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Immunology > L2 - humoral immunity > Flashcards

L2 - humoral immunity Flashcards

1
Q

oes innate immunity generates immunological memory?

A

No
The adaptive
–Highly specific
–Generates immunological memory

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2
Q

what are the immunoglobulins?

A

A group of proteins produced by B lymphocytes that contribute to the humoral immune response. The different types of immunoglobulins include IgA, IgG, IgM, IgE, and IgD.

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3
Q

what are the 2 functional parts of immunoglobulins?

A

Immunoglobulins (antibodies) have two functional parts: the Fc region and the Fab region. The two enzymes papain and pepsin can be used to identify the different functional parts.

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4
Q

what is teh immunoglobulin FC region?

A
  • -Contains the constant region
  • -Formed by heavy (H) chains
  • -Determines the antibody isotype (e.g., IgA, IgG, IgM)
  • -Binds complement (IgG, IgM)
  • -Binds various immunological cells, such as macrophages, to stimulate phagocytic or cytotoxic activity
  • -Contains the carboxy-terminal
  • -Has many carbohydrate side chains
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5
Q

what is the immunoglobulin Fab region?

A
  • -Contains the variable/hypervariable region
  • -Formed bylight (L) chains and heavy chains (H)
  • -Recognizes and binds to antigens via epitope
  • -Determines the idiotype, which is specific for one antigen only
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6
Q

what is the immunoglobulin idiotype?

A

The three-dimensional characteristic of an immunoglobulin variable region that imparts the immunoglobulin specificity for a given antigen.

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7
Q

what regions of immunoglobulins determine idiotype vs isotype?

A

Fab vs Fc

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8
Q

how immunoglobulins acquire their antigen specificity/

A
  • -Occurs by somatic hypermutation and affinity maturation
  • -Alterations take place in the variable region.
  • -Normal response to antigenic stimulation: B lymphocytes with varying immunoglobulin alleles (i.e., polyclonal proliferation)
  • -Malignant lymphocyte proliferation: predominance of B lymphocytes with a single immunoglobulin variable domain (i.e., monoclonal proliferation)
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9
Q

what is the somatic hypermutation?

A

A process in which a gene locus undergoes a rate of mutation that is 100,000-1,000,000 times greater than the rate of mutation in the rest of the genome. Typically results in single-base substitutions. Normally occurs only in proliferating B cells to generate antibodies against specific antigens.

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10
Q

what is the affinity maturation?

A

A process in which B cells interact with T-helper cells to produce antibodies with higher affinity for specific antigens. Mechanisms leading to increased affinity include somatic hypermutation and clonal selection.

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11
Q

what is the isotype switching?

A
  • -Within the germinal centers of lymph nodes, activated B cells change the antibody isotype in response to specific cytokines that are released by Th cells. IgM, the primary antibody on B cells before getting activated, is switched to IgA, IgE, or IgG. IgM is also secreted by plasma cells (stimulated by IL-6).
  • -A mechanism that changes the type of immunoglobulin produced by a mature B cell, usually from IgM to another isotype (e.g., IgE, IgA, and IgG). The heavy chain constant region (Fc region) is changed while the heavy chain variable region, which is specific to the antigen, remains the same.
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12
Q

isotype switching occurs by changes in the heavy chain variable region.True/False

A

False
The heavy chain constant region (Fc region) is changed while the heavy chain variable region, which is specific to the antigen, remains the same.

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13
Q

does immunoglobulin diversity require antigen exposure?

A

No

  • -Does not require antigens
  • -Random recombination of certain genes during B cell maturation in bone marrow
  • -Light chain: VJ genes
  • -Heavy chain: V(D)J genes
  • -Terminal deoxynucleotidyl transferase (TdT) randomly adds nucleotides to the DNA.
  • -Recombination of light chains with heavy chains occurs randomly.
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14
Q

what is the TdT?

A

specialized DNA polymerase expressed at high levels in immature T and B cells. It is helpful in the diagnosis of acute lymphoblastic leukemia.

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15
Q

what are the immunoglobulin genes?

A
  • V variable
  • D diversity (heavy chains only)
  • J joining
  • C constant
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16
Q

D gene is only for the light chains. True/False

A

False

  • -Light chain: VJ genes
  • -Heavy chain: V(D)J genes
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17
Q

B cells mature in the thymus.True/False

A

False

  • -Major component of the adaptive immune system (especially humoral immune response)
  • -Originate in the bone marrow, where they develop to mature, naive B cells
  • -Mature B cells circulate in between the blood and secondary lymphatic organs (e.g., lymph nodes, spleen, MALT)
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18
Q

how B cells are activated?

A
  • -Activation of mature B cells: occurs in response to an antigen
  • -Each B cell responds to a specific antigen depending on its unique B-cell receptor.
  • -Nonprotein antigens: B cell activation occurs independently
  • -Protein or peptide antigens: B cell activation involves Ig class switching, which requires the involvement of T-helper cells
  • -After activation: B cells differentiate into plasma cells that produce and secrete antibodies (see immunoglobulins), e.g., to opsonize bacteria which facilitates phagocytosis.
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19
Q

do proteins lead to B cell activation independently by themselves?

A

No

  • -Nonprotein antigens: B cell activation occurs independently
  • -Protein or peptide antigens: B cell activation involves Ig class switching, which requires the involvement of T-helper cells
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20
Q

describe Th cell‑independent activation of B cells (1° response

A
  • -Immediate response to an antigen → leads to production of IgM antibodies
  • -Polysaccharide, lipid, and lipopolysaccharide (LPS) antigens activate B cells and induce antibody production without any further stimulation by T-helper cells.
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21
Q

does class switching occur in B cell-independent activation?

A

No Ig class-switching occurs without T-helper cells.

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22
Q

what type of antigens activate B cells independently?

A

Polysaccharide, lipid, and lipopolysaccharide (LPS) antigens activate B cells and induce antibody production without any further stimulation by T-helper cells.

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23
Q

describe B cell activation via Th cells (2° response)

A
  • -Requires activation of CD4+T-helper cells
  • -B lymphocytes recognize protein/peptide antigens via their B-cell receptors (membrane‑bound immunoglobulins, IgD or IgM) → B cell receptor-mediated endocytosis of the BCR/antigen complex → breakdown of antigen into small fragments by lysosomal proteases → presentation of antigen fragment via MHC class II receptors on B cell surface to Th cells → interaction between Th2 cells and B lymphocytes → T cell‑dependent activation of B cells (plasma cells) → immunoglobulin production
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24
Q

what are th4r B cell receptors?

A

membrane‑bound immunoglobulins, IgD or IgM

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25
Q

how affinity maturation occurs?

A
  • -A process in which B cells interact with Th cells within the germinal center of secondary lymphoid tissue in order to secrete immunoglobulins with higher affinity for specific antigens.
  • -Mechanisms that lead to increased affinity
    1) Somatic hypermutation: Point mutations that create random alterations in the variable region of the antibody gene.
    2) Clonal selection: B cells that possess antibodies with higher affinity for the antigen have a survival advantage through positive selection → proliferate and predominate within the follicle.
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26
Q

what are the mechanisms that lead to affinity maturation?

A

1) Somatic hypermutation: Point mutations that create random alterations in the variable region of the antibody gene.
2) Clonal selection: B cells that possess antibodies with higher affinity for the antigen have a survival advantage through positive selection → proliferate and predominate within the follicle.

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27
Q

how isotype switching occurs?

A
  • -B cell class switching occurs via two signaling mechanisms
    1) signal = activation: Antigen bound to MHC II molecule binds to the T-cell receptor on the surface of T-helper cells.
    2) signal = CD40 membrane receptor on the B cell binds to CD40 ligand (CD40L) on the surface of CD4+ T cell (CD40L/CD40) → Released cytokines determine immunoglobulin class switching.
  • -IL-4, IL-13 stimulates class switching to IgE.
  • -IL-5, TGF-β stimulates class switching to IgA.
  • -IFN-β stimulates class switching to IgG.
  • -The resulting antibody has the same affinity for the antigen but a different function.
  • -Isotype switching is irreversible.
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28
Q

does isotype switching is reversible?

A

no

29
Q

what cytokines determines class switching to IgA?

A
  • -IL-4, IL-13 stimulate class switching to IgE.
  • -IL-5, TGF-β stimulate class switching to IgA.
  • -IFN-β stimulates class switching to IgG.
30
Q

the second signal for class switching is the binding of CD40 L on B cell to CD 40 on CD4+ T cell. True/False

A

False

CD40 membrane receptor on the B cell binds to CD40 ligand (CD40L) on the surface of CD4+ T cell (CD40L/CD40)

31
Q

how do B lymphocytes return to the bloodstream?

A

through thoracic duct

32
Q

what is the thoracic duct?

A

The largest lymphatic channel in the body. Drains the lower limbs, pelvis, abdomen, left side of the thorax, left upper limb, and left side of the head and neck. Originates from the cysterna chyli (below the diaphragm), passes through the aortic hiatus, lies in the posterior mediastinum, and terminates by draining into the junction of the left subclavian and internal jugular veins.

33
Q

what is the structure of the lymph node?

A
  • -Bean-shaped organ surrounded by fibrous capsule with trabeculae
  • -Numerous afferent lymphatic vessels enter through the capsule.
  • -The trabecular sinus leads lymph from the subcapsular sinus to the medullary sinus.
  • -The hilus allows blood vessels and efferent lymphatic vessel to enter or leave the lymph node
  • -The entering artery and vein branch into a large capillary network, which forms the post-capillary high endothelial venules.
34
Q

how many afferents and efferents have lymph nodes?

A

Typically only one efferent lymphatic vessel or a small number of these vessels leave the lymph node, compared to the larger number of afferent lymphatic vessels that enter the lymph node through the cortex.

35
Q

Lymph node parenchyma can be divided into the …

A

cortex, paracortex, and medulla.

36
Q

describe the cortex of the lymph node

A
  • -Lymphoid follicles: site of B lymphocyte storage, differentiation, and proliferation
  • -Primary follicle (inactive): aggregates of naive B lymphocytes
  • -Secondary follicle (active): dense mantle zone surrounding a pale germinal center
37
Q

what are the germinal centers?

A

Germinal centers develop following antigen contact. They are the site of B lymphocyte activation, which leads to somatic hypermutation and affinity maturation.

38
Q

what is the paracortex of the lymph node?

A
  • -T lymphocytes and high endothelial venules

- -Site of T-cell activation

39
Q

what are the high endothelial venules?

A

High endothelial venules allow circulating B and T lymphocytes to enter or leave the lymph node.

40
Q

site of negative vs positive selection of B cells?

A

BM vs secondary lymphoid organs

41
Q

does isotype switching require T cell help?

A

Yes

Antigen bound to MHC II molecule binds to T-cell receptor on the surface of T-helper cells.

42
Q

what are the classes of immunoglobulins?

A
  • -IgM
  • -IgG
  • -IgE
  • -IgA
  • -IgD
43
Q

what is the largest antibody?

A

IgM

IgM antibodies are too large to pass through the placenta and are not transferred to the infant via breast milk.

44
Q

describe IgM

A
  • -Largest antibody, located on the surface of B cells as a monomer and circulating as a pentamer (with J chain)
  • -Formed early (evidence of recent infection)
  • -Activates complement
  • -Blood group antibodies
  • -Immune response (early reaction) antibodies, e.g., anti-HBc (hepatitis C core) IgM antibody
45
Q

IgM is a dimer. True/False

A

False

located on the surface of B cells as a monomer and circulating as a pentamer (with J chain)

46
Q

what is the first antibody produced in response to an infection?

A

IgM

47
Q

describe IgG

A
  • -Most abundant immunoglobulin in blood serum
  • -Delayed formation during the course of infection (IgM-IgG switch); ensures long‑term immunity
  • -Titer determination for follow‑up: high affinity and specificity
  • -Can be free-floating in serum or bound to the surface of lymphocytes
  • -The only immunoglobulin that can cross the placenta and thus convey passive immunity to the child
  • -Activates complement
  • -Opsonization of bacteria
  • -Neutralization of viruses and toxins
  • -Rhesus antibodies
  • -Immune response (late reaction) antibodies, e.g., anti‑Hbc IgG
  • -Allergy: mediation of type II hypersensitivity, type III hypersensitivity
48
Q

The only immunoglobulin that can cross the placenta and thus convey passive immunity to the child?

A

IgG

49
Q

IgG is a monomer or dimer?

A

monomer

50
Q

what is the role of IgG in response to infection?

A
  • -Delayed formation during the course of infection (IgM-IgG switch); ensures long‑term immunity
  • -Titer determination for follow‑up: high affinity and specificity
51
Q

how IgG fights bacteria?

A
  • -Activates complement
  • -Opsonization of bacteria
  • -Neutralization of viruses and toxins
52
Q

blood group vs rhesus antibodies?

A

IgM vs IgG

53
Q

IgA is a monomer or dimer?

A

Monomer in circulation and dimer when secreted

54
Q

describe IgA

A
  • -Monomer in circulation and dimer when secreted
  • -Most abundant immunoglobulin in the body but has a low serum concentration
  • -Found especially on mucosal surfaces and in bodily fluids
  • -Prevents binding of pathogens to host cells
  • -Secretory component protects IgA from proteases (e.g., in the gastrointestinal tract)
  • -IgA antibodies to tissue transglutaminase are present in gluten‑sensitive enteropathy (celiac disease)
  • -Important in defense against intestinal infections (e.g., giardiasis)
55
Q

what is the most abundant antibody in the body?

A

IgA

56
Q

what is selective IgA deficiency?

A

The most common primary immunodeficiency syndrome. Patients have an isolated deficiency of IgA, with normal serum levels of IgG and IgM. Clinical manifestations are highly variable and range from asymptomatic to recurrent sinopulmonary (mostly caused by encapsulated bacteria, e.g., S. pneumoniae, H. influenzae) and GI infections (e.g., due to Giardia lamblia), as secretory IgA antibodies are a crucial part of mucosal defense.

57
Q

IgA are found especially on…

A
  • -mucosal surfaces and in bodily fluids
  • -found in tears, saliva, mucus, and breast milk. The IgA content of breast milk is responsible for maternal passive immunity in breastfed newborns.
58
Q

describe IgE

A
  • -Defense against parasites
  • -Binds to mast cells → cross-linking → release of histamine (involved in allergic diseases)
  • -Binds to basophils
  • -Allergy: mediation of immediate‑type reaction (type I hypersensitivity - e.g.., anaphylaxis)
59
Q

IgE is a monomer or dimer?

A

monomer

60
Q

what are the effector functions of antibodies?

A
  • Neutralization
  • Complement Activation
  • Opsonisation
  • Antibody-directed cellular cytotoxicity
61
Q

what is the antibody-dependent cellular cytotoxicity?

A

ADCC is independent of the immune complement system that also lyses targets but does not require any other cell. ADCC requires an effector cell which classically is known to be natural killer (NK) cells that typically interact with immunoglobulin G (IgG) antibodies. However, macrophages, neutrophils, and eosinophils can also mediate ADCC, such as eosinophils killing certain parasitic worms known as helminths via IgE antibodies.
ADCC is part of the adaptive immune response due to its dependence on a prior antibody response

62
Q

how antibodies neutralize toxins?

A

1) toxin binds to cell surface receptor
2) endocytosis of toxin-receptor complex
3) dissociation of the toxin to release active chain that poisons the cell
4) neutralizing antibody binds to the toxin and prevents from it binding to cell surface receptor

63
Q

how antibodies neutralize bacteria?

A

antibodies against adhesins block colonization and uptake of bacteria

64
Q

which pathway of complement activation is dependent on antibodies?

A
  • -Classical pathway: activated by IgM or IgG complexes binding to the pathogen (via C1)
  • -Alternative pathway: activated directly by pathogen rather than by antigen-antibody complexes (via C3)
  • -Lectin pathway (via C1-like complex)
65
Q

what is the opsonization?

A

the process of altering bacteria to increase their susceptibility to phagocytosis.

  • -IgM and IgG antibodies
  • -C3b and IgG are the two main opsonins for bacteria (via C3b).
66
Q

how humoral immunity is assessed?

A 
•	Clinical history
•	Measurement of Immunoglobulins:
--IgG subclasses, complement activity
•	Serum protein electrophoresis
•	Functional assessment of antibody production
–	Naturally occurring antibody
–	Vaccine induced antibodies
–	Test vaccination
•	B cell Numbers (Tonsils/Blood/BM)
•	B cell proliferation – not routine
67
Q

what is the immunologic memory?

A

The ability of the immune system to recognize antigens from previous encounters and quickly and efficiently initiate an immune response to subsequent exposure to the antigen.

68
Q

how memory B cells are formed?

A
  • -Specialized plasma cells that have the ability to persist for decades following the elimination of an antigen and produce high-affinity antibodies throughout their lifespan.
  • -Undergo proliferation, somatic hypermutation, clonal selection, and antigen switching
  • -Since memory B cells have undergone somatic hypermutation and clonal selection, they have the ability to rapidly produce high-affinity antibodies following subsequent exposure to the antigen.
  • -Arrested in their differentiation and persist in the marginal zone of follicles
  • -Selection of memory B cells is dependent upon sustained stimulation of their CD40 receptor by CD154-positive T cells.
  • -Memory B cells secrete high-affinity antibodies and accelerate the secondary immune response to the antigen.

Immunology (9 decks)

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