Autoimmunity Flashcards
Autoimmunity
Immune reactions directed at self-antigens.
No cure for most.
Allergic vs autoimmune hypersensitivity depends on
Antigen and duration of response
Autoimmunity. What antigen and what duration?
Environmental antigen and chronic duration.
Lately limited to type II, III, and IV hypersensitivities.
Does not resolve with removal of environmental agent.
Does autoimmunity resolve with removal of environmental agent?
NO
Allergies, however, will resolve if you remove the ag.
Allergy. What antigen and duration?
Environmental antigen and limited duration. Allergies resolve with removal of environmental antigen.
How many autoimmune diseases known?
Over 80
What % of autoimmune patients are women
75%
Single gene or multigenic?
multi. Makes it harder to pinpoint what causes someone to develop an autoimmune disease.
Most affected organs and tissues
Bone marrow Lining of joints Blood vessels Connective tissues Endocrine glands Kidneys Muscles Skin
3 main things that can cause autoimmunity
- Multigenic.
- Hormonal
- Environmental triggers
- Infections
- drug induced
- toxins
All of these cause a breakdown of central or peripheral tolerance, resulting in an autoimmune disease.
What is a gene and what is an allele?
Gene= make Allele= model
There are MHCI and MHCII associated alleles that can increase risk of certain diseases.
Non HLA alleles include co-stimulatory molecules and cytokines.
MHCI associated allele
HLA B27. Can be a risk for acute anterior uveitis.
If not due to infection or injury and seems idiopathic, check to see if patient has this allele.
What 3 things could cause the breakdown of central and peripheral tolerance?
Faulty clonal deletion. Auto-reactive lymphocytes mature.
Loss of T reg cells. Results in hyper responsive T and B lymphocytes with prolonged immune response.
Abnormal expression of MHCII molecules.
Immunoprivileged organs
Eyes, BBB, testes. Prevents immune cells from entering organs.
What antigens can be used to cause an autoimmune disease
Sequestered Ag’s in immunopriviledged organs. AKA the lymphocytes have not had central tolerance to these antigens.
Infectious disease. Molecular mimicry. Requires original insult- exposure to pathogen before cross reactivity.
Type II auto antibodies directed at auto-antigens
Anti: DNA IgG (Rheumatoid factor) phospholipids (cardiolipin- component of bacterial and mitochondrial membrane) erythrocyte lymphocyte
4 autoimmune diseases type II
Acute rheumatic fever. due to strep.
Pernicious anemia. Loose ability to transport via B12 from gut to blood stream. Auto abs block transport molecule in Gi tract.
Myasthenia gravis. Auto Abs block muscle function.
Graves disease. Auto Abs stimulate thyroid gland.
Rheumatic fever
Strep pyogenes bacteria has M protein that is similar to proteins on valve in heart. Body will attack heart. Molecular mimicry.
Ocular manifestations of myasthenia gravis
Diplopia, ptosis, blurred vision
Ocular manifestations of graves disease
Proptosis (Thyroid Hormone acts on levator) which can cause exposure keratopathy.
Periorbital edema, abnormal EOMs, and optic nerve compression.
Type III infectious initiation (2)
reactive arthritis
Poststreptococcal glomerulonephritis
Type III undetermined initiation (2)
SLE, rheumatoid arthritis
Rhematoid arthritis shows which 2 types of hypersensitivities
Type III and IV
Uveitis could be due to which 2 autoimmune diseases
SLE, Reactive arthritis
PUK could be due to which 2 autoimmune diseases
Rheumatoid, polyarteritis nodosa (knots in artery)
K-sic could be secondary to which autoimmune disease
Sjogrens
Type IV autoimmune diseases
Chrons
Type I diabetes
MS
Rheumatoid Arthritis
How do systemic autoimmune diseases present?
Wide range of antigens and widespread damage
Ex: SLE, MS, scleroderma.
Could be types II, III, or IV
Who is more likely to be diagnosed with SLE
African american women that are genetically predisposed.
Auto antibodies against many cells and tissues in body.
How to be diagnosed with SLE
Must have greater than or equal to 4 symptoms to be diagnosed (out of 11)
Ocular manifestations of SLE
Episcleritis/scleritis
Neuro-ophthalmic lesions
Retinal vasculopathy (cotton wool spots due to complexes settling–> Hypoxic cells–> swelling)
Bulls eye maculopathy (sign of long term plaquenil use)
Primary and secondary forms of Sjogrens
Primary: Lymphocyte infiltration of salivary and lacrimal gland.
Secondary: Immune complex accumulation in salivary and lacrimal glands.
