Date: Tuesday, March 18th, 2025
Format: In-person
Location: Highfield Campus (see timetable for specific room and time)
Exam Structure: 40 questions covering innate and adaptive immunity
Special Consideration: Extra time available for eligible students via student office
Instructions: Students must remain seated if they finish early.
Common Autoimmune Diseases:
Multiple sclerosis
Systemic Lupus Erythematosus
Rheumatoid arthritis
Breakdown of immune system functioning leading to autoimmune diseases.
Plasticity of the immune system regarding pathogen recognition and its consequences.
Key Points:
Effectors of acquired immunity: antibodies, T-cells
Antigen presentation by professional antigen-presenting cells (APCs)
Mechanisms of tolerance.
Statistics (2018 data):
Approximately 4 million cases in the UK
1 in 5 individuals affected
75% of cases occur in women.
Autoimmune diseases rank as the 4th largest cause of disability among women.
Rheumatoid Arthritis affects approximately 1 in 100 individuals.
Steps of Pathogen Recognition by APCs:
APC recognizes a pathogen.
Internalization and antigen processing.
Peptide presented via MHC class II.
Interaction of TCR complex with the peptide.
Danger signal and co-stimulation.
T cell proliferation and cytokine response.
Activation of B cells and CD8 T cells to launch a full immune response.
Normal CD4 T cell response: involves MHC-antigen and co-stimulation interactions.
The immune system typically distinguishes between self and non-self.
Autoimmune diseases arise when:
Control processes are interrupted, leading to lymphocyte suppression failure.
Cells/tissues are altered and mistaken for non-self.
Factors that may trigger autoimmune processes include:
Bacteria, viruses, toxins, and certain drugs.
Genetic predisposition to autoimmune disorders.
Tolerance: The immune system's ability to avoid attacking self-antigens.
Breakdown of tolerance leads to autoimmune disease.
Tolerance mechanisms include:
Central tolerance (during T cell maturation in the thymus).
Peripheral tolerance (involving signals from normal cellular tissue).
MHC molecules are critical antigen-presenting structures.
They partly determine immune responses to antigens and are implicated in susceptibility and development of autoimmune diseases.
Peter C. Doherty and Rolf M. Zinkernagel won the Nobel Prize in 1996 for discoveries related to specificity in cell-mediated immune defense.
Only viral infected cells are eliminated by cytotoxic T cells, not free virus or antigen.
Key differences exist in responses between T cells and B cells.
T cells develop in the thymus with processes of:
Central Tolerance: Reactive T cells against self are eliminated; involves positive and negative selection.
Peripheral Tolerance: T cells in circulation depend on signals from normal tissues to survive; failure results in autoimmunity.
Various stages of T cell development (e.g., precursor, immature thymocyte) illustrate gene rearrangement and selection processes.
Negative selection for B cells occurs in the bone marrow; cross-linking of IgM can lead to apoptosis of self-reactive B cells.
Immature B cells undergo receptor editing or deletion if they strongly react to self-antigens.
Chronic activation through inappropriate immune responses can lead to detrimental effects on the body, necessitating therapeutic interventions.