islet of the
Langerhans are destroyed by lymphocytes. Experiments on
NOD mouse found that T cells play the decisive role in IDDM.
• The experimental autoimmune encephalomyelitis
rat/mouse is the model animal for multiple sclerosis. When
injected with myelin basic protiens or proteolipids, the rodent
In essence, autoimmunity arises from defects in self-
tolerance mechanisms and abnormalities in cellmediated and antibody-mediated immunity.
Self-tolerance mechanism failure to produce
autoantibodies against self-antigens because: 1) clonal
deletion of self-reactive cells, 2) tolerance of TH and B
cells to self-antigens, 3) clonal ignorance whereby selfreactive lymphocytes remain dormant.
Some viruses and bacterial antigens can act as poly-clonal activators that activate
self-reactive B cells which leads to tissue damages and diseases.
Molecular mimicry by cross-reactive microbial antigens. This describes a
condition where surface antigens on microbes resemble self-antigens of the
body. This results in an immune assault against the microbial antigens and the
self-antigens which they resemble.
Availability of sequestered (isolated) self-antigens. Antigens which have
been isolated from the immune system during embryonic stages become
exposed during injury or trauma.
These sequestered antigens may be released and exposed to immune cells
which lack self-tolerance leading to the development of an autoimmune
Aberrant (Unusual) Expression of MHC Class II Molecules.
This occurs when MHC class II proteins are expressed on non-immune
cells, self-antigens presented by them will activate TH cells which in turn
activate cell-mediated immunity and humoral immunity against the selfantigens
Currently, autoimmune responses and diseases
are treated via chemotherapeutic methods and
Organ ablation is the removal of the affected
organ, in some cases followed by organ
Treatments are mainly aimed at suppressing an
autoimmune response with the use
immunosuppressive drugs, cytotoxic drugs,
plasmapheresis, and organ ablation (removal of
a target organ is indispensable.)
Non-steroidal anti-inflammatory drugs mitigate
inflammations by slowing migration of
Cytotoxic drugs inhibit the antigen-activated T-
Plasmapheresis is the exchange of the affected
person’s plasma containing autoantibodies with
plasma containing normal antibodies.
Immunosuppression (e.g., prednisone,
Removal of thymus (some MG patients)
Plasmapheresis (remove Ab-Ag complexes)
T-cell vaccination (activate suppressing T
Block MHC with similar peptide
anti-CD4 monoclonal Ab
anti-IL2R monoclonal Ab
Main Thesis: Research is being done on model
animals in order to develop alternative ways
aimed at inducing tolerance to the specific selfantigens, or removing self-reactive B and T
Tolerance Induction. This is achieved by the oral
administration of the self-antigen, which elicits the
autoimmune response, into the body. This
method attempts to reintroduce specific immunity
Monoclonal Antibody Against Autoantigens. Monoclonal
antibodies bind to cells bearing the specific antigens which
leads to the blocking or destruction of the cell. However,
the removal of the irritating antigen does not activate the
production of autoantibodies.
Blockage of MHC Molecules. Blocking peptides, which
have a different amino acid sequence from the antigen, are
made to bind to the antigen-binding cleft on the MHC class
II molecules. This prevents MHC class II from binding to the
antigens and thereby autoimmune response.
Induction of T-cell suppression. In the case of the EAE
mouse, the administration of low doses of MBP-specific T
cells immunized the mice so that when low doses of MBP is
introduced the mice did not develop encephalitis.
Role of MHC. MHC class II molecules are more associated with
autoimmunity because MHC class II are involved in the selection
and activation of TH. TH cells in turn mediate the activation
humoral and cell-mediated immune responses for both normal
immunity and autoimmunity.
Role of TH cells in autoimmunity. Abnormalities in TH cells may
lead to the production autoantibodies because TH are necessary
for the production of antibodies.
Role of T-cell receptors autoimmunity. T-cells obtained from
patients with MS and myasthenia gravis show a preferential
expression of the TCR variable gene in the self-reactive T-cells.
The absence of the CTLA-4 gene which codes for CTLA-4
receptor that inhibits autoimmune response can result in fatal
autoimmune response and massive tissue damage
The important genes that regulate the development of
autoimmunity are located within MHC.
MHC have got critical role in maturation of T cell & induction of
MHC II genes are directly responsible for auto antigen
processing and presentation.
The structure of Ag binding groove will determine , if specific Ag
will trigger an AU response.
Kindt, Thomas. Barbara Osbourne. Richard
Goldsby.Kuby Immunology. (2006).6th Edition.
Pearson Education, New York.
Tortora, Gerard. Berdell Funke. Christine Chase.
Microbiology: An introduction. (2010). 10th Edition.
Benjamin Cummings, New York.
Kahn, Fahim. Elements of Immunology. (2009).
First Edition. Pearson, New York.