Exam questions 22, 23

Question 1

Pattern-Recognition Receptors (PRRs) cellular locations and examples

Answer 1

Cell surface: TLR4, recognizes lipopolysaccharides (LPS). Endosome: TLR7, detects viral RNA. Cytosol: RIG-I, recognizes viral RNA.

Question 2

Phagocytosis definition and activation

Answer 2

Phagocytosis: Engulfment of particles like microbes. Phagocytic cells: Macrophages, neutrophils, dendritic cells. Activation: Indirect via opsonins (e.g., CRP, MBL) or direct via PRRs (e.g., TLRs).

Question 3

Inflammasome definition and activation

Answer 3

Cytosolic multiprotein complex that induces inflammation. Activation: NLRs detect PAMPs, leading to IL-1β production and inflammasome assembly. Outcome: Release of IL-1β and IL-18.

Question 4

Complement system activation pathways

Answer 4

Classical: C1q binds antibody-antigen complexes. Lectin: MBL binds mannose on microbial surfaces. Alternative: Spontaneous C3 hydrolysis or C3b binding to microbial surfaces.

Question 5

Complement deficiencies and autoimmunity

Answer 5

C1q, C2, C4 deficiency leads to impaired clearance of apoptotic cells, increasing self-reactive lymphocyte activation and promoting autoimmunity.

Question 6

C5 deficiency and Neisseria infection

Answer 6

C5 deficiency prevents MAC formation, leading to susceptibility to Neisseria bacteria.

Question 7

B cell development stages and locations

Answer 7

V(D)J recombination: Bone marrow. Switch to IgD: Periphery. Somatic hypermutation: Germinal centers. Class-switch recombination: Germinal centers. Secreted antibodies: Periphery.

Question 8

RAG1/2 activity in B cells

Answer 8

RAG1/2 is involved in V(D)J recombination during B cell development.

Question 9

AID/UNG activity in B cells

Answer 9

AID and UNG are involved in somatic hypermutation and class-switch recombination in B cells.

Question 10

Ig region changes in B cell development

Answer 10

V(D)J recombination: Variable region. IgM to IgD switch: Constant region. Somatic hypermutation: Variable region. Class-switch recombination: Constant region. Antibody secretion: Constant region.

Question 11

MHC molecules diversity

Answer 11

Polymorphism: Multiple alleles for MHC genes. Polygeny: Multiple MHC genes encoding different molecules. Codominant expression: Both maternal and paternal alleles are expressed. Promiscuity: Each MHC molecule binds multiple peptides.

Question 12

Cross-presentation and its importance for CD8+ T cells

Answer 12

Cross-presentation: Dendritic cells present extracellular antigens on MHC I. Importance: Activates CD8+ T cells to respond to intracellular pathogens or tumors.

Question 13

Type I interferons in viral defense

Answer 13

Critical for defense against viruses. Effects: Induces ISGs to restrict viral replication, enhance antiviral defenses, and alert neighboring cells.

Question 14

Cytokine influence on CD4+ T cell response

Answer 14

Polarizing cytokines (e.g., IL-12, IL-4) guide differentiation into Th1, Th2, etc., influencing immune responses during infection.

Question 15

IL-2 in CD4+ T cell differentiation

Answer 15

IL-2 drives T cell proliferation, clonal expansion, and survival.

Question 16

Th1 cells in intracellular bacterial infections

Answer 16

Th1 cells produce IFN-γ to activate macrophages for intracellular pathogen destruction.

Question 17

Tolerance definition

Answer 17

Tolerance refers to unresponsiveness to self-antigens, preventing autoimmune reactions.

Question 18

Thymic selection in T cell development

Answer 18

Positive selection: Tests T cells for MHC recognition. Negative selection: Eliminates self-reactive T cells to maintain tolerance.

Question 19

Regulatory T cells and mechanisms of tolerance

Answer 19

Tregs suppress immune responses via IL-10, TGF-β secretion and CTLA-4 expression to reduce co-stimulatory signals.

Question 20

Clinical outcome without functioning Treg cells

Answer 20

Severe autoimmunity and inflammation, as seen in IPEX syndrome.

Question 21

Checkpoint immunotherapy concept

Answer 21

Blocks inhibitory signals (e.g., PD-1, CTLA-4) on T cells, allowing them to attack tumors. Example: Anti-PD-1 antibodies.

Question 22

Cancer immunoediting and checkpoint blockade

Answer 22

Immunoediting: Tumor cells evolve to evade immune detection. Low-immunogenic tumor cells may not respond to checkpoint blockade.

Question 23

NK cell recognition of infected or cancerous cells

Answer 23

NK cells detect the absence of MHC I or recognize stress ligands on target cells, triggering killing.

Question 24

Helminth infection immune response

Answer 24

Type II immune response.

Question 25

Intestinal epithelial cells detecting worm infection

Answer 25

IECs detect worms, releasing alarmins (e.g., IL-25, IL-33, TSLP) to activate immune responses.

Question 26

Immune cells in response to worm infection

Answer 26

ILC2 and Th2 cells produce IL-4, IL-5, and IL-13. Eosinophils are recruited and degranulate to kill worms. B cells produce IgE, triggering eosinophil action.