Immunobiology Flashcards (Lecture 1-8)

1
Q

innate immune system

A

consists of complement, granulocytes, NK cells, antigen presenting cells

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2
Q

Adaptive (specific) immune system

A

B cells, T cells, to antibodies

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3
Q

Immune system organs- primary lymphoid organs

A

Bone marrow, thymus

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4
Q

Basophyls

A

Similar to mast cells but found in blood.Release inflammatory mediators (histamine, cytokines).
Support adaptive immunity, particularly antibody responses.

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5
Q

Neutorphyls

A

Most abundant white blood cells.
First responders to infections.
Short-lived but potent:
- Phagocytose microbes.
- Secrete cytokines.
- Form Neutrophil Extracellular Traps (NETs) to trap bacteria.

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6
Q

Monocytes/Macrophages

A

Monocytes in blood migrate to tissues to become macrophages.
Functions:
- Phagocytosis (engulfing pathogens).
- Cytokine secretion.
- Antigen presentation to T cells.

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7
Q

Antigen Presenting Cells

A

Capture and present antigens to T cells.
Types:
- Macrophages.
- Dendritic cells.
- B cells.

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8
Q

Immune system organs- Secondary lymphoid organs

A

Spleen, lymph nodes, peyer’s patches, appendix, tonsils and adenoids

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9
Q

Inflammatory mediators

A

Increased blood flow causes increased capillary permeability, attracts cells, alerts immune system, clotting.

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10
Q

Innate immune response to cuts

A

Mast cells secrete histamine that cause nearby capillaries to dilate. Neutrophils and monocytes leave capillaries. Antigen presenting cells, Etc. I missed the rest of the tutorial slide

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11
Q

What are Eosinophils

A

Attack parasites and helminths. Derived from myeloid progenitors in bone marrow.
Contain granules with enzymes that:
- Attack parasites and helminths.
- Can also damage host tissue.
Increase during inflammation and allergic responses.

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12
Q

Natural Killer (NK) Cells

A

Target and destroy infected or cancerous cells. Recognize stressed cells lacking MHC-I. Release perforins and granzymes to induce cell death. AntiVIRAL immunity.

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13
Q

Dendritic Cells

A

Strategically positioned in tissues.Function: Detect pathogens and Present antigens to T cells in lymph nodes.

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14
Q

Cell morphology

A

Shape, size, and internal structures (microscopy).

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15
Q

Surface molecule expression

A

Using flow cytometry and CD markers.

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16
Q

CD Nomenclature (Cluster of Differentiation)

A

CD molecules help in classifying immune cells.
- CD1 to CD371 represent various immune markers.
- Groups of antibodies recognizing the same molecule form a “cluster”

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17
Q

Reside in epithelial tissues.Different types:

A

ILC1 (defense against viruses).
ILC2 (allergic inflammation).
ILC3 (gut barrier function).
ILC4 (form secondary lyphoid tissues)
ILC5 (Anticribrobia peptides, phaogcyte)

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18
Q

Myeloid Cells

A

Myeloid cells include:
- Phagocytes (neutrophils, monocytes/macrophages).
- Granulocytes (mast cells, eosinophils, basophils).
These cells originate from common myeloid progenitors.

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19
Q

Mast Cells

A

Immature mast cells migrate to tissues where they mature.
Reside in skin, lungs, gut (exposed to the environment).
Function:
- Release histamine and cytokines during allergic reactions.
- Long-lived cells.

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20
Q

What are the three main components of the immune system?
A: Epithelial barriers, immune cells, and immune molecules (cytokines, plasma proteins).

A

Innate immunity: Rapid, non-specific, no memory.
Adaptive immunity: Slower, highly specific, provides long-term memory.

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21
Q

What are the primary lymphoid organs and their function?

A

Bone marrow: Produces all blood cells, site of B-cell maturation.
Thymus: Site of T-cell maturation.

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22
Q

What are the secondary lymphoid organs, and what do they do?

A

Lymph nodes, spleen, and mucosa-associated lymphoid tissue (MALT).
Function: Site where immune responses are initiated.

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23
Q

What is the main function of lymph nodes?

A

Filter lymph, trap pathogens, and activate lymphocytes.

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24
Q

What is the role of the spleen in immunity?

A

Filters blood, removes old RBCs, and traps bloodborne antigens.

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25
Q

What are phagocytes, and what is their function?

A

Cells that engulf and digest microbes, including neutrophils and macrophages.

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26
Q

Which innate immune cells release histamine and inflammatory mediators?

A

Mast cells, basophils, and eosinophils.

27
Q

What are dendritic cells, and why are they important?

A

Antigen-presenting cells (APCs) that bridge innate and adaptive immunity by activating T cells.

28
Q

What are natural killer (NK) cells, and what do they do?

A

Lymphocytes that kill virus-infected and cancerous cells by releasing perforins and granzymes.

29
Q

What are B cells and T cells, and how do they differ?

A

B cells: Produce antibodies.
T cells: Direct cell-mediated immunity.

30
Q

What are the five hallmarks of the innate immune system?

A

Rapid response (within hours).
Short duration (response fades quickly).
Repetitive response (same reaction every time).
Interacts with adaptive immunity.
Does not attack self (tolerance to host tissues).

31
Q

How does the innate immune system recognize pathogens?

A

Through pattern recognition receptors (PRRs) that detect pathogen-associated molecular patterns (PAMPs).

32
Q

What are PAMPs and DAMPs?

A

PAMPs (Pathogen-Associated Molecular Patterns) – Microbial molecules (e.g., LPS, viral RNA).
DAMPs (Damage-Associated Molecular Patterns) – Host molecules from injured or stressed cells.

33
Q

What are Toll-Like Receptors (TLRs)?

A

Membrane-bound PRRs that recognize extracellular and endosomal pathogens.

34
Q

Where are TLRs located?

A

Cell surface (detect extracellular microbes) and endosomes (detect viral RNA).

35
Q

What signaling pathway is activated by TLR engagement?

A

The NF-κB pathway, which induces inflammatory cytokine expression.

36
Q

What adaptor protein is used by most TLRs?

A

MyD88 (except for TLR3, which uses TRIF).

37
Q

What are the steps of phagocytosis?

A

Recognition (microbe binds PRRs).
Engulfment (phagosome forms).
Fusion (phagosome + lysosome = phagolysosome).
Microbial killing (by ROS, NO, enzymes).

38
Q

How do neutrophils kill microbes?

A

Through phagocytosis, release of reactive oxygen species (ROS), and Neutrophil Extracellular Traps (NETs), netosis.

39
Q

What are antimicrobial peptides (AMPs), and how do they work?

A

Small proteins (e.g., defensins) that disrupt bacterial membranes, causing lysis.

40
Q

What is the difference between alpha-defensins and beta-defensins?

A

Alpha-defensins: Produced by leukocytes and Paneth cells (gut).
Beta-defensins: Produced by epithelial cells (continuous secretion).

41
Q

What are NOD-Like Receptors (NLRs), and where are they located?

A

Cytoplasmic PRRs that detect intracellular bacterial components and stress signals.

42
Q

What are NOD1 and NOD2, and what do they recognize?

A

NOD1 → Recognizes Gram-negative bacteria (Meso-DAP).
NOD2 → Recognizes both Gram-negative & Gram-positive bacteria (MDP).

43
Q

How does NOD receptor signaling work?

A

NOD receptors activate RIPK2, which triggers NF-κB to induce inflammation.

44
Q

What is the function of DAMP recognition in innate immunity?

A

Detects host cell damage, triggering inflammation.

45
Q

What is an example of a DAMP-recognizing receptor?

A

TLR9, which detects unsequestered host DNA as a danger signal.

46
Q

What is the complement system?

A

A system of circulating and membrane-bound proteins that assist immune responses by:
- Opsonizing pathogens (C3b).
- Inducing inflammation (C3a, C5a).
- Forming Membrane Attack Complex (MAC) (C5b-C9).

47
Q

What are the three pathways of complement activation?

A
  1. Alternative pathway: Direct activation by microbial surfaces (innate immunity).
  2. Classical pathway: Triggered by antigen-antibody complexes (adaptive immunity).
  3. Lectin pathway: Initiated by mannose-binding lectin (MBL) binding to microbial sugars.
48
Q

What is C3 “tick-over” in the alternative pathway?

A

C3 undergoes spontaneous low-level hydrolysis to C3b.
If C3b binds a microbial surface, it initiates the alternative pathway.
If no microbe is present, C3b is quickly inactivated in the fluid phase.

49
Q

What are the functions of C3a, C3b, C5a, and MAC?

A

C3a & C5a: Anaphylatoxins (cause inflammation, recruit immune cells).
C3b: Opsonization (coating pathogens for phagocytosis).
MAC (C5b-9): Pore-forming complex that lyses pathogens.

50
Q

What diseases are associated with complement deficiencies?

A

C3 deficiency → Severe, recurrent pyogenic bacterial infections.
C2 deficiency → Autoimmune diseases (lupus-like symptoms).
C1 inhibitor (C1-INH) deficiency → Hereditary angioedema (excess inflammation, swelling).
DAF (Decay-Accelerating Factor) deficiency → Paroxysmal nocturnal hemoglobinuria (PNH) (uncontrolled complement activation on RBCs).

51
Q

What is the role of MHC in immunity?

A

MHC molecules present peptide antigens to T cells.
MHC Class I → presents intracellular peptides to CD8+ cytotoxic T cells.
MHC Class II → presents extracellular peptides to CD4+ helper T cells.

52
Q

How are antigens processed for MHC Class I vs. MHC Class II?

A

MHC I Pathway (Cytosolic Pathway):
- Proteasome degrades intracellular proteins.
- Peptides are transported into the ER via TAP (Transporter Associated with Antigen Processing).
- Loaded onto MHC I and transported to the cell surface.
MHC II Pathway (Endocytic Pathway):
- Antigens are phagocytosed and degraded in endosomes/lysosomes.
- Invariant chain (Ii) blocks premature peptide binding in the ER.
- HLA-DM removes CLIP, allowing antigenic peptides to load onto MHC II.

53
Q

What is cross-presentation and why is it important?

A

Cross-presentation: APCs can present extracellular antigens on MHC I to activate CD8+ T cells.
Importance: Allows DCs to stimulate cytotoxic T cell responses against viruses and tumors, even if they don’t infect APCs directly.

54
Q

What is MHC polymorphism and why is it significant?

A

MHC genes are highly polymorphic, meaning many alleles exist within the population.
Ensures diversity in antigen presentation and prevents pathogen escape.

55
Q

What are the functions of B cells?

A

Produce antibodies for humoral immunity.
Differentiate into plasma cells (secrete antibodies) or memory B cells (long-term immunity).

56
Q

What are the key structural features of an antibody?

A

2 heavy chains + 2 light chains (Y-shaped structure).
Fab region (binds antigen) and Fc region (binds receptors for effector functions).

57
Q

What are the 5 antibody isotypes and their roles?

A

IgM- First antibody produced, strong complement activation.
IgG- Most abundant, neutralization, opsonization, ADCC.
IgA- Mucosal immunity, protects gut & respiratory tract.
IgE- Binds mast cells → involved in allergies & helminth defense.
IgD- Functions in B cell development.

58
Q

What is somatic hypermutation and affinity maturation?

A

Somatic hypermutation: B cells undergo mutations in the variable region to increase antibody affinity.
Affinity maturation: Selection for higher-affinity B cells in germinal centers.

59
Q

What is class switching and why is it important?

A

Class switching: B cells change antibody isotype (IgM → IgG, IgA, etc.).
Does not change antigen specificity.
Requires T cell help (CD40-CD40L interaction).

60
Q

What are the two main types of T cells and their functions?

A

CD8+ Cytotoxic T Cells: Kill virus-infected or cancerous cells.
CD4+ Helper T Cells: Activate macrophages, B cells, and other immune cells.

61
Q

How do T cells recognize antigens?

A

T Cell Receptors (TCRs) bind peptide-MHC complexes.
CD4+ T cells → Recognize MHC Class II.
CD8+ T cells → Recognize MHC Class I.

62
Q

How are TCRs generated?

A

V(D)J recombination generates TCR diversity.
Junctional diversity (nucleotide additions) increases specificity.

63
Q

What are the stages of T cell selection in the thymus?

A

Positive Selection (Cortex):
- Ensures T cells recognize self-MHC.
- Cells that fail → die by neglect.
Negative Selection (Medulla):
- Removes self-reactive T cells.
- Prevents autoimmunity.

64
Q

What are the major T cell subsets and their roles?

A

Th1- Activates macrophages, fights intracellular pathogens.
Th2- Helps B cells, fights helminths, mediates allergic reactions.
Th17- Enhances neutrophil response, protects barrier tissues.
Treg- Suppresses immune responses, prevents autoimmunity.