AIM Step 10
3rd Year MBBS
Blood and Immunology
3rd Year MBBS
Blood and Immunology
Student Memory Support
Hypersensitivity, Immune Tolerance, Autoimmunity, Immunodeficiency and Immunomodulatory Drugs
High-yield memory reinforcement for rapid KMU revision.
1. High-Yield Flashcards
Tap each question to reveal the answer.
Which antibody and effector cell are central to immediate type I hypersensitivity?
IgE and mast cells.
What is the basic mechanism of type III hypersensitivity?
Immune-complex deposition followed by complement activation and inflammation.
Which hypersensitivity type is mediated predominantly by sensitized T lymphocytes?
Type IV hypersensitivity.
What is immune tolerance?
Specific immunological unresponsiveness to an antigen, especially self-antigens.
Name three important peripheral tolerance mechanisms.
Anergy, regulatory T-cell suppression and deletion.
What causes hyperacute graft rejection?
Pre-existing recipient antibodies causing endothelial injury and thrombosis.
Which tissues are important targets of graft-versus-host disease?
Skin, gastrointestinal tract and liver.
What is the fundamental abnormality underlying autoimmune disease?
Loss of self-tolerance with activation of autoreactive lymphocytes.
Which adaptive immune cell is progressively impaired and depleted in HIV infection?
CD4-positive T lymphocytes.
Which chemokine co-receptors facilitate HIV entry after gp120 binds CD4?
CCR5 or CXCR4.
How do cyclosporine and tacrolimus suppress T-cell activation?
They inhibit calcineurin and reduce IL-2 transcription.
How does sirolimus differ mechanistically from tacrolimus?
Sirolimus inhibits mTOR and blocks IL-2-driven lymphocyte proliferation.
Which enzyme is inhibited by mycophenolate?
Inosine monophosphate dehydrogenase.
Which lymphocyte marker is targeted by rituximab?
CD20 on B lymphocytes.
Why are several immunosuppressive drugs commonly combined after transplantation?
To suppress multiple immune pathways while reducing reliance on a very high dose of one agent.
2. Mnemonics
Mnemonic Title: Hypersensitivity Types
ACID
Meaning: Anaphylactic = Type I, Cytotoxic/antibody-mediated = Type II, Immune complex = Type III, Delayed = Type IV.
Mnemonic Title: Peripheral Tolerance
ARD
Meaning: Anergy, Regulatory T-cell suppression, Deletion.
Mnemonic Title: Major Immunodeficiency Groups
BTPC
Meaning: B-cell, T-cell, Phagocyte and Complement defects; combined defects involve both major adaptive arms.
3. Memory Tables
Immediate vs Delayed Hypersensitivity
| Feature | Immediate | Delayed |
|---|---|---|
| Main type | Type I | Type IV |
| Main mediator | IgE and mast cells | Sensitized T cells |
| Timing | Minutes after re-exposure | Develops over many hours |
| Example | Anaphylaxis | Contact dermatitis |
Major Immunophilin-Binding Drugs
| Drug | Key Target | Main Effect | High-Yield Toxicity |
|---|---|---|---|
| Cyclosporine | Calcineurin | Reduced IL-2 transcription | Nephrotoxicity |
| Tacrolimus | Calcineurin | Reduced IL-2 transcription | Nephrotoxicity, glucose disturbance |
| Sirolimus | mTOR | Reduced IL-2-driven proliferation | Marrow suppression, hyperlipidemia |
4. Rapid Revision Points — Last-Minute Revision
Must Remember:
- Type II hypersensitivity may destroy cells, inflame tissues or alter receptor function.
- Central tolerance acts during lymphocyte development; peripheral tolerance controls escaped self-reactive cells.
- Chronic graft rejection produces progressive vascular narrowing and interstitial fibrosis.
- In GVHD, immunocompetent donor T cells attack recipient tissues.
- Autoimmune disease reflects loss of tolerance in a genetically susceptible host, often with an environmental trigger.
- Primary immunodeficiencies include defects of B cells, T cells, combined immunity, phagocytes and complement.
- HIV persists after viral DNA integrates into the host-cell genome.
- Corticosteroids suppress immunity by altering gene transcription through intracellular glucocorticoid receptors.
- Mycophenolate limits guanine nucleotide synthesis and therefore lymphocyte proliferation.
- Combination immunosuppression improves pathway coverage but increases infection, toxicity and interaction risks.
Common KMU Trap:
Hyperacute rejection depends on pre-existing recipient antibodies, whereas acute rejection may involve newly activated T cells and/or antibodies.
Hyperacute rejection depends on pre-existing recipient antibodies, whereas acute rejection may involve newly activated T cells and/or antibodies.
5. Clinical Memory Hooks
Wheezing and hypotension minutes after allergen exposure
→
IgE-mediated mast-cell activation and systemic immediate hypersensitivity
→
IgE-mediated mast-cell activation and systemic immediate hypersensitivity
Transplanted organ fails immediately with vascular thrombosis
→
pre-existing antibodies causing hyperacute rejection
→
pre-existing antibodies causing hyperacute rejection
Stem-cell transplant followed by rash, diarrhea and liver injury
→
donor T cells causing graft-versus-host disease
→
donor T cells causing graft-versus-host disease
Transplant patient develops nephrotoxicity during calcineurin-inhibitor therapy
→
think cyclosporine or tacrolimus
→
think cyclosporine or tacrolimus
6. Starred High-Yield Exam Points
“`
- ⭐ Type I hypersensitivity: IgE cross-linking on mast cells produces rapid mediator release.
- ⭐ Type IV hypersensitivity: sensitized T lymphocytes mediate delayed inflammation or direct cellular injury.
- ⭐ Graft rejection vs GVHD: recipient attacks graft in rejection; donor lymphocytes attack recipient in GVHD.
- ⭐ HIV: progressive loss and dysfunction of CD4-positive T cells produces acquired immunodeficiency.
- ⭐ Calcineurin inhibitors: cyclosporine and tacrolimus reduce IL-2 transcription; nephrotoxicity is a major adverse effect.
- ⭐ Rituximab: targets CD20-positive B lymphocytes and is used in selected B-cell malignancies and autoimmune diseases.
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