Aaaai

Front 1

Proteins

Back 1

Excellent immunogens, antigen presented to MHC class I- and MHC class II-restricted cells.
o T-lymphocyte-dependent antigens.
o Immunizations which are protein based antigens include diphtheria and tetanus.

Front 2

Polysaccharides

Back 2

T-lymphocyte-independent antigens.
o The meningococcal and 23 valent pneumococcal immunizations are examples of T lymphocyte independent antigens.

Front 3

Composite of antigens

Back 3

Proteins, Polysaccharides, NA, and Lipids

Front 4

Lipids

Back 4

MHC-like CD1 molecules bind lipid antigens that are recognized by natural killer T lymphocytes (NKT cells), γδ T lymphocytes, and other lipid antigen-specific T lymphocytes.

Front 5

Antigenic Determinants as recognized by B Lymphocytes

Back 5

Linear determinants or tertiary structure. Carbohydrates, amino acids, and nucleic acids. Four to eight residues. Polysaccharides are considered T-lymphocyte-independent (TI) antigens.

Front 6

Proteins

Back 6

Excellent immunogens, antigen presented to MHC class I- and MHC class II-restricted cells.
o T-lymphocyte-dependent antigens.
o Immunizations which are protein based antigens include diphtheria and tetanus.

Front 7

Polysaccharides

Back 7

T-lymphocyte-independent antigens.
o The meningococcal and 23 valent pneumococcal immunizations are examples of T lymphocyte independent antigens.

Front 8

Composite of antigens

Back 8

Proteins, Polysaccharides, NA, and Lipids

Front 9

Lipids

Back 9

MHC-like CD1 molecules bind lipid antigens that are recognized by natural killer T lymphocytes (NKT cells), γδ T lymphocytes, and other lipid antigen-specific T lymphocytes.

Front 10

Antigenic Determinants as recognized by B Lymphocytes

Back 10

Linear determinants or tertiary structure. Carbohydrates, amino acids, and nucleic acids. Four to eight residues. Polysaccharides are considered T-lymphocyte-independent (TI) antigens.

Front 11

Superantigens bind to the Vbeta region of TCR and outside of the peptide binding group on MHC molecules.

Back 11

Front 12

Hapten

Back 12

Antigen that requires covalent linkage to a carrier to stimulate immune response (eg, penicillin is a hapten).

Front 13

Carrier:

Back 13

A macromolecular substance to which a hapten is coupled in order to produce an immune response against the hapten.

Front 14

Adjuvant:

Back 14

Molecules that enhance the immune response. Adjuvants release bound antigens to antigen-presenting cells (APCs) over a prolonged period, interact with toll-like receptors, and stimulate chemokine and cytokine release. Examples include the following: Alum. Freund’s adjuvant: emulsified bacterial products (eg, bacille Calmette-Guérin (BCGs]). Incomplete Freund’s adjuvant: water in oil emulsification. Ribi adjuvant system: Squalene-Tween80-water and oil emulsification. Titermax: copolymers polyoxypropylene (POP) and polyoxyethylene (POE).

Front 15

Epitope (Antigenic determinant):

Back 15

Antigenic component identified by a unique antibody. May represent linear amino acid sequence or antigenic tertiary structure.

Front 16

Superantigen:

Back 16

Antigens that activate a large number of polyclonal T lymphocytes. Examples of microbial toxin superantigens are provided

Front 17

Superantigens binds to the ___ of the TCR

Back 17

Superantigens bind to the Vβ chain of the T cell receptor (TCR) bypassing the need for the specific major histocompatibility complex (MHC), peptide, or TCR trimolecular complex required for signal 1 (Figure 1-1).

Front 18

Antigenic Determinants recognized by B cells

Back 18

Linear determinants or tertiary structure. Carbohydrates, amino acids, and nucleic acids. Four to eight residues. Polysaccharides are considered T-lymphocyte-independent (TI) antigens.

Front 19

AD Recognized by T lymphocyte:

Back 19

Linear determinants. Amino acid peptides. Eight to 30 amino acids (MHC class I 8-11 aa and MHC class II 10-30 aa).

Front 20

MHC I are constitutively expressed by _____ and induced by ______

Back 20

Most nucleated cells; IFN gamma

Front 21

MHC 2 are constitutively expressed by _____ and induced by ______

Back 21

APC (Dendritic cells, Macrophages,
and B lymphocytes), thymic
epithelia, and activated T
lymphocytes; IFN gamma

Front 22

Map of the MHC Genome; encoded on short arm Chr 6

Back 22

Front 23

Class III region encodes for

Back 23

Proteins of the complement system: Factor B, C4a, C4b, and C2. Cytokines: tumor necrosis factor (TNF)α, and lymphotoxins α and β. Heat shock proteins.

Front 24

Class I encodes for

Back 24

HLA E: NK cell recognition. HLA F: localized to endoplasmic reticulum and Golgi apparatus. HLA G: on fetal-derived placental cells. HLA H: involved in iron metabolism.

Front 25

For MHC Class I, polypeptides remain sequestered in the endoplasmic reticulum by interacting with:

Back 25

Calnexin, Calreticulin, Erp57, and Tapasin.

Front 26

Organisms that enter the cytoplasm are degraded to antigenic peptides by the

Back 26

proteasome:
o The proteasome is a multi-subunit proteinase. Four seven-membrane rings have catalytic subunits.
o Examples of subunits are: low molecular mass polypeptide (LMP) 7 and LMP2.
o LMPs are encoded in MHC class II locus.

Front 27

Antigenic peptides are transported into the endoplasmic reticulum by transporter associated with antigen processing (TAP) proteins.

Back 27

Energy-dependent transport of peptides.
o Composed of two subunits: TAP1 and TAP2, both of which must be present for function.
o TAP proteins are encoded in MHC class II locus.

Front 28

Post transport into ER, antigenic peptides are..

Back 28

loaded onto newly synthesized MHC class I polypeptides. MHC class I and antigenic peptide are transported to cell surface. Stable MHC class I expression requires presence of antigenic peptide.

Front 29

In MHC 2 Extracellular antigen is endocytosed (directly via Fc or complement receptors) and compartmentalized in cytosolic phagosomes.

Back 29

Phagosomes fuse with lysosomes. The resulting phagolysosome degrades the microbe into antigenic peptides.

Front 30

Newly synthesized MHC class II molecules are synthesized in the endoplasmic reticulum and transported to the phagolysosome, forming the MHC class II vesicle. The MHC class II binding cleft is occupied by

Back 30

invariant chain (Ii) prior to antigen loading.

Front 31

In the MHC class II vesicle, the Ii is degraded by proteolytic enzymes, leaving behind a

Back 31

short peptide named class II-associated invariant chain peptide (CLIP).

Front 32

_____ removes CLIP and allows antigenic peptides to be loaded in the MHC binding cleft. MHC class II and peptide are transported to cell surface.

Back 32

HLA-DM

Front 33

HLA-DM

Back 33

is an intracellular protein that is involved in MHC class II antigen processing and does not present antigenic peptides nor is it a component of MHC class II.

Front 34

MHC I Mutation, inheritence, and syndrome

Back 34

Genes encoding for transporter associated with antigen presentation (TAP) – essential for MHCI expression.; AR; Sinopulmonary infections, granulomatous skin lesions, and necrobiosis lipoidica.

Front 35

MHC1 Lab/Tx

Back 35

CD8 Lymphopenia, PBMC on flow cytometry lack MHC class I.; Treat pulmonary infections like CF (aggressive toileting and chest PT)

Front 36

MHC2 defx (Mutation/inheritence, syndrome)

Back 36

Genes encoding for mutations in several transcription factors required for MHC class II expression: MHC2TA, RFX5, FRXAP, and FRXANK.; Diarrhea, hepatosplenomegaly, transaminitis, sclerosing cholangitis (Cryptosporidium parvum), pulmonary infections (Pneumocystis jiroveci, encapsulated bacteria, Herpesviridae, and respiratory syncytial virus [RSV]), and meningitis.

Front 37

MHC2 defx (Lab/Tx)

Back 37

CD4 Lymphopenia (reversed CD4:CD8) Lack of HLA DR/DP/DQ on lymphocytes, delayed-type hypersensitivity test (DTH). Hypogammaglobulinemia. Absent germinal centers from LN.; HSCT

Front 38

Tolerance

Back 38

is defined as unresponsiveness to an antigen. This can be to self-antigens, self-tolerance, or to foreign antigens. Self-tolerance is part of the normal function of educating the immune system not to react to itself.

Front 39

Tolerogens

Back 39

are antigens that induce tolerance. A foreign antigen that becomes a tolerogen is conditional. The antigen may only induce tolerance under certain conditions, like age or the amount of antigen being at a very low or high concentration.

Front 40

Anergy

Back 40

is a state of unresponsiveness to antigenic stimulation. The antigen is recognized by the immune cell; but weak signaling, due to a lack of costimulus, leads to anergy. Other factors include antigen type and antigen dose.

Front 41

Central tolerance occurs is the lymph organs. T lymphocytes are educated and tolerized in

Back 41

Thymus

Front 42

For T-lymphocyte central tolerance, it is a T lymphocyte precursor that is exposed to a self-antigen in the thymus. The T lymphocyte is exposed to a self-antigen, which yields two fates:

Back 42

apoptosis, which is also known as negative selection, or development into a regulatory T (Treg) cell, which will migrate to the periphery. Knowledge of T lymphocyte tolerance is limited to CD4+ T lymphocytes, including Treg cells.

Front 43

For B-lymphocyte central tolerance, the precursor B lymphocyte is exposed to a self-antigen in the bone marrow during development. The immature B lymphocyte is exposed to self-antigen, which yields three fates:

Back 43

apoptosis (or negative selection), receptor editing, or anergy.

Front 44

Receptor Editing

Back 44

reactivates recombination activation gene (RAG)-1 and RAG-2, which rearrange the Ig light chain, producing new receptor specificity.

Front 45

Receptor editing is seen in ____ concentration of antigen.

Back 45

high; In low antigen concentration, the B lymphocyte may become anergic to the self-antigen.

Front 46

In both T and B lymphocytes, peripheral tolerance occurs in peripheral tissues when a mature lymphocyte encounters a self-antigen.

Back 46

In the case of a T lymphocyte, if recognition of self-antigen occurs, the T lymphocyte may be induced to undergo apoptosis, may become anergic, or a Treg cell that confers suppression. In this situation, a B lymphocyte will either become anergic or be deleted through apoptosis.

Front 47

The two main factors determining tolerance or negative selection are _______ and ______ to the TCR.

Back 47

concentration and affinity; high concentration and high affinity --> negative selection

Front 48

The thymus presents self-antigens through thymic antigen-presenting lymphocytes that process antigen in the context .

Back 48

of HLA class I and II

Front 49

This gene promotes expression of non-thymic tissue antigens in the thymus!

Back 49

; AIRE, Mutation in the AIRE gene produces disorders such as autoimmune polyglandular syndrome (APS). Lymphocytes are not deleted or tolerized to endocrine-related self-antigens. The endocrine organs are attacked by autoreactive T lymphocytes and autoantibodies.

Front 50

Peripheral T-Lymphocyte Tolerance

Back 50

—Peripheral tolerance has the same outcomes as central tolerance: anergy, deletion, or regulation. Lack of a second signal or lack of innate costimulation (eg, micro environment) produces anergy of the peripheral T lymphocytes.

Front 51

Anergy in these T lymphocytes is maintained by

Back 51

TCR-signaling, ubiquitin ligases, which target proteins for degradation, and inhibitor costimulatory molecules, such as CTLA-4 and PD-1. Dendritic cells may also present self-antigen without expression of costimulator molecules

Front 52

Once a cell is anergic,

Back 52

costimulation will not restore activation.

Front 53

Dendritic cells that are not activated that are or immature still present self-antigen on their surfaces. These cells in an immature state do not express receptors, thus antigen presented to T lymphocytes will

Back 53

will not have a second signal resulting in tolerance. This presentation of antigen by the dendritic cell is ongoing, which reminds cells not to be self-reactive

Front 54

Treg cells are mainly thymic emigrants that respond to self-antigen. Despite being self-reactive, they are allowed to escape the thymus and, instead, help to

Back 54

maintain self-tolerance. Characteristically, they express CD25 (ie, the interleukin [IL]-2R α chain).

Front 55

Treg cells: Their survival depends on IL-2 and transforming growth factor β (TGFβ). Tolerance or regulation is maintained by secretion of IL-10 and TGFβ.

Back 55

IL-10 targets macrophages and dendritic cells, and TGFβ inhibits lymphocytes and macrophages.

Front 56

Apoptosis is a key regulator of self-reacting T lymphocytes. Self-antigens repeatedly recognized by a T lymphocyte without costimulation can activate Bim,

Back 56

proapoptotic member of the Bcl-2 protein family. Bim works through a mitochondrial pathway.

Front 57

Cells presenting self-antigen without innate response or costimulation have other receptors on their surfaces,

Back 57

such as Fas Ligand (FASL) (CD95L) on the T lymphocyte. FASL is upregulated on repeatedly activated T lymphocytes. FASL can interact with FAS (CD95) on the same cell or nearby cells, either deleting a self-reactive T lymphocyte or causing the death of an activated cell, thereby down-regulating the immune response. The FAS:FASL interaction signals through the caspase system.

Front 58

Mutations in FAS or Caspase 10

Back 58

as autoimmune lymphoproliferative syndrome (ALPS). The lymphocytes do not know when to die. They accumulate in the lymph organs. There is a lack of tolerance, producing autoimmune problems.

Front 59

Central B-lymphocyte tolerance can include deletion or receptor editing. Receptor editing reactivates

Back 59

RAG-1 and RAG-2 when a high affinity self-antigen is recognized by a B cell receptor (BCR). The RAG enzymes will give the BCR a new light chain.

Front 60

___ light chains are rearranged first. If receptor editing is needed, a ___ light chain will be used.

Back 60

kappa, lambda

Front 61

If both recombinations recognize a self-antigen, the immature B lymphocyte

Back 61

deleted

Front 62

Chronic antigen recognition down-regulates CXCR5,

Back 62

inhibiting B lymphocyte homing and interaction with T lymphocyte, which yields death.

Front 63

Tolerance features

Back 63

Front 64

In central tolerance, the T lymphocyte can be deleted by negative selection of high affinity self-antigens or apoptosis; or some “self recognizers”

Back 64

can be released into the periphery to become regulator cells to maintain tolerance.

Front 65

B-lymphocyte central tolerance can yield deletion; but, prior to deletion, _________ may save the B lymphocyte from negative selection.

Back 65

receptor editing

Front 66

Peripheral tolerance can result in deletion or anergy. Anergy occurs with ____________ without a second signal and/or inflammation.

Back 66

antigen exposure

Front 67

A and G are purines,

Back 67

composed of two fused rings of carbon and nitrogen.

Front 68

T and C are pyrimidines,

Back 68

are composed of one simple ring of carbon and nitrogen.

Front 69

Double helix winds around ______ to form _________

Back 69

histones; chromatin

Front 70

X opens the chromatin to allow transcription. ____________ represses gene expression and is reduced in X

Back 70

trasncription; histone deacetylation; COPD

Front 71

RNA

Back 71

Protein synthesis occurs via RNA. Composed of nucleotides. Contains the pyrimidine uracil (U), instead of T. mRNA is copied from DNA and travels to ribosome. tRNA transports amino acids to ribosome. rRNA and protein combine to make ribosomes.

Front 72

Mutations result from changes in the nucleotide sequence of genes (Table 1-8). Germline mutations can be passed down via X

Back 72

reproductive cells

Front 73

Somatic mutations involve cells outside the reproductive system and generally do not get passed to

Back 73

subsequent generation

Front 74

Frameshift

Back 74

Caused by the insertion or deletion of a number of nucleotides then evenly divisible by three, which causes the incorrect translation of amino acids downstream from the mutation.

Front 75

Point

Back 75

Type of point mutation, where a single nucleotide substitution causes the translation of a different amino acid.

Front 76

Nonsense

Back 76

Type of point mutation, where a single nucleotide substitution causes an early stop (or termination) codon.

Front 77

Silent

Back 77

Does not cause a change in amino acid sequence.

Front 78

Neutral

Back 78

Causes a different but similar amino acid to be translated.

Front 79

X can be described as changes in gene function that occur without a change in the sequence of DNA. These changes occur as a result of the interaction of the environment with the genome.

Back 79

Epigenetics

Front 80

X AND Y likely play a crucial role in the epigenetic regulation of immune system genes.

Back 80

DNA Methylation, Histone acetylation

Front 81

SNP associated with increased incidence of eczema and asthma.

Back 81

Fillagrin,

Front 82

SNP a/w increased in asthma

Back 82

17q12-21; ORMDL3

Front 83

SNPs associated with both increased as well as reduced risk of development of asthma and atopy.

Back 83

5q22-32, CD14, LPS receptor

Front 84

SNP found to protect against nonatopic asthma.

Back 84

3p21-22, CCR5, Chemokine Receptor

Front 85

SNP confers increased risk for asthma, rhinitis, atopic dermatitis, and increased specific IgE.

Back 85

XPR, TLR 7 & 8, pattern recognition receptor for viral ssRNA

Front 86

SNP associated with increased risk of asthma, bronchial hyperresponsiveness, and skin-test responsiveness. SNP may be linked to response to montelukast.

Back 86

5q31, IL13, Cytokine that induces IgE secretion, mucus production, and collagen synthesis.

Front 87

Argenteum (Arg) or Arg phenotype with decreased albuterol response compared to Gly/Gly phenotype at residue 16.

Back 87

ADRB2, B2 receptor, adrenaline/noradrenaline receptor

Front 88

SNP confers risk of asthma and bronchial hyperresponsiveness

Back 88

ADAM33, Type 1 membrane e pt; involved in cell/cell intxns.

Front 89

Immunoglobulins (Igs) are glycoprotein molecules produced by B lymphocytes and plasma cells in response to an immunogen.

Back 89

Ig is the key component of humoral immunity. The earliest cell in B-lymphocyte lineage that produces Ig is the pre-B lymphocyte. An adult human produces approximately 2-3 grams of Ig every day.

Front 90

The Ig molecule is a polypeptide heterodimer that is composed of

Back 90

two identical light chains and two identical heavy chains connected by disulfide bonds (Figure 1-6). Each chain consists of two or more Ig domains, which are compact, globular structures of approximately 110 amino acids containing intrachain disulfide bonds.

Front 91

Heavy chains are designated by letters of the Greek alphabet (ie, γ, α, μ, ε, δ) for Ig classes: G, A, M, E, and D, respectively. Human IgG consists of four isotypes:

Back 91

IgG1, IgG2, IgG3, and IgG4.

Front 92

The constant (C) regions of IgG, IgA, and IgD consist of only X CH domains.

Back 92

3

Front 93

In IgM and IgE, the C regions consist of X CH domains.

Back 93

4

Front 94

Ig structure

Back 94

Front 95

Light chains κ and λ are identified by their

Back 95

C region

Front 96

An Ig molecule has either X or Y but never one of each.

Back 96

kk, or lambda/lambda

Front 97

An individual B lymphocyte will produce only

Back 97

κ or λ chains but never both.

Front 98

The ratio of κ-bearing lymphocytes to λ-bearing lymphocytes can be used as an indication

Back 98

clonality and is, therefore, useful in diagnosing and typing B lymphocyte lymphomas.

Front 99

Hinge regions are X and provide Ig flexibility.

Back 99

proline rich

Front 100

Ig fragments are produced from enzymatic cleavage of the Ig molecule. Enzymatic digestion provides useful reagents for determining Ig function and activity. Papain cleaves Ig above the hinge (as seen in Figure 1-6) and results in X and Y fragment.

Back 100

2 Fab (antigen binding) and one Fc (Crystallizable)

Front 101

Pepsin cleaves Ig below the hinge at multiple sites and produces

Back 101

F(ab′)2, which contains interchain disulfide bonds, and exhibits two antigen-binding sites..

Front 102

F(ab) can X but not Y, F(ab')2 can _____

Back 102

F(ab) can bind but not crosslink; and F(ab′)2 both binds and crosslinks

Front 103

Variable regions VL and VH form the antigen-binding sites that consist of

Back 103

complementarity determining regions (CDRs) of about ten amino acids and account for antibody diversity.

Front 104

There are X CDRs in each V region; Y is the most variable and, typically, has the most extensive contact with the antigen.

Back 104

3; CDR3

Front 105

Constant regions CH and CL are located at C-terminals of the Ig molecule. Only X mediates effector functions by binding to Fc receptors or binding complement.

Back 105

CH

Front 106

Most variable part of the Ig

Back 106

CDR3

Front 107

Two forms of Ig exist that differ in the X (membrane vs secreted)

Back 107

amino acid sequence of the C-terminal end of the CH.

Front 108

Membrane-bound Ig (or surface Ig) is attached to the B lymphocyte surface by its transmembrane region.

Back 108

Once Ig molecules bind to antigens and are cross-linked, they serve as B lymphocyte antigen receptors that mediate B lymphocyte activation.

Front 109

Secreted Ig molecules lack transmembrane regions and circulate in

Back 109

plasma, mucosal sites, and interstitial fluids. Secreted Ig can be in the form of monomers (all Ig), dimers (IgA), or pentamers (IgM).

Front 110

Dimers or pentamers are formed by

Back 110

tail pieces connected by disulfide bonds to joining (J) chain.

Front 111

Affinity

Back 111

strength of the binding between each molecule of Ig and antigen epitopes, and is indicated by Kd. A numerically lower Kd indicates higher affinity.

Front 112

Avidity

Back 112

It is an estimate of the overall strength of the binding between Ig and antigen. A low-affinity IgM can produce a high-avidity interaction by simultaneous binding to multiple antigen epitopes, through 10 contact sites on each IgM molecule.

Front 113

Ig Superfamily

Back 113

group of proteins that share similar structure to Ig by having one or more domains composed of 70-110 amino acids, most typically containing an intrachain disulfide loop. Examples of Ig superfamily members are TCR, MHC molecules, CD4, CD8, B7-1, B7-2, Fc receptors, KIR, and VCAM-

Front 114

Ig can recognize highly diverse antigens through

Back 114

linear and conformational determinants found in various macromolecules (ie, proteins, polysaccharides, and lipids).

Front 115

TCRs only recognize

Back 115

linear determinants of peptides presented by MHC molecules.

Front 116

IgM is the first

Back 116

produced after birth, the first to reach adult level, and the first to be synthesized following antigenic stimulation.

Front 117

Only IgG crosses placenta. IgG level reaches a nadir around

Back 117

four to six months after birth due to declining in passively-transferred maternal IgG.

Front 118

IgA is produced in the highest quantity daily, and is found in higher concentrations

Back 118

in the respiratory and GI mucosal surfaces.

Front 119

In the gastrointestinal tract, IgA is produced by plasma cells in the lamina propria and is transported across the mucosal epithelium by

Back 119

poly-Ig receptor (transcytosis).

Front 120

Rheumatoid factor (RF) is an antibody against the

Back 120

Fc portion of IgG. RF is most commonly IgM, but can also be any other isotype.

Front 121

fixes complement most efficiently of any Ig isotype.

Back 121

IgM

Front 122

The shortest half-life of all IgG subclasses is IgG3.

Back 122

IgG3

Front 123

Ig Isotype Summary

Back 123

Front 124

Antigen recognition by Ig initiates a humoral immune response. Ig selectively captures antigens and microbial pathogens, including bacteria and viruses through noncovalent, reversible binding through the

Back 124

Ig V regions.

Front 125

Ig-mediated effector functions include:

Back 125

neutralization of microbes or toxins, opsonization, ADCC, and immediate hypersensitivity (IgE).

Front 126

Variability in the structures of the antigen-binding site of Ig and TCR.

Back 126

Large antibody and TCR repertoires, potentially in excess of 109 structurally-distinct antibodies and even more TCRs.

Front 127

Variation in inherited (germline) V, D and, J elements in Ig and TCR.

Back 127

Inherited structural differences create different basic structural frameworks.

Front 128

Combinatorial diversity (somatic recombination)

Back 128

Result of different V, D, and J segment rearrangement in developing B and T lymphocytes. Moderate levels of immune receptor diversity.

Front 129

Junctional diversity

Back 129

Random (nontemplated) addition or removal of nucleotide sequences at junctions between V, D, and, J regions.

Front 130

Somatic Hypermutation

Back 130

Point mutations in V regions of Ig in rapidly dividing B lymphocytes.Selected increase (or decrease) in antibody affinity.

Front 131

Receptor Editing

Back 131

Changes in Ig specificity that express self-reactive antibody achieved through secondary rearrangements.

Front 132

Somatic hypermutation leads to changes

Back 132

V not C

Front 133

Class switch recombination changes

Back 133

C not V

Front 134

Alternative splicing

Back 134

changes Ig from transmembrane to secretory form.

Front 135

Class Switch Recombination

Back 135

Change in heavy chain C regions, with same V region at the gene locus.

Front 136

Affinity maturation

Back 136

Process of somatic hypermutation and selective survival of B lymphocytes that produce high affinity antibodies.

Front 137

Alternative splicing

Back 137

Splicing at different locations in the 3′ of C region exons.

Production of membrane-bound or secreted Ig forms.

Splicing at different location of the C-terminal of the IgM gene.

Production of IgD from the same RNA transcript with IgM. Not conventional class switch.

Front 138

Each Fc receptor functions as a receptor specific for the CH region of the Ig molecule (Table 1-12). FCRs contain domains for

Back 138

Ig-binding and signaling components.

Front 139

FcγRI

Back 139

CD64; High; Macrophages, neutrophils, eosinophils; Phagocytosis

Front 140

FcγRIIIA

Back 140

CD16; Low; NK cells ADCC

Front 141

FcγRIIIB

Back 141

CD16; Low; Neutrophils Phagocytosis (poor)

Front 142

FcεRI

Back 142

High; Mast cells, basophils, eosinophils; Degranulation; ADCC

Front 143

FcεRII CD23 (not 32!)

Back 143

Low; Neutrophils, eosinophils, monocytes; Unknown

Front 144

T lymphocyte progenitors arise in the bone morrow and travel to the thymus as

Back 144

CD4-, CD8-, double negative, and CD3+ cells.

Front 145

Naïve T lymphocytes recirculate through the lymph nodes looking for their unique protein antigen as displayed in the context of an HLA molecule

Back 145

Class I for CD8 T cells and HLA Class II for CD4 T cells.

Front 146

Naïve T lymphocytes require X to present the antigens.

Back 146

dendritic cells

Front 147

Effector T lymphocytes respond to

Back 147

variety of antigen-presenting cells. (Since they have been activated, they are “ready to go”. They also remember and/or kill.)

Front 148

The most important cytokine produced during activation is the T lymphocyte survival signal,

Back 148

provided by IL-2 and its receptor CD 25.

Front 149

(Common gamma chain of IL2R is shared by receptors

Back 149

for IL2,4,7,9,15,21; mutations in common gamma chain result in XSCID)

Front 150

Proliferation is clonal. It is stimulated by IL-2.

Back 150

Clonal expansion preserves the specificity of the T lymphocyte for its particular antigen.

Front 151

Effector cells react to antigens. In the CD4+ lineage, they induce differentiation of the T lymphocyte response,

Back 151

Th1, Th2, Treg, and Th17.

Front 152

In CD8

Back 152

cells become cytolytic.

Front 153

Effector cells function to eliminate antigen. With the decline in antigen stimulation,

Back 153

there is a decline in T lymphocyte activity and achievement of homeostasis.

Front 154

Memory cells are a subset of the clonally-expanded population.

Back 154

These cells are long-lived and functionally quiet. They provide a rapid secondary response.

Front 155

Lymphocyte Differentiation

Back 155