Diseases of Immunity: Immune-Mediated Disorders

Master hypersensitivity, autoimmunity, immunodeficiency, transplant rejection, and amyloidosis for clinical practice

Role Play

Created byISO Horizon

Last updated 6/2026

English

What you'll learn

Explain innate and adaptive immunity, antigen presentation, and immunological memory
Differentiate the four Gell and Coombs hypersensitivity reactions with classic disease examples
Analyze mechanisms of self-tolerance and how their breakdown causes autoimmunity
Compare systemic and organ-specific autoimmune diseases including SLE, RA, and MS
Recognize primary immunodeficiency patterns from SCID to common variable immunodeficiency
Trace HIV pathogenesis from CD4 depletion to AIDS-defining opportunistic infections
Distinguish hyperacute, acute, and chronic graft rejection and graft-versus-host disease
Identify major immunosuppressive drug classes and their mechanisms of action
Classify amyloidosis subtypes and connect each to its underlying immunopathology
Apply immunological reasoning to interpret real clinical presentations

Course content

19 sections • 28 lectures

Innate Immunity: The First Line of Defense10:19
Explore the rapid, non-specific arm of immunity that greets every pathogen, including physical and chemical barriers, neutrophils, macrophages, dendritic cells, natural killer cells, the complement cascade, and pattern recognition receptors such as Toll-like receptors. Examine how pathogen-associated molecular patterns and damage-associated molecular patterns trigger inflammation, cytokine release, and the recruitment of leukocytes to infected tissues. Understand why innate immunity buys time for adaptive responses to mature and how its dysfunction sets the stage for many of the disorders covered later, framing the cellular cast and molecular signals that recur throughout immune-mediated disease.
Adaptive Immunity: T Cells, B Cells, and Specificity12:34
Step into the world of lymphocytes and the exquisitely specific defenses they mount. Learn how T cells mature in the thymus, how B cells develop in the bone marrow, and how somatic recombination generates the astronomical receptor diversity that lets the body recognize virtually any antigen. Distinguish CD4+ helper subsets such as Th1, Th2, Th17, and regulatory T cells from CD8+ cytotoxic T cells, and contrast humoral immunity driven by plasma cell antibody production with cell-mediated immunity. Understand clonal selection, affinity maturation, and class switching as the engines that tailor responses to specific threats.
Antigen Presentation and the MHC System11:57
Unpack how the immune system shows fragments of proteins to T cells through the major histocompatibility complex, called HLA in humans. Compare MHC class I, which presents endogenous peptides to CD8+ T cells on virtually every nucleated cell, with MHC class II, which presents exogenous peptides to CD4+ T cells on professional antigen-presenting cells like dendritic cells, macrophages, and B cells. Examine the endogenous and exogenous processing pathways, the role of TAP transporters and invariant chain, and why HLA polymorphism underlies transplant compatibility and many autoimmune disease associations.
Immunological Memory and Vaccination Principles8:41
Discover how the immune system remembers past encounters and responds faster and stronger on re-exposure. Compare primary and secondary immune responses, the kinetics of IgM versus IgG production, and the formation of long-lived memory T and B cells in lymphoid tissues. Examine how vaccines exploit these mechanisms using live attenuated, inactivated, subunit, conjugate, and mRNA platforms to generate protective memory without disease. Understand why memory is the cornerstone of immunity and how its failure or misdirection leads to chronic infection, immunodeficiency, or autoimmune disease.
Cytokines, Chemokines, and Immune Communication8:52
Learn the molecular language the immune system uses to coordinate complex responses. Walk through key cytokine families including interleukins, interferons, tumor necrosis factor, and colony-stimulating factors, and see how chemokines direct leukocyte trafficking to sites of inflammation. Understand the JAK-STAT signaling pathway, the concept of cytokine pleiotropy and redundancy, and how cytokine storms drive severe pathology in conditions like sepsis, macrophage activation syndrome, and severe viral infections. This molecular toolkit reappears in every hypersensitivity, autoimmune, and immunodeficiency disorder you will encounter.
Section 1 Quiz: Foundations of the Immune Response
Roleplay: Foundations of the Immune Response

Type I Hypersensitivity: Allergies and Anaphylaxis10:11
Examine the IgE-mediated immediate hypersensitivity reactions that drive allergic disease worldwide. Trace the sensitization phase in which allergens such as pollens, foods, or insect venoms prime Th2 responses, leading to IgE production and mast cell coating via FcεRI receptors. Understand how re-exposure triggers degranulation releasing histamine, tryptase, leukotrienes, and prostaglandins, producing vasodilation, bronchoconstriction, and increased vascular permeability. Distinguish the early-phase response from the late-phase eosinophil-rich inflammation, and connect mechanisms to clinical syndromes including allergic rhinitis, urticaria, food allergy, and life-threatening anaphylaxis.
Asthma as an Immune-Mediated Airway Disease12:57
Dive deep into bronchial asthma as a chronic Th2-driven inflammatory disorder of the airways. Understand how IgE, mast cells, eosinophils, and cytokines like IL-4, IL-5, and IL-13 produce airway hyperresponsiveness, smooth muscle hypertrophy, mucus hypersecretion, and goblet cell metaplasia. Distinguish atopic from non-atopic asthma, examine the role of viral infections and environmental triggers, and explore airway remodeling with subepithelial fibrosis as a long-term consequence. Connect these mechanisms to the clinical hallmarks of wheezing, dyspnea, and reversible airflow obstruction, and understand why targeted biologics against IgE, IL-5, and IL-4Rα are transforming severe asthma care.
Type II Hypersensitivity: Antibody-Mediated Tissue Damage9:24
Investigate how IgG and IgM antibodies directed against cell-surface or extracellular matrix antigens cause disease through three mechanisms: complement-mediated lysis, opsonization with phagocytosis, and antibody-dependent cellular cytotoxicity. Survey landmark conditions including autoimmune hemolytic anemia where antibodies coat red blood cells, Goodpasture syndrome with anti-glomerular basement membrane antibodies attacking lung and kidney, pemphigus vulgaris with anti-desmoglein antibodies disrupting epidermal adhesion, and ABO-incompatible transfusion reactions. Also examine antibody-mediated receptor dysfunction such as Graves disease stimulation of TSH receptors and myasthenia gravis blockade of acetylcholine receptors.
Type III Hypersensitivity: Immune Complex Disease10:39
Understand how circulating or in situ antigen-antibody complexes deposit in tissues and trigger destructive inflammation through complement activation and neutrophil recruitment. Trace the pathogenesis of serum sickness following exposure to foreign proteins, the Arthus reaction as a localized immune complex phenomenon, and post-streptococcal glomerulonephritis. Explore lupus nephritis as the prototype of immune complex deposition with characteristic full-house immunofluorescence and subendothelial, subepithelial, and mesangial deposits visualized on electron microscopy. Connect tissue tropism of immune complexes — kidneys, joints, skin, and small vessels — to the clinical patterns of vasculitis and glomerulonephritis seen in practice.
Type IV Hypersensitivity: Cell-Mediated Delayed Reactions8:51
Explore delayed-type hypersensitivity in which sensitized T cells, not antibodies, drive tissue injury hours to days after antigen exposure. Distinguish CD4+ Th1-mediated reactions producing macrophage activation and granuloma formation from CD8+ cytotoxic T cell-mediated direct killing of target cells. Walk through the tuberculin skin test, contact dermatitis to poison ivy, nickel, and latex, granulomatous diseases including tuberculosis and sarcoidosis, and chronic transplant rejection. Understand how persistent antigens that resist clearance drive granuloma formation with epithelioid macrophages, multinucleated giant cells, and surrounding lymphocytic cuffs that define this immunopathology.
Comparing the Four Hypersensitivity Types8:53
Consolidate your understanding by comparing the four hypersensitivity types side by side across mediator, timing, mechanism, and representative diseases. Examine why Type I is immediate and IgE-driven, Type II involves IgG and IgM against fixed cellular antigens, Type III features soluble immune complex deposition, and Type IV is delayed and T cell-mediated. Recognize that many real-world diseases involve more than one mechanism simultaneously, such as systemic lupus erythematosus combining Types II and III, and that mastering this framework gives you a reliable diagnostic lens for any immune-mediated condition you encounter.
Section 2 Quiz: Hypersensitivity Reactions
Roleplay: Hypersensitivity Reactions

Self-Tolerance and Its Breakdown9:32
Investigate the mechanisms that normally prevent the immune system from attacking the body's own tissues, then examine how they fail. Distinguish central tolerance, mediated by negative selection of autoreactive T cells in the thymus and B cells in the bone marrow with help from the AIRE transcription factor, from peripheral tolerance, which relies on regulatory T cells expressing FOXP3, anergy, and activation-induced cell death. Explore how genetic susceptibility tied to HLA alleles, environmental triggers including infections through molecular mimicry, hormonal influences explaining female predominance, and epitope spreading collectively unleash autoimmunity.
Systemic Lupus Erythematosus11:00
Examine the prototypical systemic autoimmune disease characterized by autoantibodies against nuclear antigens and multi-organ involvement. Understand the pathogenesis of impaired apoptotic debris clearance leading to anti-double-stranded DNA, anti-Sm, anti-Ro, and anti-La antibodies. Walk through the classic clinical manifestations including malar rash, discoid lesions, photosensitivity, oral ulcers, polyarthritis, serositis, hematologic cytopenias, neuropsychiatric features, and lupus nephritis with its six-class WHO classification. Connect Type II and Type III hypersensitivity mechanisms to the immune complex deposition and direct antibody-mediated injury that produce the disease's protean presentations.
Rheumatoid Arthritis10:52
Explore the chronic systemic autoimmune disease that attacks synovial joints and extra-articular tissues. Trace pathogenesis from anti-citrullinated protein antibodies and rheumatoid factor production through synovial pannus formation, with infiltration of T cells, B cells, macrophages, and fibroblast-like synoviocytes producing TNF-alpha, IL-6, and IL-17. Understand how this leads to cartilage erosion, subchondral bone destruction, and the characteristic symmetric polyarthritis of the small joints with morning stiffness, ulnar deviation, swan neck, and boutonnière deformities. Survey extra-articular manifestations including rheumatoid nodules, interstitial lung disease, vasculitis, and the association with Felty and Caplan syndromes.
Systemic Sclerosis and Sjögren Syndrome7:46
Compare two systemic autoimmune diseases with distinct fingerprints. In systemic sclerosis, examine the triad of microvascular injury, immune activation, and excessive fibrosis driven by TGF-beta, distinguishing limited cutaneous scleroderma with anti-centromere antibodies and CREST features from diffuse cutaneous disease with anti-Scl-70 antibodies and aggressive internal organ involvement. In Sjögren syndrome, explore lymphocytic infiltration of exocrine glands producing keratoconjunctivitis sicca and xerostomia, with anti-Ro and anti-La antibodies, and connect the disease to an elevated risk of mucosa-associated lymphoid tissue lymphoma.
Organ-Specific Autoimmunity: Endocrine Targets9:07
Focus on autoimmune diseases that selectively destroy or stimulate specific endocrine organs. Examine Type 1 diabetes mellitus as T cell-mediated destruction of pancreatic beta cells with insulitis and autoantibodies against insulin, GAD65, and IA-2. Compare Hashimoto thyroiditis, where lymphocytic infiltration with germinal centers and anti-thyroid peroxidase and anti-thyroglobulin antibodies cause hypothyroidism, with Graves disease, where stimulating TSH-receptor antibodies cause hyperthyroidism with ophthalmopathy and pretibial myxedema. Connect HLA associations, environmental triggers, and clinical presentations to underlying immunopathology.
Multiple Sclerosis and Myasthenia Gravis11:08
Examine two organ-specific autoimmune diseases of the nervous system with very different mechanisms. In multiple sclerosis, trace the Th1 and Th17-driven inflammatory demyelination of central nervous system white matter, producing the characteristic perivenular plaques with oligodendrocyte loss and relative axonal preservation, and connect this to relapsing-remitting and progressive clinical courses with optic neuritis, sensory disturbance, and motor symptoms. In myasthenia gravis, explore antibody-mediated blockade and internalization of nicotinic acetylcholine receptors at the neuromuscular junction, producing fatigable weakness, ptosis, diplopia, and the characteristic association with thymic hyperplasia and thymoma.
Section 3 Quiz: Autoimmune Diseases
Roleplay: Autoimmune Diseases

Primary Immunodeficiencies: An Overview7:24
Survey the landscape of primary immunodeficiencies as inherited disorders affecting specific arms of the immune system, each producing recognizable infection patterns. Understand the diagnostic principle that defects in humoral immunity predispose to encapsulated bacterial infections, T cell defects to viral and opportunistic infections, phagocyte defects to catalase-positive organisms, and complement defects to Neisseria and immune complex disease. Introduce the warning signs that should prompt evaluation, including recurrent severe infections, unusual organisms, family history, and failure to thrive, setting up the specific syndromes covered in subsequent lectures.
Severe Combined Immunodeficiency and DiGeorge Syndrome10:38
Examine two devastating T cell immunodeficiencies. In severe combined immunodeficiency, explore the genetic causes including X-linked common gamma chain mutations, adenosine deaminase deficiency, and RAG mutations, all producing profound absence of functional T cells and often B cells, presenting in infancy with persistent thrush, diarrhea, failure to thrive, and opportunistic infections that are fatal without hematopoietic stem cell transplantation. In DiGeorge syndrome, trace the 22q11.2 microdeletion that disrupts third and fourth pharyngeal pouch development, producing thymic aplasia, parathyroid hypoplasia with hypocalcemia, conotruncal cardiac defects, and characteristic facial features.
B Cell Immunodeficiencies7:05
Focus on disorders of humoral immunity that leave patients vulnerable to encapsulated bacterial infections. Examine X-linked Bruton agammaglobulinemia, where mutations in BTK halt B cell maturation at the pre-B stage, producing absent immunoglobulins of all classes and recurrent pyogenic sinopulmonary infections after maternal antibody wanes around six months of age. Contrast common variable immunodeficiency, a heterogeneous adult-onset disorder with low IgG, IgA, or IgM despite present but dysfunctional B cells, producing recurrent infections plus a paradoxical predisposition to autoimmune cytopenias, granulomatous disease, and lymphoma. Also touch on selective IgA deficiency as the most common primary immunodeficiency.
Other Primary Immunodeficiencies7:47
Round out your understanding of primary immunodeficiencies with disorders affecting innate immunity and combined pathways. Examine chronic granulomatous disease with NADPH oxidase defects producing recurrent infections with catalase-positive organisms and granuloma formation, Chediak-Higashi syndrome with giant lysosomal granules and impaired phagolysosome fusion, and leukocyte adhesion deficiency with impaired neutrophil migration. Touch on Wiskott-Aldrich syndrome with the triad of eczema, thrombocytopenia, and immunodeficiency, ataxia-telangiectasia with DNA repair defects, and hyper-IgM syndrome with class-switching failures. Connect each defect to its characteristic infection pattern.
HIV Pathogenesis and Immune Destruction11:50
Investigate how the human immunodeficiency virus systematically dismantles adaptive immunity. Trace the viral life cycle from CD4 and CCR5 or CXCR4 receptor binding through reverse transcription, integration, and viral replication that progressively depletes CD4+ T helper cells. Understand the routes of transmission, the dynamics of acute viremia with the seroconversion illness, the long clinical latency with ongoing lymphoid tissue destruction, and the catastrophic immune collapse that defines acquired immunodeficiency syndrome. Explore mechanisms of CD4 depletion including direct cytopathic effects, apoptosis, syncytium formation, and immune-mediated killing of infected cells.
AIDS-Defining Illnesses and Clinical Progression8:11
Connect HIV-induced immunodeficiency to the spectrum of opportunistic infections and malignancies that define AIDS. Walk through the CD4 count thresholds at which specific complications emerge, from oral candidiasis and tuberculosis at moderate immunosuppression to Pneumocystis jirovecii pneumonia, cerebral toxoplasmosis, cryptococcal meningitis, cytomegalovirus retinitis, and Mycobacterium avium complex at severe immunosuppression. Examine AIDS-defining malignancies including Kaposi sarcoma driven by HHV-8, primary central nervous system lymphoma associated with Epstein-Barr virus, and aggressive B cell lymphomas, alongside HIV-associated neurocognitive disorder and wasting syndrome.
Section 4 Quiz: Immunodeficiency Disorders
Roleplay: Immunodeficiency Disorders

Graft Rejection Mechanisms7:25
Explore how the immune system recognizes and attacks transplanted tissue through three distinct timing patterns. In hyperacute rejection, examine preformed recipient antibodies against donor ABO or HLA antigens triggering immediate complement-mediated vascular thrombosis within minutes. In acute rejection, distinguish cellular rejection driven by CD4+ and CD8+ T cells recognizing donor MHC through direct and indirect pathways from antibody-mediated rejection with C4d deposition in peritubular capillaries. In chronic rejection, trace the indolent fibrosis, vasculopathy, and parenchymal loss driven by chronic low-grade alloimmune injury that ultimately limits long-term graft survival despite modern immunosuppression.
Graft-Versus-Host Disease8:06
Examine the unique immunological reversal that occurs when transplanted immune cells attack the recipient. Trace the pathogenesis of graft-versus-host disease in hematopoietic stem cell transplantation, where donor T cells recognize recipient HLA mismatches and minor histocompatibility antigens as foreign. Distinguish acute graft-versus-host disease with its classic triad of dermatitis with maculopapular rash, hepatitis with cholestasis, and enteritis with secretory diarrhea, from chronic graft-versus-host disease resembling autoimmune connective tissue diseases with lichenoid skin changes, sicca syndrome, and bronchiolitis obliterans. Connect risk factors, prevention strategies, and the beneficial graft-versus-leukemia effect.
Immunosuppression Principles8:53
Survey the major drug classes used to control alloimmune and autoimmune responses, organized by mechanism. Examine calcineurin inhibitors like cyclosporine and tacrolimus that block T cell activation, mTOR inhibitors like sirolimus that interrupt proliferation signals, antimetabolites like mycophenolate and azathioprine that limit lymphocyte expansion, and corticosteroids with their broad anti-inflammatory effects. Introduce biological agents including anti-thymocyte globulin, anti-CD20 rituximab, and TNF-alpha inhibitors. Connect each agent to its targets in the immune response and to characteristic toxicities including infection, malignancy, nephrotoxicity, and metabolic complications that shape long-term patient management.
Amyloidosis as an Immune-Related Disease7:28
Investigate amyloidosis as a heterogeneous family of diseases unified by extracellular deposition of misfolded protein fibrils with characteristic beta-pleated sheet structure. Distinguish AL amyloidosis derived from immunoglobulin light chains in plasma cell dyscrasias such as multiple myeloma, AA amyloidosis derived from serum amyloid A in chronic inflammatory and autoimmune diseases like rheumatoid arthritis and familial Mediterranean fever, and beta-2 microglobulin amyloidosis in long-term dialysis patients. Examine clinical patterns including restrictive cardiomyopathy, nephrotic syndrome, hepatosplenomegaly, peripheral neuropathy, and macroglossia, and understand the diagnostic role of Congo red staining with apple-green birefringence.
Putting It All Together: The Immune System in Disease8:45
Synthesize the course by tracing how every immune-mediated disorder shares a common cast of cells, cytokines, and antibodies playing different roles. Compare how hypersensitivity, autoimmunity, immunodeficiency, transplant rejection, and amyloidosis all reflect the same machinery either overreacting, misdirecting against self, failing to act, recognizing alloantigens, or producing misfolded proteins. Examine emerging therapeutic frontiers including biologic agents targeting specific cytokines and cell populations, checkpoint inhibitors that unleash anti-tumor immunity, CAR-T cell therapy, and tolerance induction strategies, and understand why mastering immune-mediated disease mechanisms is essential to modern clinical practice.
Section 5 Quiz: Transplantation and Amyloidosis
Roleplay: Transplantation and Amyloidosis

Requirements

Basic understanding of human anatomy and physiology
Familiarity with general cellular and molecular biology concepts
Introductory knowledge of microbiology and pathogen types
Comfort with medical terminology used in clinical settings
Prior exposure to general pathology principles is helpful but not required

Description

This course contains the use of artificial intelligence.

Why do some bodies attack themselves, fail to defend against ordinary microbes, or react violently to harmless pollens? The immune system is one of medicine's most powerful and most dangerous biological networks, and when it misfires the consequences range from a stubborn rash to life-threatening anaphylaxis, organ failure, or fatal infection. This course gives you a rigorous, clinically grounded tour of immune-mediated disease, translating dense immunology into the recognizable syndromes you will encounter on the wards, in pathology, and on board examinations.

You will begin with a focused review of the normal immune response, covering innate and adaptive immunity, antigen presentation through the MHC system, T and B cell activation, immunological memory, and the cytokine networks that coordinate every immune reaction. From there you will walk through the four classical Gell and Coombs hypersensitivity reactions, mastering IgE-mediated allergy and anaphylaxis, antibody-mediated cytotoxicity, immune complex disease, and delayed cell-mediated reactions including granulomatous inflammation. You will study self-tolerance and its breakdown, then dissect systemic autoimmune diseases such as lupus, rheumatoid arthritis, and systemic sclerosis alongside organ-specific disorders including Type 1 diabetes, Hashimoto thyroiditis, multiple sclerosis, and myasthenia gravis.

The course then explores primary immunodeficiencies including SCID, DiGeorge syndrome, Bruton agammaglobulinemia, and common variable immunodeficiency, before tackling HIV pathogenesis and the AIDS-defining illnesses that mark immune collapse. You will examine transplant immunology including hyperacute, acute, and chronic rejection, graft-versus-host disease, and the major immunosuppressive drug classes used in clinical practice. The course closes with amyloidosis as an immune-related systemic disease, tying together the unifying themes of immune-mediated pathology.

Designed for medical, pathology, and immunology students as well as clinicians who want a comprehensive refresher, this course turns intimidating immunopathology into clear, memorable mechanisms you can apply at the bedside. Enroll now and build the durable mental framework you need to reason through any immune-mediated disease with confidence.

Who this course is for:

Medical students preparing for pathology and immunology examinations
Pathology residents and fellows seeking a structured immunopathology review
Immunology students wanting clinically anchored disease mechanisms
Practicing clinicians refreshing their understanding of immune-mediated disease
Physician assistants, nurse practitioners, and advanced healthcare trainees

Diseases of Immunity: Immune-Mediated Disorders

What you'll learn

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Course content

Section 1: Foundations of the Immune Response6 lectures • 52min

Section 2: Hypersensitivity Reactions7 lectures • 1hr 1min

Section 3: Autoimmune Diseases7 lectures • 59min

Section 4: Immunodeficiency Disorders7 lectures • 53min

Section 5: Transplantation and Amyloidosis6 lectures • 41min

Fundamentals of Immune System Dysfunction0

Autoimmune Diseases: When Self Becomes the Enemy0

Allergic Diseases and Hypersensitivity Reactions0

Immunodeficiency Disorders0

Transplant Immunology and Rejection0

Requirements

Description

Who this course is for: