The document summarizes a chapter about autoimmunity and autoimmune diseases from three perspectives: 1) It outlines several key autoimmune diseases, their causes from abnormal immune responses against self-antigens, and their symptoms. 2) It discusses the use of animal models to study the mechanisms and potential treatments of autoimmune diseases. 3) It examines current therapeutic approaches that aim to suppress autoimmune responses through drugs or removal of target organs, and potential alternative strategies like inducing tolerance to self-antigens.

1. Autoimmunity
and
Autoimmune
Disease
A Unit By Unit Chapter Review
By
Delia Brett & Rhondene Wint

2. Outline
•
•
•
•
•
Summary of each unit with relevant points
Critical assessment of the chapter
Comparative Review
Checkpoints
Conclusion

3. Introduction
• A review is a critical evaluation of a text, event,
object, or phenomenon. Reviews can consider
books, articles, entire genres or fields of literature,
architecture, art, etc.
• Above all, a review makes an argument. The most
important element of a review is that it is a
commentary, not merely a summary. It allows you
to enter into dialogue and discussion with the
work‟s creator and with other audiences.

4. Introduction
• Team 13 has been assigned the task of writing a
literature review of Chapter 20 titled “Autoimmunity
and Autoimmune Diseases” from the textbook “
Elements of Immunology” by F. Kahn.
• The contents of the aforementioned chapter will be
compared to chapter 19 –”Disorders of the Immune
System” of another textbook “Microbiology: An
Introduction” by Totora,Funke Case.

5. Unit 20.1
• Summary – Autoimmune disease arises from an
immune reaction against self-antigens which evokes
the production of humoral mediated, cell mediated
or complement mediated immunity.
• Organ specific autoimmune diseases affect tissues of
a single organ or gland.
• Systemic autoimmune diseases affect multiple
organs/glands,

6. Unit 20.2 Single Organ Autoimmune
Disease
• Main Thesis: The clinicopathological features of
popular organ-specific autoimmune diseases:
• Hashimoto’s Thyroiditis- The body produces
autoantibodies and TDTH cells against thyroid antigens
leading to enlarged thyroid gland, goitre and
hyperthyroidism.
• 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, weakness,weight loss and fatigue.

7. • 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. Symptoms include
bleeding disorders.
• 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.

8. • Insulin Dependent Diabetes Mellitus Type I Diabetes. This
disease is caused by a directed attack on the insulin-producing
cell β-cells 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 contraction

9. Unit 20.3 Systemic Autoimmune Diseases
• Main Thesis: The clinicopathological features of
popular organ-specific autoimmune diseases:
• 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.
• Symptoms: erythrematosus skin rashes,
glomerulinephritis, fever, malaise, weight loss

10. • 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. 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,.

11. • Sceleroderma- characterised by the deposition of
excess collagen in the connecting tissues which
results in the thickening of the skin and gradual
skin lightening.
• 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-

12. Unit 20.4 Animal Models of Autoimmune Diseases
• Main Theses:
• 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 human counterparts.
• Autoimmunity arises from defects in self-tolerance
mechanisms and abnormalities in cell-mediated
and antibody-mediated immunity

13. • 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

14. Mechanisms of induction of immunity
Unit 20.5.2
• Normal individuals fail 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.

15. • 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 selfantigens 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 response.
• 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

16. Unit 20.5 Therapeutic Approaches to
Autoimmune Diseases
• Main Thesis: Currently, autoimmune responses
and diseases are treated via
chemotherapeutic methods and organ
ablation.
• 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.)

17. • Non-steroidal anti-inflammatory drugs mitigate
inflammations by slowing migration of lymphocytes;
cytotoxic drugs inhibit the antigen-activated T-cells;
plasmapheresis is the exchange of the affected
person‟s plasma containing autoantibodies with
plasma containing normal antibodies.

18. 20.6 Other Strategies
• Main Thesis: Research is being done on model
animals in order to develop alternative ways aimed
at inducing tolerance to the specific self-antigens,
or removing self-reactive B and T lymphocytes.
• 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 toward
self-antigens

19. •
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.

20. Unit 20.7 Role of MHC, TH cells and TCR in
autoimmunity
• 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

21. Critical Assessment
Pros, Cons, Comments

22. PROS
• In unit 20.1 we commend the insertion of diagrams
which illustrated the regions of the body affected
by autoimmune diseases. This gave us a mental
picture of what the symptoms would be like for a
particular autoimmune disease.

23. PROS
• Throughout the chapter, the author provided side
notes which provided supplementary information
about a certain subject like summaries, historical
background and new developments which were
informative.

24. PROS
• Some of the autoimmune diseases were identifiable
and were well discussed. For example, we knew of
persons who have lupus but we didn‟t that it was
autoimmune disease

25. PROS
• (Delia) The use of diagrams showing the
mechanisms of how an autoimmune disease
develops helped elucidate some of the diseases
discussed in units 20.2 and 20.3

26. CONS
• We both rue that the author did not organise the
organ-specific and systemic autoimmune diseases
in units 20.2 and 20.3 in a table. That would have
made the units more reader-friendly and easier to
memorise.

27. CON
• The major disadvantage was the apparent
incoherence of the presentation of the content.
Although the chapter titled “Autoimmunity and
Autoimmune Disease” the author took a while to
define and explain “autoimmunity” but instead
focused on autoimmune diseases.

28. CON
• In unit 20.1, we felt that the mechanisms of autoimmunity,
which he explained all the way in unit 20.5, should have been
discussed instead. This would have laid a stronger foundation
in understanding the autoimmune diseases.
• By the time we should be learning what causes autoimmune
diseases in the first place, we were wearied by the kinds of
autoimmune diseases and model animals.

29. COMPARATIVE REVIEW
Microbiology vs. Immunology

30. • As an immunology textbook, one would think that
Elements of Immunology would do a better job of
explaining mechanism of self-tolerance, which is
essential to autoimmunity than Microbiology. It did not
even measure up.
• Microbiology actually explained the mechanisms of self
tolerance, whilst Immunology only mentioned that
autoimmunity results from defects in self-tolerance
mechanisms.
• However, Immunology was more in depth in regards to
the mechanisms leading to autoimmunity.

31. • In the end, “Elements of Immunology” provided
more content in the relevant areas; however
“Microbiology: An Introduction” was better at
condensing the information so that the essential
points are captured.
• Furthermore, Microbiology looks more readerfriendly than Elements of Immunology.
• In concluding, we honestly found Elements of
Immunology too narrative and vague sometimes in
that it failed to define key terms. Nonetheless, we
recommend the text to other students who are not
visual learners.

32. REFERENCES
• College of Arts and Sciences. The Writing Centre:
Book Review. Retrieved from
file:///C:/Users/User/Documents/Immuno/Book%20R
eviews%20-%20The%20Writing%20Center.htm on
Spetember 20, 2013
• 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.