Notes on Immunopathology

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Cells of immune system:

• Innate and acquired (specific).

• IgM = synthesized at birth; congenital infection if already present in newborn.

• IgG = synthesized at 2 months of age; maternally derived if present in newborn.

MHC:

• Chromosome 6.

• Class I: present on all nucleated cells; recognized by CD8 T cells and NK cells.

• Class II: present on B cells, macrophages, and dendritic cells; recognized by CD4 T cells.

• HLA-B27: ankylosing spondylitis.

• HLA-DR2: MS.

• HLA-DR3/4: type 1 DM.

HLA:

• Tested in donor and acceptor graft recipient.

• Tested HLA-A, -B, and -C; also determining any disease risk.

Types of immune cells:

CD-4 secrete:

IL-2:

• Causes CD4/8 proliferation.

Gamma-interferon:

• Macrophage activation.

CD-8:

• Kill virus-infected cells.

Hypersensitive reactions:

Type I (immediate) Hypersensitive reaction:

• IgE mediated allergy.

• May cause anaphylactic shock.

• Mast cells activated; inflamed response.

• Allergens to APCs to CD-4 TH-cells to IL to B cell maturation.

IL-4:

• IgM switched to IgE synthesis.

IL-5:

• Epsinophils.

• Early (histamine, chemotactic factors) and late (prostaglandins, leukotrienes) phase reactions by mast cells.

Treatment:

Desensitization therapy: IgG injections; IgG coats allergens, and prevents mast cells from binding to them.)

Tests:

• Scratch test: wheal-and-flare reaction

• Radioimmunosorbent test: IgE antibody detection in serum.

Type II Hypersensitive reaction:

Examples:

• Goodpasture's syndrome, autoimmune hemolytic anemia of newborn, myasthenia gravis, Grave's disease.

• Antibody-dependent cytotoxic reactions.

Complement-dependent (IgG, IgM):

• Lysis by MAC.

• Phagocytosis.

Complement-independent (IgG, IgE).

Tests:

• Coombs' test: indirect (antibodies in serum) and direct (C3b or IgG).

Type III Hypersensitive reaction:

• Antigen-antibody complexes activate complement.

• Eg., serum sickness, SLE.

• First exposure: antibody synthesis.

• Second exposure: antibody-antigen deposition; complement activation by C5a.

• Arthus reaction seen.

Tests:

• Immunofluorescent staining.

Type IV Hypersensitive reaction:

• Cellular immunity.

• Antibody-independent T cell-mediated reactions.

• Eg., contact dermatitis, cytotoxicity.

• antibody-independent T-cell mediated reactions.

• Delayed reaction hypersensitivity: CD4 activated.

• Cell-mediated cytotoxicity; CD8 activated.

Tests:

• Patch test; skin reaction to Candida.

Transplantation immunology:

• ABO blood group compatibility.

• Best chance of success with matching HLA-A,-B,-D loci.

Rejection reactions:

Hyperacute:

• Recipient ABO incompatibility or preformed anti-HLA antibodies react against donor.

• Type II hypersensitivity reaction.

• Eg., blood group A person receives blood group B heart.

Acute:

• Type IV: CD4 T cells activate macrophages; CD8 proliferation; donor-graft destruction.

• antibody-mediated type II hypersensitivity reaction: CD4 T cells activate B-cells.

Treatment:

• Immunosupressive agents; risk for cervical squamous cell cancer, malignant lymphoma, squamous cell carcinoma of skin.

Chronic:

• Irreversible reaction that occurs over months to years.

Graft-vs-host reaction:

• Donor T cells activate host CD4/8 T cells.

• Bile duct necrosis, jaundice, diarrhea, dermatitis.

Systemic lupus erythematous (SLE):

• Child-bearing age.

• B-cell activation after exposure to certain triggers (eg., procainamide).

• Affects: blood, lymph nodes, joints, skin, heart, lungs, and kidneys.

• IgG anti-SS-A (Ro) antibodies cross placenta and cause neonatal heart block.

Drug-induced SLE:

• Procainamide, and hydrazaline.

• Findings: Anti-histone antibodies; low CNS and renal involvement.

Lab findings in SLE:

• ANA in almost all cases.

• Anti-dsDNA antibodies and anti-Sm antibodies: very specific.

• Anti-Ro antibodies.

• Anti-phospholipid antibodies: vessel damage and thrombosis.

• Anti-cardiolipin antibodies: may generate false-positive syphilis test.

Systemic sclerosis (scleroderma):

• Small vessel endothelial damage; ischemic injury.

• Excess cytokines cause excess collagen synthesis.

• Raynaud's phenomenon.

• Tightened facial features; also affects GI, lungs, kidneys.

• Calcification of subcutaneous tissue, dysphagia, esophageal reflux.

• Lungs, kidneys also affected.

• Serum ANA +.

• Anti-topoisomerase antibody.

• Anti-centromere antibodies.

• CREST syndrome.

Dermatomyositis (PM/DM):

• Women 40-60 age.

• Two types: PM (no skin involvement) and DM (skin involvement).

• Malignant neoplasms like lung cancer.

• Muscle pain, atrophy, raccoon eyes.

• Serum ANA +; increased CK.

Mixed connective tissue disease:

• Similar to SLE, systemic sclerosis, PM/DM.

• Anti-ribonucleoprotein antibodies.

Immune disorders:

Bruton's agammaglobinemia:

• B cells fail to mature; mutated tyrosine kinase; XR.

IgA deficiency:

• IgA B cells fail to mature.

Common variable immunodeficiency:

• B-cells fail to become plasma cells.

DiGeorge syndrome:

• 3rd and 4th pharyngeal pouches fail to develop; no thymus / parathyroid.

SCID:

• Adenosine deaminase deficiency; B/T cells fail to develop.

AIDS:

• RNA retrovirus.

• HIV 1: US.

• HIV 2: developing countries.

• HIV envelope protein gp120 attaches to CD4 T-cell.

• Infects all APCs.

• Macrophages and dendritic cells are reservoirs for the virus.

Tests:

• ELISA (screening), Western blot (confirmatory test), p24 antigen (indicates active viral replication).

Phases:

• Acute, latent, early symptomatic.

• CD4 T-cell count less than 200 cells/mL.

• Most common infection: cryptococcosis.

Complement disorder:

Hereditary angioedema:

• AD; deficiency of C1 esterase inhibitor; swelling of face and oropharynx.

• Classic and complement pathways.

• MAC is common for both pathways.

• C4/C2 decreased: classic pathway activated.

• Factor B decreased: alternate pathway activated.

• C3 decreased: activation of either system.

Amyloidosis:

• Fibrillar protein deposition causing organ dysfunction.

• Abnormal protein folding.

• Beta-pleated sheets.

• Apple green-colored birefringence in polarized light.

• Eosinophilic staining with H and E stain.

• Three major types of amyloid proteins: AL, AA, A-beta.

• Systemic: primary or secondary; multiorgan; seen in tuberculosis and rheumatoid arthritis.

• Localized: confined to a specific organ; seen in Alzheimer's disease.

• Hereditary: AR disorder involving AA amyloid.

• Tests: immunoelectrophoresis, tissue biopsy.

Additional Reading:

Basic Pathology

1. Cell Injury
2. Inflammation and Repair
3. Immunopathology
4. Water, Electrolyte, Acid-Base, Hemodynamic Disorders
5. Genetic and Developmental Disorders
6. Environmental Pathology
7. Nutritional Disorders
8. Neoplasia
9. Vascular Disorders
10. Heart Disorders
11. Red Blood Cell Disorders
12. White Blood Cell Disorders
13. Lymphoid Tissue Disorders
14. Hemostasis Disorders
15. Blood Banking and Transfusion Disorders
16. Upper and Lower Respiratory Disorders
17. Gastrointestinal Disorders
18. Hepatobiliary and Pancreatic Disorders
19. Kidney Disorders
20. Lower Urinary Tract and Male Reproductive Disorders
21. Female Reproductive and Breast Disorders
22. Endocrine Disorders
23. Musculoskeletal Disorders
24. Skin Disorders
25. Nervous System Disorders
26. Notes on Tissue Regeneration
27. A Table of Bleeding Disorders
28. FAQ on Structure and Function of Red Blood Cells
29. FAQ on Components of Blood
30. Notes on Hemostatic Mechanisms
31. What is Fever?
32. What is Edema?
33. FAQ on Blood Pressure
34. FAQ on principles of fluid and flow dynamics of Blood
35. Causes of Thrombocytopenia
36. Squamous cell carcinoma of head and neck mucosa
37. Four tumors which never metastasize to the brain
38. What is caustic injury?
39. What causes Peripheral Edema?

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