Immunology – Pathology · FCPS Part 1

One Liners

AIDS screening = ELISA
AIDS Confirmatory = Westren Blot
Cryptosporidia is a protozoan parasite that causes severe, chronic, watery diarrhea in immunocompromised individuals, particularly those with advanced HIV/AIDS.
Cryptococus = microscopically as an "oval cell with a halo" = in an immunosuppressed patient
Raspergillus = Chronic fungal infection causing rhinosinusitis with granuloma
Pneumocysitosis carini = HIV most serious complication
Mucormycosis Facial pain, headache, and a characteristic black necrotic eschar in the nasal cavity or palate in a patient with Diabetic Ketoacidosis (DKA) are classic diagnostic features of Rhinocerebral Mucormycosis
Most common system organ involved with histoplasmosis = Reticuoendothelial
Thermophillic actinomyces = Farmers lung & Humidifier fever
HLA B27 = Causes ankylosing spondolitis
Aspergillosis = Non fungal rhinits
Birbeck granules are distinctive, rod- or tennis-racket-shaped cytoplasmic inclusions seen on electron microscopy = Langerhans cells.

HIV

IMMUNE DYSFUNCTION

Hypersensitivity Reactions

Hypersensitivity occurs when an immune response causes tissue injury.

Four types

Type	Mechanism	Main mediators	Examples
I	Immediate hypersensitivity	IgE, mast cells	Anaphylaxis, allergic rhinitis, urticaria
II	Antibody-mediated	IgG or IgM against cell or matrix antigens	Autoimmune hemolytic anemia, Goodpasture syndrome
III	Immune-complex mediated	Antigen–antibody complexes and complement	SLE, serum sickness, Arthus reaction
IV	Delayed T-cell-mediated	T lymphocytes and macrophages	Contact dermatitis, tuberculin reaction

Type I Hypersensitivity

Mechanism

Initial allergen exposure promotes Th2 responses.
IL-4 and IL-13 support IgE class switching.
IgE binds FcεRI receptors on mast cells.
Re-exposure cross-links surface-bound IgE.
Mast cells release histamine and other inflammatory mediators.

Examples

Anaphylaxis.
Allergic rhinitis.
Atopic asthma.
Urticaria.
Some food allergies.

MCQ tip: Type I = IgE + mast cells + immediate reaction.

Type II Hypersensitivity

Antibodies react with antigens on cells or extracellular structures, producing injury or altered cellular function.

Mechanisms include:

Complement activation.
Opsonization and phagocytosis.
Antibody-dependent cellular cytotoxicity.
Receptor stimulation or blockade.

Examples

Disorder	Mechanism
Autoimmune hemolytic anemia	Antibody-mediated red cell destruction
Goodpasture syndrome	Antibodies against basement membrane antigens
Myasthenia gravis	Antibodies impair acetylcholine receptor function
Graves disease	Antibodies stimulate TSH receptors
Pemphigus vulgaris	Antibodies against desmosomal proteins

Dental relevance

Pemphigus vulgaris frequently presents with painful oral erosions and may show a positive Nikolsky sign.

Type III Hypersensitivity

Antigen–antibody complexes form and deposit in tissues, activating complement and recruiting inflammatory cells.

Examples

Systemic lupus erythematosus.
Serum sickness.
Arthus reaction.
Certain forms of glomerulonephritis (Post Streptococcal)

Remember: Type III = immune-complex deposition.

Type IV Hypersensitivity

Type IV reactions are mediated by sensitized T lymphocytes rather than antibodies.

Mechanisms

Th1 cells activate macrophages.
Th17 cells promote inflammatory cell recruitment.
Cytotoxic T cells can directly damage target cells.

Examples

Contact dermatitis.
Tuberculin skin test.
Granulomatous inflammation.
Certain transplant rejection reactions.

MCQ tip: Type IV = T-cell mediated and classically delayed 48–72 hours.

Autoimmune Diseases

Autoimmune diseases occur when immune tolerance to self-antigens is lost.

Disease	Major association
SLE	ANA, anti-dsDNA, anti-Sm
Rheumatoid arthritis	Rheumatoid factor and anti-CCP
Sjögren syndrome	Anti-SSA/Ro and anti-SSB/La
Systemic sclerosis	Anti-centromere or anti-Scl-70
Polymyositis/dermatomyositis	Inflammatory muscle disease; selected myositis antibodies

Systemic lupus erythematosus

A multisystem autoimmune disorder involving autoantibody formation and immune-complex-mediated tissue injury.

Typical features include:

Malar rash.
Photosensitivity.
Arthritis.
Renal disease.
Hematologic abnormalities.
Oral ulcers.

Sjögren syndrome

Characterized by autoimmune damage to exocrine glands.

Typical findings:

Xerostomia.
Keratoconjunctivitis sicca.
Increased dental caries risk.
Salivary gland enlargement in some patients.

Dental relevance: Sjögren syndrome is particularly important because reduced salivary flow can cause rampant caries, oral candidiasis and swallowing difficulties.

Immunodeficiency Disorders

Primary immunodeficiencies

Disorder	Main defect	Classic clue
DiGeorge syndrome	Thymic developmental abnormality	T-cell deficiency, hypocalcemia
Bruton agammaglobulinemia	BTK mutation	Very low B cells and immunoglobulins
SCID	Severe defects in T-cell development/function, often affecting other lymphocytes	Severe recurrent infections in infancy
Common variable immunodeficiency	Impaired antibody production	Recurrent sinopulmonary infections
Wiskott–Aldrich syndrome	WAS gene defect	Eczema, infections, thrombocytopenia with small platelets
Chronic granulomatous disease	NADPH oxidase defect	Recurrent infections with catalase-positive organisms
Leukocyte adhesion deficiency	Defective leukocyte adhesion	Delayed umbilical cord separation, recurrent bacterial infections

Secondary immunodeficiencies

May occur with:

HIV infection.
Malnutrition.
Immunosuppressive medications.
Malignancy.
Chronic systemic disease.

HIV/AIDS

HIV targets CD4-positive cells, progressively impairing cellular immunity.

AIDS may be diagnosed by a CD4 count below 200 cells/µL or by the presence of an AIDS-defining condition in a person with HIV.

Oral manifestations of HIV

Oral candidiasis.
Oral hairy leukoplakia.
Recurrent oral ulceration.
Kaposi sarcoma.
Certain periodontal diseases.

Antibodies

Feature	🟦 IgG	🟩 IgA	🟥 IgM	🟨 IgE	🟪 IgD
Main location	Blood + tissues	Mucosal secretions	Mainly blood	Mast cells & basophils	Surface of naïve B cells
Structure	Monomer	Dimer in secretions	Pentamer	Monomer	Monomer
Most abundant in serum	✅ Yes	No	No	No	No
First antibody produced	No	No	✅ Yes	No	No
Major antibody in secondary response	✅ Yes	Important	Less important	No	No
Crosses placenta	✅ Yes	❌	❌	❌	❌
Complement activation	Yes	Weak/No	Strongest	❌	❌
Opsonization	✅ Major	Limited	Limited	❌	❌
Mucosal protection	Some	✅ Major	❌	❌	❌
Breast milk	Some	✅ Major	❌	❌	❌
Allergy / anaphylaxis	❌	❌	❌	✅ Major	❌
Helminth/parasite defense	Some	Some	❌	✅ Major	❌
B-cell receptor	❌	❌	✅	❌	✅
Key association	Placenta + opsonization + long-term immunity	Mucosa + secretions	First + pentamer + complement	Allergy + parasites	Naïve B cells

RECAP

Feature	Type I	Type II	Type III	Type IV
Other name	Immediate / Anaphylactic	Antibody-mediated / Cytotoxic	Immune-complex	Delayed-type
Main mediator	IgE	IgG, IgM	IgG, IgM	T cells
Target	Allergens	Antigens on cells, tissues or receptors	Soluble antigen-antibody complexes	Antigens recognized by T cells
Main cells	Mast cells, basophils, eosinophils	Neutrophils, macrophages, NK cells	Neutrophils	T lymphocytes, macrophages
Complement	Usually not important	Often important	Very important	❌ Not involved
Mechanism	Allergen → IgE → mast-cell degranulation	Antibody binds target → destruction or altered function	Immune complexes deposit → complement → inflammation	T cells release cytokines and/or directly kill cells
Onset	Minutes	Hours	Hours–days	48–72 h
Hallmark	Allergy / histamine	Antibody attacks specific target	Immune-complex deposition	Delayed T-cell response
Examples	Anaphylaxis, allergic rhinitis, asthma, urticaria	Graves, myasthenia gravis, Goodpasture, autoimmune hemolytic anemia, erythroblastosis fetalis	SLE, serum sickness, Arthus reaction, post-streptococcal GN	TB skin test Contact dermatitis type 1 DM sarcoidosis Hashimoto thyroiditis acute interstitial nephritis, aplastic anemia

Molecule / Component	Primary Secretory Source / Origin	Major Functions & Immunological Roles
Interleukin-2 (IL-2)	Activated CD4+ Helper T cells	* Autocrine and paracrine growth factor for T cells * Drives T-cell proliferation and clonal expansion * Enhances NK cell activity and cytotoxic T-cell function
Interleukin-1 (IL-1)	Activated Macrophages, monocytes, dendritic cells, and endothelial cells	* Pro-inflammatory mediator * Acts on the hypothalamus to induce fever * Stimulates endothelial adhesion molecules and acute-phase protein release
Interleukin-6 (IL-6)	Macrophages, dendritic cells, T cells, and endothelial cells	* Stimulates hepatic synthesis of acute-phase proteins (e.g., CRP) * Promotes B-cell differentiation into antibody-secreting plasma cells * Induces fever and neutrophil production
Complement C3b	Cleavage product of C3 (produced primarily by Hepatocytes)	* Functions as a powerful opsonin for phagocytosis * Binds antigen-antibody complexes for clearance * Forms part of C5 convertase to initiate the membrane attack complex (MAC)