Autoimmune diseases occur when the immune system mistakenly attacks and damages healthy body tissues. There are two main types - organ-specific diseases like Graves' disease which target a single organ, and systemic diseases like lupus that affect multiple body systems. Common symptoms include fatigue, joint pain, and skin rashes. While causes are unclear, genetics and environmental factors likely play a role. Treatment focuses on reducing immune system activity through medications like steroids, methotrexate, or targeted biologic therapies.

1. Autoimmune Diseases
Name : palani ananth.s
Class : 1st MSc microbiology
Submitted to : DR. SIVA KUMARTHANGAVEL

2. Autoimmune Diseases
▪ Autoimmune diseases is a group of disorders in which tissue injury is caused by humoral (by
auto-antibodies ) or cell mediated immune response ( by auto-reactiveT cells ) to self
antigens.
▪ Normally, the immune system does not attack the self . However, there is a large group of
autoimmune diseases in which the immune system does attack self-cells.
▪ The attack can be directed either against a very specific tissue or to a large no. of tissues.
▪ Once started, autoimmune diseases are hard to stop.
▪ An autoimmune disorder may result in:
 The destruction of one or more types of body tissue
 Abnormal growth of an organ
 Changes in organ function

3. SYMPTOMS
The symptoms of autoimmune disease vary depending on the disease as well as the person's immune system.
Common symptoms include:
▪ Anxiety or depression
▪ Blood sugar changes
▪ Digestive or gastrointestinal problems
▪ Dizziness
▪ Elevated fever and high body temperature
▪ Extreme sensitivity to cold in the hands and feet
▪ Fatigue
▪ Infertility
▪ Inflammation
▪ Irritability

4. Causes of autoimmunity

5. Autoimmune Diseases
▪ Autoimmunity Classification Can be classified into clusters that are either organ-specific or
systemic .

6. ORGAN-SPECIFIC AUTOIMMUNE DISEASES
In this type, the immune response is directed to a target antigen unique to a single organ or
gland.The cells of the organ may be damaged directly by humoral or cell- mediated effector
mechanisms. Alternatively, the antibodies may overstimulate or block the normal functions of
the target organ e.g. Graves disease.
. A.Direct Cellular Damage where lymphocytes or antibodies bind to cell- membrane
antigens, causing cellular lysis and/or an inflammatory response in the organ as a result of
which the damaged cellular structure is replaced by connective tissue (scar tissue) and the
function of the organ declines.
B. Stimulating or Blocking Auto-antibodies where antibodies act as agonists, binding to
hormone receptors in lieu of the normal ligand and stimulating inappropriate activity.This
usually leads to an over-production of mediators or an increase in cell growth.
Conversely, antibodies may act as antagonists, binding hormone receptors but blocking
receptor function.This generally causes impaired secretion of mediators and gradual atrophy of
the affected organ.

7. GRAVE’S DISEASE
Graves' disease is an autoimmune disease in which the patient's own immune system attacks
the thyroid gland, causing it to produce too much thyroxine.Thyroxine (T4) is a hormone
produced by the thyroid gland that has four iodine molecules attached to its molecular
structure.T4, as well as other thyroid hormones help regulate growth and control metabolism
in the body.

8. GRAVE’S DISEASE
ImportantThyroid-Related Hormones and Elements
TSH
T3
T4
Iodine
Thyroid Stimulating Hormone; secreted by the pituitary gland. Stimulates the thyroid, causing it
to release thyroid hormones.
Triiodothyronine; a less abundant but more potent thyroid hormone. Aids in regulating
metabolism and heart rate.
Thyroxine; the most important thyroid hormone. Processes iodine in the thyroid, affects
mitochondrial activity, regulates protein synthesis and breakdown and carbohydrate
metabolism.This hormone stimulates the central nervous system and the endocrine system,
and remains active in the body for up to a month.Too much thyroxine can cause over-
stimulation of the nervous/endocrine systems as well as increased metabolism
An important element necessary for healthy thyroid functioning.Too much stored iodine in the
thyroid is a sign of Iodine hyperthyroidism. Iodine deficiency or allergy can result in a goiter
(swollen thyroid gland).

9. ORGAN-SPECIFIC AUTOIMMUNE DISEASES
•Production of thyroid hormones is regulated by thyroid-stimulating
hormones (TSH)
•The binding ofTSH to a receptor on thyroid cells activates adenylate cyclase
and stimulates the synthesis of two thyroid hormones: thyroxine and
triiodothyronine
•A person with Grave’s Disease makes auto-antibodies to the receptor forTSH.
The binding of these auto-antibodies to the receptor mimics the normal action
ofTSH, without the regulation, leading to overstimulation of the thyroid
•The auto-antibodies are called long- acting thyroid stimulating hormones

10. Symptoms :
▪ Anxiety
▪ Breast enlargement in men (possible)
▪ Double vision
▪ Eyeballs that stick out (exophthalmos)
▪ Eye irritation and tearing
▪ Fatigue
▪ Goiter (possible)
• Heat intolerance
• Increased appetites
• Increased sweating
• Insomnia
• Irregular menstrual periods in women Muscle
• weakness Nervousness Rapid or irregular heartbeat
(palpitations or arrhythmia)
• Restlessness and difficulty sleeping
• Shortness of breath with activity Weight loss
(rarely, weight gain)

11. Tests to diagnose Graves' disease
Thyroid function tests -A blood sample is sent to a lab to see if your body has the right
amount of thyroid hormone (T4) andTSH. A high level of thyroid hormone in the blood plus a
low level ofTSH is a sign of overactive thyroid. Sometimes, routine screening of thyroid
function reveals mild overactive thyroid in a person without symptoms. In such cases, doctors
might suggest treatment or watchful waiting to see if levels return to normal.
Radioactive iodine uptake (RAIU) - An RAIU tells how much iodine the thyroid takes up.The
thyroid takes up iodine and uses it to make thyroid hormone.A high uptake suggests Graves'
disease.This test can be helpful in ruling out other possible causes of overactive thyroid.
Antibody tests -A blood sample is sent to a lab to look for antibodies that suggest Graves'
disease.

12. Treatment
Treatment is aimed at controlling your overactive thyroid. Medicines called beta-blockers are
often used to treat symptoms of rapid heart rate, sweating, and anxiety until the
hyperthyroidism is controlled. Hyperthyroidism is treated with one or more of the following:
Antithyroid medications and Radioactive iodine
Surgery If you have radiation or surgery, you will need to take replacement thyroid hormones
for the rest of your life, because these treatments destroy or remove the gland.

13. SYSTEMIC AUTOIMMUNE DISEASES
In this type, the immune response is not directed to a target antigen unique to a single organ or
gland, rather it is directed to any different organs, tissues, and cells of the body.
Eg- Systemic lupus erythematosus.
Systemic lupus erythematosus.
▪ The word “lupus” comes from the latin word “for wolf” –means- “ to reflect the mask like
appearance”, that client have when they have a lupus facial rash.
▪ The rash is red and thus the word erythematosus, meaning reddened, was added to describe
the disease.

14. SYSTEMIC AUTOIMMUNE DISEASES
Characteristics of SLE
▪ Appearance of blood red spots over the bridge of nose & cheeks.The lesions take the shape
of a butterfly.
▪ Connective tissues of the skin, kidney, heart. Speel & blood vessels are severely damaged
resulting in joint pain, fever & anemia.
▪ Glomerulonephritis due to deposition of immune complex in the glomerulus region.
▪ It is a systemic disease affecting the whole body

15. SYSTEMIC AUTOIMMUNE DISEASES
Affects the
▪ Skin
▪ Joints
▪ Serous membranes
▪ Renal system
▪ Hematologic system
▪ Neurologic system

16. RISK FACTORS
▪ Most clients with lupus have the systemic type, but a small percentage have the type that
affect only the skin , a condition called “DISCOID LUPUS ERYTHEMATOSUS”.
▪ Discoid lupus is not life threatening.
▪ SLE can be life threatening -progressive systemic inflammatory disease that can cause major
body organ and system failure.
▪ Although this definition seems similar to the definition of rheumatoid arthritis; one distinct
difference exists, client with SLE typically have more body organ development earlier in their
disease than the clients with R.A.

17. SYSTEMIC LUPUS ERYTHEMATOSUS (SLE)
• Chronic, multi-system inflammatory disease with protean manifestations and remitting
course
Clinical manifestations
– Musculoskeletal (joint and muscle pain)
– Dermatological (malar rash)
– Renal (glomerulonephritis)
Female to male ratio of 9:1
Etiology is unknown
• Genetics, race, hormones, environment

18. Diagnosis
General tests
▪ C Reactive Protein
▪ Autoantibody titers (anti DNA, anti phospholipids, etc)
▪ Presence of Rheumatoid Factor
Disease specific tests
▪ Neurological exam – MS
▪ Fasting glucose

19. Treatment
Anti-inflammatory drugs
• NSAIDS, Corticosteroids
Immunosuppressant drugs
• Methotrexate
• Radiation
• Plasmapheresis
Cell Blocking Reagents
• aCD20 (Rituxan)
• aCD3 (Teplizumab)
Cytokine Blocking Reagents
•TNF (Humira, Enbrel)

20. Current Therapies
• Immunosuppressive drugs - corticosteroids, azathioprine - slows the proliferation of
lymphocytes
• Cyclosporine A - blocks signal transduction mediated by theTCR (inhibits only antigen-
activatedT cells while sparing non- activated ones)
•Thymectomy - removal of thymus from patients with myasthenia gravis
• Plasmapheresis - removes antigen-antibody complexes for a short- term reduction in
symptoms

21. Summary
▪ Autoimmune diseases and conditions exist when body produces abnormal cells, which attack
body, itself
• Most autoimmune diseases strike women more than men
▪ The causes of autoimmune diseases are not but some autoimmune diseases seem torun in
families
▪ Strike any part of the body, symptoms vary widely and diagnosis and treatment are often
difficult
• Medical science is striving to design therapies that prevent autoimmune diseases