Immunology Mid-Exam

1. Bonds between Ag & Ab (covalent vs non-covalent)

The bonds that hold the antigen to the antibody combining site are all non-covalent in nature. These
include hydrogen bonds, electrostatic bonds, Van der Waals forces and hydrophobic bonds. Multiple
bonding between the antigen and the antibody ensures that the antigen will be bound tightly to the
antibody.

Since antigen-antibody reactions occur via non-covalent bonds, they are by their nature reversible.

2. Hapten

Hapten is small molecule that elicits (trigger) an immune response only when conjugated to a larger

molecule, called a carrier molecule.

The term hapten is derived from the Greed haptein, meaning to fasten. Hapten can become tightly

fastened to a carrier molecule, most often a protein, by a covalent bond. The hapten-carrier complex
stimulates the production of antibodies, which the unbound hapten cannot do, and become immunogenic
(capable of eliciting an immune response).
3. Adjuvant
Adjuvants are added to vaccines to active and enhance the response to antigen. Adjuvant (meaning
helper) serves to trigger the innate immune response and establish a state of inflammation at the site of
vaccination. The inflammation is necessary for initiating an adaptive immune response against the
antigens in the vaccine.
4. What types of cells are directly involved in eradicating/killing/lysing the virally-infected cells?

In innate immunity: Natural Killer Cells

Adaptive Immunity: Cytotoxic T-Cells

(Type I & Type II Interferon trigger cellular reactions, involving the NK cells and cytotoxic T cells
during adaptive immunity reactions in response to the viral infection.)
MHC Class I molecules is the eradication of virally infected cells.
5. T cells markers

Effector CD4+ Th-1 & Th-2 cells

Effector CD8+ T cytotoxic cells

CD4+/Foxp3+ T regulatory cells

6. B cells markers

Immature B Cell
Membrane IgM expressed

Mature Nave B Cell

IgM and IgD expreesed

IgM Ab-secreting Plasma cells

Isotype switching

All

isotypes

Abs-secreting

Plasma cells

7. T cells co-receptors
CD4, CD8, alternatively B7 (CDC activated)
8. B cells co-receptors
CD19, CR2 and CD81

Interaction of BCR with Ag generate a signal that is necessary

but is not sufficient to activate nave B cell

The addition signals that are required are delivered in several

ways:

Involvement of the B cell co-receptor, consisting of CD 19,

CD2 and CD 81 chain.

Activation by T helper cells via B and Th cells interaction.

9. Co-stimulatory molecules (B, T & DC)

CD28 receptors and CD40L ligands are expressed on the T cells

B7 ligands and CD40 receptors are expressed on DC and B cells

(B7.1 ligand is CD80, and B7.2 is also called CD86)

Include B7.1 and B7.2 proteins on professional antigen-presenting cells which engage molecules
CD28 and CTLA-4 on T cells

CD40 ligand serves a co-stimulatory role when it binds to CD40 on B cells.

10. Ig molecule, heavy chains designations: Greek vs. English

Differences in the heavy chain C regions define five main isotypes:

IgG

IgM

IgD

IgA

IgE

Blue Constant region

Red - Variable region
The light chains have only two isotypes, or classes: kappa (k) & lambda (l), with no functional
differences.

11. In NK cells, the cytotoxic granules formation is constitutive or inflammation-induced?

Constitutive
12. Antibody-dependent cellular cytotoxicity (ADCC)

Antibody binds antigens on the surface of target cell.

Fc receptors on NK cell recognize bound antibody.

Cross-linking of Fc receptors signals the NK cell to kill the target cell.

Target cell dies by apoptosis.

13. Fab vs. Fc portions of an Antibody (Ab)

Fab (Fragment antigen binding) consists of a light

chain and N-termini part of a heavy chain held
together by disulfide bond.

Fc (Fragment crystallizable) consists of the carboxylterminal halves of the two heavy chains disulfidebonded to each other by the residual hinge region.

14. FcgR, FcmR, FcaR, FceR

FceR: receptor present on surface of mast cells, baspohils and activated eosinophiles that binds free
IGE with high affinity

FcgR: receptor present on various cell types that are specific for Fc regions of IGG antibodies

FcaR: found on the surface of neutrophils, eosinophil, monocytes, some macrophages (including
Kupffer cells), and some dendritic cells, It signals by associating with two FcR signaling chains.
Another receptor can also bind IgA, although it has higher affinity for another antibody called IgM.

FCmR: IgA and IgM, B cells Mesangial cells Macrophages.

15. Primary immune response vs. Secondary immune response

Primary immune response (first exposure to a pathogen) takes 10-17 days to get going and destroy
the pathogen. During this time many B and T cells are generated to engage the pathogen.

Secondary immune response (second exposure to pathogen) is much faster taking 2-7 days as the
memory cells quickly clone more B and T cells to attack the pathogen.

19. MHC structure: protein and DNA levels

An MHC class I molecule is composed of one

membrane-bound heavy chain and noncovalently bonded 2 micro-globulin.

The heavy chain has three extracellular

domains (1, 2, 3)

1 & 2 domains form the peptide binding

site (Ag-derived)

An MHC class II molecule is composed of two membrane-bound chains: chain and chain. Each
of them has two extracellular domains.

1 & 1 domains form the binding site for the Ag-derived peptide.

All protein from MHC I and MHC II are different from their counterparts.

20. Complement components in all three complement activation pathways

Alternative- C3Bb, C3bBb, C3B2Bb, C3 and C5 convertase

Lectin- C4b2a classical C3 convertase, c5 convertase

Classical c4b2a classical C3 and C5 convertase

21. Plasma cells: what hemopoietic cell linage they belong?

Lymphocyte lineage
22. MHC Class I and Class II expression (on what type of cells)

MHC I all nucleated cells

MHC II on selected cells, and is mostly limited to cells involved in Ag-presentation:

Dendritic cells

Macrophages

B cells

Epithelial cells in the thymus

23. Isotype switching in the immunoglobulin molecules occurs:

Germinal Centers in Lymph Node (secondary
lymphoid tissue) under the influence of factors produced
by DC and Th cells.

24. Highest concentrations of the different isotypes of the Ig/Abs in

IgG, IgM, monomeric IgA (heart color) predominate in Blood

Dimeric IgA in fluids.

IgE is associated with epithelia.

The fetus has IgG

After birth dimeric IgA from mothers milk.

Primary- IgM more than any other.

Secondary- IgG more than any other.
25. Primary vs. secondary encounter/infection with the same type of virus (pre-formed anti-viral
antibodies, their role in mechanisms of the anti-viral immune response)

Primary immune response (first exposure to a pathogen) takes 10-17 days to get going and destroy
the pathogen. During this time many B and T cells are generated to engage the pathogen.

Secondary immune response (second exposure to pathogen) is much faster taking 2-7 days as the
memory cells quickly clone more B and T cells to attack the pathogen.

26. What is Immunogenicity and what are its defining factors

The ability of a molecule or substance to provoke an immune response.

Factors include structures as organic molecule, proteins. Temp/pH no effect on induction.

27. Chemokine molecules (few major of them that mediate cells of the immune response trafficking and
homing in the secondary lymphoid tissues and centers of inflammation)

Large group of small proteins involved in guiding white blood cells to sites where functions are
needed, central role in inflammatory response

CCR7: lymphoid tissue, responsible for both B and T cells, not cell specific

28. What are two signals during DC /nave T cell interactions that are required for T cells activation?

1st: TCR and MHC class II presenting antigen

2nd: CD-28 on nave T cell and B7 of dendritic cell.

29. What are two signals during DC /activated T cell interactions that are required for suppressing
the T cells activation?

Binding of MHC class II peptide complex to the

TCR and CD4 induces signal 1 in the T cell.

Positive co-stimulation (signal 2) is provided by

binding of CD80 or CD86 to CD28, whereas binding
to CTLA4 will inhibit T cell activation.

30. How the anergy status is induced in the T cells?

Anergy: state of non-responsiveness to an antigen.
Achieved through lack of second signal to enter activated status, peripheral tolerance to self antigens
31. Humoral vs cellular immunity

Humoral: eliminates extracellular pathogens (bacteria, toxins, virus in blood or fluid)

Cellular: eliminates intracellular pathogens (viruses)

Cellular vs. Humoral immunity

Cellular: adaptive immune response in which antigen-specific effector T cells dominate, cannot be
transferred.

 Humoral: Immunity mediated by antibodies and can be transferred.

32. The role of IL-2 in T cells proliferation

It is a protein that regulates the activities of white blood cells (leukocytes, often lymphocytes) that
are responsible for immunity. IL-2 is part of the body's natural response to microbial infection, and
in discriminating between foreign ("non-self") and "self".

Antigen binding to the TCR stimulates the secretion of IL-2, and the expression of IL-2 receptors IL2R. The IL-2/IL-2R interaction then stimulates the growth, differentiation and survival of antigenspecific CD4+ T cells and CD8+ T cells. As such, IL-2 is necessary for the development of T cell
immunologic memory, which depends upon the expansion of the number and function of antigenselected T cell clones.

33. Is co-stimulation (2nd signals between CD28 and B7.1 or B7.2) needed for the effector cells
function?
No. This signal 2 is not required for interaction between effector Tc cells and the target cells.
34. The possible outcomes of opsonization of the pathogen with Abs

Phagocytosis of pathogen.

Classical pathway of complement fixation.

35. TCR complex and its 8 chains functions

and chains of TCR antigen recognition
and chain
2 chains
2 (Zeta) chains - signal transduction
In this complex the CD3 proteins and the (Zeta) chain transmit
signals to the cells interior after antigen has been recognized by the
: chain heterodimer.

36. Is inflammatory response always good for the general health condition?

Not always, because sometimes the body attacks itself (autoimmunity) or overreacts, this could be
detrimental. Prolonged inflammation, known as chronic inflammation, leads to a progressive shift in
the type of cells present at the site of inflammation and is characterized by simultaneous destruction
and healing of the tissue from the inflammatory process.

Mononuclear cells (monocytes, macrophages, lymphocytes, plasma cells), fibroblasts

Leads to tissue destruction, fibrosis, necrosis

Non-immune diseases with etiological origins in inflammatory processes include cancer,

atherosclerosis, and ischemic heart disease

37. T-independent Ag Response.

ONLY B cell is needed for Abs formation (usually a weaker response and not so long lasting)

These Ags are usually polymers- present a large number of identical Ag epitopes to specific B cell.

Activates the specific B cell (CLONAL SELECTION) to divide and differentiate into an Ab
producing plasma cell

Only IgM (primitive response) produced (no switching to IgG).

38. CCR7

Receptor expressed in various lymphoid tissues and activates B and T cells. It has been shown to
control the migration of memory T cells home to secondary lympho-organ, such as lymph nodes, as
well as stimulate dendritic cell maturation.

Chemokine receptor 7; provides the balance between immunity and tolerance.

39. Immunoglobulins are produced by?

Plasma cells (B-cell lineage)
40. Ratio of CD4 vs. CD8 cells = 2:1
There is twice as much CD4 than CD8.
41. Major function of Abs in anti-viral immunity?
During the extracellular presence of the viruses, antibodies have a neutralizing effect. They block
viruses from binding to epithelial/host cells.
42. Mechanisms of central vs. peripheral tolerance

Central tolerance: occurs in primary lymphoid organs (thymus & BM), thymic deletion of
autoreactive T cells, BM deletion of autoreactive B cells.

Peripheral tolerance: occurs throughout body, deletion & anergy induction in autoreactive T cells,
T- reg policing, splenic deletion of autoreactive B cells.

Central tolerance involves positive and negative selection. Peripheral tolerance involves anergy.
43. Role of the complement system in anti-bacterial and anti-viral immunity
Complement plays a role in innate immunity by opsonizing bacterial and extracellular viral peptides
for phagocytosis and forming pores/lysis of bacterial and virally-infected eukaryotic cells.

44. CD40 and CD40L: what type of cells are expressed on, and their role in immune reactions (during
interactions between B/T cells; B/DC cells; T/DC cells)

B/T cells: The CD40 on B cells interact with the CD40L on Nave T cells, which results in B cells
differentiation into plasma cells (with IL-10) or memory cells (with IL-4).

T/DC: The CD40 L on T cells interacts with the CD40 on DCs that causes T cell proliferation into
Th1 and Th2.

45. Physiologic role of cross-linking of the receptors during (phagocytosis, B cell activation)
Cross-linking occurs as a result of binding of Fab arms of the IgM molecule on the B cell to
repetitive epitopes on the bacterial cell. Cross-linking causes clustering of BCRs and initiation of signaling
pathways
46. Ag-binding strength to change by physical parameters, such as Temperature and pH?
Antigen-binding STRENGTH is not affected by temperature and pH, but the RATE of binding is
affected.
47. Which receptors can interact with MHC Class I?
CD8, TCRs, and inhibitory receptors on self-MIC will interact with NKFR on NK once infected.
48. B cells activation process includes the following:
Recognition of antigen and processing; affinity maturation; clonal expansion; isotypes switching.

49. Differences between primary vs. secondary and beginning vs. advanced stage of immune
responses? Why secondary response is faster?

Primary beginning: innate immunity Primary advanced: innate immunity and adaptive begins
Secondary responses: combination of both.

Secondary responses are faster due to immunological memory from the adaptive primary response.

50. NK cells: in anti-viral infection; cytotoxic granules (pre-formed vs. induced; do not kill self-cells
because?
Cytotoxic granules are pre-formed. Natural killer cells do not kill self cells because of the presence
of inhibitory receptors (KIRs) on the NK cell and MHC I on the self cell.