Defends body against injury Responds after the inflammatory response Works in background of an already activated inflammatory response
The Immune Response differs from inflammatory response
Differs in that it remembers and responds more quickly to foreign substances that enter the body a second time.
Foreign substances against which the immune response defends the body. Autoimmune disease parts of an individuals own body become antigens.
Cells involved in the Immune Response
1. T lymphocytes 2. B lymphocytes 3. Natural killer cells 4. Macrophages 5. Cytokines
Originate in bone marrow and travel to thymus. Thymus gets small as get older (processed into mature cells). FIRST LINE OF DEFENSE AGAINST INTRACELLULAR BACTERIA.
Plasma cells derived from stem cells in bone marrow. 20-25% of WBC
Natural killer cells and Macrophages
Involved in phagocytosis
A T cell receptor located on surface of T cell. Linked to protein complex (CD3). Used to recognize antigens and fight them off. Inherited and is in all cells except natural kill cells.
Essential for activity of T cells
Types of T lymphocytes
1. T-helper (T4) 2.T-suppressor and T-cytotoxic (T8)
T4 cell marker - CD4. Enhance antibody response. Assists B cells in producing antibodies.
T8 marker. Suppress or turn off the functioning B lymphocytes.
T8 marker. Surveillance against or attacking tumor cells directly.
Normal blood ratio
CD4:CD8 ratio is 2:1
CD4 cells are selectively lost and the CD4 and CD8 ratio is less than 1:0
Two groups of T-helper cells
T-helper-1 (Th1) T-helper-2 (Th2)
Cells that synthesize interleukin-2 (IL2) and interferon-gamma(IFN-y). Stimulate macrophages to become phagocytic and mediate the formation of granulomas to influence the immune system.
Synthesizes IL-4, IL-5 and IL-13. Secretion of IgE and other immunoglobulins and activation of eosinophils which influence immune system.
Two types of B lymphocytes
Plasma cells B memory cells
B lymphocytes become plasma cells...
When stimulated by antigen
Produce specific antibody needed to fight the antigen. Produce proteins called antibodies (immunoglobulins - Ig)
Types of immunoglobulins carried in blood stream
1.IgG 2.IgM 3.IgE 4.IgA 5.IgD
Digestive tract, most common, can pass to baby.
Appears first usually, largest in number.
Allergic reaction, production of histamines.
Found in saliva.
Most often found in B cells.
B memory cells
Retains memory of a previously encountered antigen. Duplicate itself. Capacity to remember.
Natural killer cells
Cells do NOT have TCR gene rearrangement. React against virus-infected cells and kill tumor and foreign cells with our previous sensitization.
Response to antigen. Present in CT. Involved in Phagocytosis. Amplify the immune system (make stronger). Does NOT remember encountered antigen.
The B and T lymphocytes that produce cytokines.
Macrophages serve as the link between...
Inflammatory and Immune Responses
Proteins that assist in communication of lymphocytes. Activate macrophages and enhance their function.
Produced by B and T cells. Cause cytokines to have different function.
Produced by macrophages (Interferon is a common monokine).
Antibody-antigen reaction (when antibodies combine with antigen).
Show levels of antibody in the blood stream.
Two major divisions of Immune Response
1. Humoral Response 2. Cell-mediated Response (they are inter-related)
Produces antibodies. B lymphocytes are primary cells. Defend against bacteria and viruses.
Lymphocytes working alone. T lymphocytes are assisted by macrophages.
Using antibodies produced by another person. Natural = from mother to child Acquired = immunization/injection
Body produces antibodies to protect against antigens. Natural = getting sick Acquired = vaccine/immunization
Type I Hypersensitivity Reaction
Anaphylaxis. Occurs within mins. Plasma cells produce IgE. IgE causes mast cells to release histamine. Life threatening. ASTHMA ATTACK, ALLERGIC RXS TO MEDICINE.
Type II Hypersensitivity Reaction
Antibodies combine with antigen. ACTIVATE IgG and IgM. Destruction of tissue. Rhesus incompatibility (RH incompatibility) - mother with negative blood type, Graves disease.
Type III Hypersensitivity Reaction
Immune complexes are deposited in various tissues and cause acute inflammation. Neutrophils are attracted to tissues. Phagocytosis and death of neutrophil. Lysosomal enzymes are released and causes tissue destruction. Systemic Lupus.
Type IV Hypersensitivity Reaction (Delayed)
Drugs act as antigens and cause an immunologically induced inflammatory response. Involved a cell-mediated immune response. T lymphocytes cause damage to the tissue cells. Tuberculin test PPD. Rejection of tissue grafts and transplanted organisms.
Canker sores. Affect about 20% of the population.
Etiology of Aphthous Ulcers
Varied, unclear. May be from foods, trauma, stress, depleted immune system, smoking, hormones, genetics, alcohol, etc.
Occurs in people who have fevers. Confused with herpes.
Histology of Aphthous Ulcers
CD4 to CD8 lymphocyte ratio decreases. Cell mediated immunity. Histocytes, PMNs and Macrophages present. T cytotoxicity ulcerations.
Types of Aphthous Ulcers
Minor Major Herpetiform
Minor Aphthous Ulcer
Most common. Discrete round to oval ulcers up to 1 cm in diameter. May be single or multiple. Surrounded by a erythematous halo. May have yellowish-white fibrinous membrane over top. Ulcers not preceded by vesicles.
Minor aphthous ulcers heal in
7-10 days. Prodomal burning for 1-2 days.
Minor aphthous ulcers occur on
Movable nonkeratinized mucosa
Major Aphthous Ulcer
More severe form. 1-3 cm in diameter, 1-10 in number. Heal with a scar. Resembles squamous cell carcinoma (biopsy to confirm). AIDS patients.
Major aphthous ulcers heal in
Major aphthous ulcers occur on
Labial mucosa, soft palate and tonsillare
Herpetiform aphthous ulcer
Greater number of lesions and more frequent recurrence. 1-3 mm in diameter and up to 100 lesions. Resemble primary herpes.
Herpetiform aphthous ulcers heal in
Herpetiform aphthous ulcers occur
Diagnosis of Aphthous Ulcers
Liquid tetracycline (herpes will not respond). Systemic disease may be associated.
Hives. Multiple areas of well demarcated swellings on skin. Pruritis (itching), Loc areas of vascular permeability. Release of histamine (IgE, IgG or IgM).
Soft, swollen areas under skin. Diffuse swelling of tissue caused by permeability of deeper BV's. Subcutaneous and submucosal CT. No pruritus (itching). Respiratory and GI. Histamine released (IgE, IgG or IgM).
Red, burning pruritus. Smooth shiny appearance, firm to palpation. Small vesicles.
Fixed drug eruption
Single or multiple. Raised, red patches or cluster of macules on skin. Pain and pruritus. Related to Type III hypersensitivity - immune complexes are deposited along the endothelial wall of BV, causing vasculitis and damage, rise to erythema and edema.
Vesticulobubous disease. Skin and mucous membranes affected. Acute or chronic. Etiology unknown (hypersensitivity).
Precipitating Factors of Erythema Multiforme
Bacterial, Fungal, Viral, Infections, Stress and Allergies (drugs)
More severe form of Erythema Multiforme. Similar skin and oral lesions, more widespread and more severe. May lead to blindness.
Stevens-Johnson Syndrome Classic traid
Eye lesions (conjunctivitis) Genital lesion Lips (encrusted and bleed)
All types of Erythema Multiforme may be mistaken for
Treatment of Stevens-Johnson Syndrome
Hospitalization, resolves in 6 weeks, systemic corticosteroid, systemic antiviral medications.
Common, chronic dermatologic disease that affects oral mucosa. Exacerbation and remission. Wickham striae (interconnecting white lines and circles). Small, papular, pinhead sized doomed or hemispheric glistening white nodules.
Most common location of Lichen Planus
Etiology of Lichen Planus
Unknown (stress, drugs or chemicals)
Types of Lichen Planus
Reticular Lichen Planus
Most common. Has gingival and skin lesions.
Gingival lesions of Reticular Lichen Planus
Wickham striae along with white slighty raised white plaque areas. Desquamative gingivitis (gingiva slough away in layers). Can be asymptomatic.
Skins lesions of Reticular Lichen Planus
2-4 mm papules. Wickham Striae. Affects lumbar region, flexor wrist and anterior surface of the ankles.
Erosive/Bullous Lichen Planus
Epithelium separates from the CT and erosions, bullae or ulcers form. Most common site is buccal mucosa. GIngival lesions look like desquamative gingivitis.
Histology of Lichen Planus
Chronic, orthokeratosis and parakeratosis, thickness of spinous layer can vary, rete ridges may be absent or hyperplastic or saw toothed, destruction of the basal cell layer, T lymphocytes.
Treatment of Lichen Planus
Corticosteroid, topical cyclosporin, may have increased risk of squamous cell carcinoma.
Reiter's Syndrome (Reactive Arthritis)
Abnormal immune response. Benign and self-limiting.
Triad of Reiter's Syndrome
Arthritis (inflammation/destruction of joints) Urethritis (inflammation of urethra) Conjunctivitis (inflammation of eye covering)
Etiology of Reiter's Syndrome
Unclear, maybe genetic. Antigenic marker (HLA-B27). Develop in 1-4 weeks after venereal or GI.
Reiter's Syndrome oral lesions
Aphthous like ulcers Red lesions Geographic tongue like lesions
Treatment of Reiter's Syndrome
Non steroidal anti inflammatory drugs
Langerhan Cell Disease (Histiocytosis X)
Eosinophils abundance, Langerhan cells (related to macrophages and histocytes), Etiology unknown.
Types of Langerhan Cell Disease
Letterer-Siwe (acute disseminated form) Hand-Schuller-Christian (chronic disseminated) Eosinophilic granuloma of bone (solitary or chronic)
Letterer-Siwe (acute disseminated form)
Acute, affects children younger than 3 years old, seldom have oral lesions, resembles lymphoma, fatal-rapid, responds to chemo therapy.
Hand-Schuller-Christian (chronic disseminated)
Affects children less than 5 years old. Triad occurs in 25% of patients.
Radiolucent area in skull (punched out) Unilateral or bilateral exophthalmus Diabetes with gradual onset (collection macrophages in sella turcica affecting the pituitary gland)
Eosinophilic granuloma of bone (solitary or chronic)
Affects older children and young adults. Involves skull and mandible. Radiographically may resemble widened PDL; circumscribed radiolucency, perapical inflammation.
Multisystem disease with skin and oral manifestation (heart and kidneys).
Signs and symptoms of Systemic lupus erythematous
Clinical: fever, weight loss, arthritis and fatigue Gen. malaise, BUTTERFLY RASH on bridge of nose, kidney failure is most significant aspect of disease. Cardiac involvement, heptomegaly, splenomegaly. RENAL FAILURE is MOST COMMON CAUSE OF DEATH. Need medical consult.
Most common initial complaint of Systemic Lupus
Arthritis and Arthralgia (pain)
Skin lesions of Systemic Lupus
Telangiectasias (red papules that look like can have black heads occurring).
Oral lesions of Systemic Lupus
Resemble lichen planus Erythema Hyperkeratosis
Chronic Cutaneous Lupus
Few or no systemic signs or symptoms. Lesions limited to skin or mucosa. Scaly, erythematous patches that increase with sun exposure. Oral lesions may be identical to erosive lichen planus.
Histology of Lupus
Increase in B lymphocyte activity and abnormal T lymphocyte function. Hyperkeratosis. Degeneration of basal cell layer.
Serious skin disease. Chronic. Autoimmune disease that affects adults from Mediterranean, South Asia or Jewish.
Oral lesions of Pemphigus Vulgaris
Ulcerations, vesicle or bullae may be first to appear. Halatosis. Vesicle or bullae that rupture and bleed leaving a denuded surface. Bulla are fragile (difficult to see). Nikolsky's sign (Bulla appear with firm pressure, desquamative gingivitis).
Skins lesions of Pemphigus Vulgaris
Erythema Vesicles Bulla Erosions Ulcers Crusted lips that bleed
Occular, oval vaginal and pharyngeal mucosa lesions. Gingiva is most common oral site. Erythematous and ulcerative gingiva (desquamative gingivitis). Nikolksy's sign. Bulla (less fragile then Pemphigus vulgaris). More serious occular involvement (scarring, symblepharons - adhesions).