1. Spleen
1. Location and Immune Response
- LUQ (Left Upper Quadrant):
- Location of the spleen.
- Beta and T Cells:
- Beta cells: Located in the pancreas (in the islets of Langerhans) and involved in insulin production.
- T cells: Part of the immune system, involved in adaptive immunity.
2. Infectious Mononucleosis:
- Cause:
- Epstein-Barr Virus (EBV).
- Clinical Features:
- Splenomegaly: Enlargement of the spleen due to infection.
- T-cell Hyperplasia: An increase in T cells as part of the immune response to the viral infection.
2. Thymus
- Origin:
- Derived from the 3rd pharyngeal pouch.
- Function:
- Responsible for the maturation of T-cells.
- T-cells are made in the bone marrow, but they mature in the thymus.
- Congenital Absence:
- If the 3rd pharyngeal pouch is absent, it leads to DiGeorge Syndrome, a condition where the thymus is underdeveloped or absent, affecting immune function and causing antibody deficiencies.
3. Antibodies and Immune Responses
| Antibody | Function | Characteristics |
|---|---|---|
| IgG | – Secondary immune response – Crosses the placenta – Complement fixation – Opsonization – More in plasma | – Main antibody in secondary immune response – Helps fix complement and aids in opsonization – Crosses placenta to provide passive immunity |
| IgA | – Present in secretions (saliva, mucus, breast milk) – More produced but drains | – Found in mucosal membranes – Lower concentration in blood but crucial for mucosal immunity |
| IgE | – Involved in HSR-1 (Type I hypersensitivity) – Plays a role in parasitic infections | – Involved in allergic reactions and parasite defense – Elevated in parasitic infections and allergies |
| IgM | – Primary immune response – Fixes complement – Pentameric structure | – First antibody produced during primary response – Fixes complement and activates immune response |
4. Types of Grafts
| Graft Type | Definition | Example |
|---|---|---|
| Autograft | Graft taken from the same body | Skin graft from one part of the body to another part of the same body |
| Isograft | Graft between identical twins (genetically identical) | Organ transplant between identical twins |
| Allograft | Graft between individuals of the same species | Kidney transplant between non-identical humans |
| Xenograft | Graft between individuals of different species | Heart valve transplant from a pig to a human |
5. Transplant Rejection
| Type of Rejection | Timeframe | Description |
|---|---|---|
| Acute Rejection | Occurs within weeks to months | – The immune system attacks the transplanted organ shortly after the transplant. |
| Chronic Rejection | Occurs within months to years | – Long-term rejection that leads to gradual deterioration of the transplanted organ over time. |
| Hyperacute Rejection | Occurs within minutes | – Immediate rejection, often due to pre-existing antibodies against the donor tissue, resulting in rapid organ failure. |
6. HSR-I (Type I Hypersensitivity Reaction)
| Type of Hypersensitivity | Mechanism | Details |
|---|---|---|
| HSR-I (Type I) | IgE-mediated | – Genetic predisposition (atopy). – Mast cells release histamine upon activation by IgE. – Conditions: Severe anaphylaxis, asthma, atopic dermatitis, allergic rhinitis. |
| HSR-II (Type II) | Antigen + Antibody Complex → Cell damage | – IgG or IgM antibodies bind to antigens on the cell surface, leading to cell damage (e.g., hemolytic anemia, autoimmune diseases). |
| HSR-III (Type III) | Antigen + Antibody + Complement Activation | – Formation of immune complexes, leading to complement activation and tissue damage (e.g., in lupus, rheumatoid arthritis). |
| HSR-IV (Type IV) | T-cell Mediated | – T-cell mediated immune response causes tissue damage (e.g., in contact dermatitis, tuberculosis, graft rejection). |
7. Complement System
- Helps to reduce infection.
- Group of 20 proteins.
- Proteins are inactive, become active during infection.
- 11 proteins are important.
- Each complement protein has 2 components.
- Example: C1 → C1a, C1b.
- Linked with T-cell mediated hypersensitivity type IV.
1. Pathways of Activation
- Classical pathway → triggered by IgG or IgM.
- Alternative pathway → triggered directly by microbial surfaces.
- Mannose-binding lectin pathway → triggered by mannose residues on microbes.
2. Important Functions
- Opsonization → C3b coats microbes, enhances phagocytosis.
- Chemotaxis → C5a attracts neutrophils.
- Membrane Attack Complex (MAC) → C5b, C6, C7, C8, C9 assemble and lyse microbes.
3. Deficiency States
- C5–C9 deficiency → recurrent Neisseria bacteremia.
- C1–C6 deficiency → recurrent pyogenic infections (pus-forming bacteria), ↑ risk of SLE.
4. Adaptive Immunity Link
- B-cell maturation → Plasma cells → Antibody production → Humoral immunity.
- T-cells → Cell-mediated immunity.
- CD4 (Helper T cells) → Support humoral immunity.
- CD8 (Cytotoxic T cells) → Directly kill infected cells.
Here are other materials for NLE NRE step 1
5. Innate Immunity
- No memory, acts immediately and non-specifically.
- Components:
- Physical barriers (skin, mucosa).
- Cells: Neutrophils, Macrophages, NK cells.
- Proteins: Complement system, acute phase proteins.
6. Adaptive Immunity
- Specific response, develops memory.
- Components:
- B-cells → mature into plasma cells → produce antibodies.
- T-cells → CD4 (helper) and CD8 (cytotoxic).
- Basis of therapeutic monoclonal antibodies.
1. Monoclonal Antibodies (Examples)
| Drug | Target | Use |
|---|---|---|
| Denosumab | RANK-L | Osteoporosis |
| Omalizumab | IgE | Asthma (allergic) |
| Palivizumab | RSV F protein | RSV bronchiolitis prophylaxis |
| Eculizumab | C5 complement | Paroxysmal nocturnal hemoglobinuria (PNH) |
| Efalizumab | CD11a (LFA-1) | Psoriasis |
| Natalizumab | α4-integrin | Multiple sclerosis |
| Trastuzumab | HER2/neu receptor | HER2+ breast cancer, gastric cancer |
