Question 1

T cells with the g/d TCR are primarily located in the:&#10;A) Bone marrow&#10;B) Lymph nodes&#10;C) Mucosal tissue&#10;D) Peripheral blood

Accepted Answer

T cells with the g/d TCR are primarily located in the mucosal tissue, where they bridge the innate and adaptive immune responses. The g/d TCR recognizes general structures on microbial surfaces, which activates the T cell and aids in localizing the pathogen until an adaptive response is mounted.

Question 2

When individuals have a congenital defect in which they lack the CD40 ligand (CD40L) on activated T cells, the outcome of that defect is:&#10;A) They are not able to make mature T or B cells&#10;B) They are only able to make CD8 cells and no other types of T cells&#10;C) They are only able to make IgM antibody and no other type of antibody&#10;D) They are not able to any antibodies at all even though B and T cells are present

Accepted Answer

The CD40/CD40L interaction is important for antibody class switching. Therefore, without that interaction individuals are only able to make the initial antibody type, which is IgM. After the IgM production, they are not able to switch to producing IgG, which is a higher-affinity antibody, so they are prone to infections, particularly bacterial and fungal infections.

Question 3

According to the clonal selection theory, the activated T cell clone produces:&#10;A) Only memory cells&#10;B) Daughter cells that all have the same TCR&#10;C) Daughter cells with different TCRs on the same cell&#10;D) Multiple types of clones that each have different TCRs

Accepted Answer

Each T cell has a receptor that recognizes one epitope. According to clonal selection theory, when a T cell recognizes its one matching epitope, that cell will begin to produce daughter cells and memory cells that have that same TCR on all progeny. The daughter cells do not have different TCRs, and the activated clone does not produce multiple types of clones with different TCRs.

Question 4

Why are the g/d T cells more similar to the innate immune response than the adaptive immune response?&#10;A) They can present antigen to other T cells.&#10;B) They are able to phagocytose pathogens.&#10;C) They do not require activation to eliminate pathogens.&#10;D) They recognize general features of pathogens rather than a specific epitope.

Accepted Answer

The g/d T cells cannot present antigen or phagocytose pathogens, and they do have to be activated to become effector cells. However, they do not recognize specific antigen as other T cells do. The g/d TCR recognizes general features of microbes, including a group of phosphorylated molecules that are common to microbes, similar to the pathogen-associated microbial pattern (PAMP) recognition by phagocytes. The limited diversity of the receptors is a feature of the innate immune system rather than the adaptive immune system.

Question 5

How are superantigens able to uniquely activate large amounts of T cells?&#10;A) Superantigens secrete many toxins that are able to activate many different T cells.&#10;B) Superantigens are able to travel to the lymph node to interact directly with more T cells.&#10;C) Superantigens bind to the TCR and MHC class II molecule outside the binding groove.&#10;D) Superantigens bind to the TCR in the binding groove like other antigens but they have more epitopes than other antigens.

Accepted Answer

The superantigens are able to bind the TCR and MHC class II molecules outside the binding groove. Therefore, they are not restricted to a few T cells that recognize a few epitopes of the antigen and the usual clonal expansion of those activated cells. Instead the superantigens are able to bind to outer portions of both the MHC class II molecule and the TCR, connecting the two cells and leading to activation of a large number of T cells. As a result of the large-scale T cell activation, large amounts of cytokines are released, which leads to increased vascular permeability, reduced blood flow, organ failure, hypovolemic shock, and potentially death.

Question 6

CD4 molecules on T cells bind to:&#10;A) CD40&#10;B) B7 molecules&#10;C) MHC class I molecules&#10;D) MHC class II molecules

Accepted Answer

CD4 molecules on T cells bind to MHC class II molecules. This interaction stabilizes the bond between the T cell and the APC and confirms that the correct cell types are interacting, thus insuring that the appropriate immune response is initiated for the type of microbe present in the body. CD40 interacts with CD40 ligand, and CD28 or cytotoxic T lymphocyte-associated antigen-4 (CTLA-4) interacts with B7 molecules. CD8 serves a similar purpose on CTLs, but the interaction is between CD8 and MHC class I molecules on infected host cells.

Question 7

How does alefacept function to reduce lesions in plaque psoriasis?&#10;A) By blocking CD28/B7 interactions and causing T cell apoptosis&#10;B) By blocking CTLA-4/B7 interactions and causing T cell apoptosis&#10;C) By blocking CD2/CD58 interactions and preventing T cell activation&#10;D) By binding to CD3 on activated T cells and preventing T cell activation

Accepted Answer

The fusion protein alefacept contains the CD58 molecule connected to an antibody. The drug will bind to endogenous CD2 on T cells, thus blocking the binding of CD2 to CD58 on the APC and preventing T cell activation.

Question 8

Which of the complementarity-determining regions (CDRs) on the a/b TCR only have contact with the MHC class II molecule and do not have contact with the antigen?&#10;A) CDR1s&#10;B) CDR2s&#10;C) CDR3s&#10;D) CDR4s

Accepted Answer

The CDR2s on the a/b TCR have contact only with the MHC class II molecules and not the antigen. The CDR1s and CDR3s have contact with the epitope, and CDR4s do not exist.

Question 9

In the function of the TCR, the purpose of the CD3 complex is to:&#10;A) Bind antigen&#10;B) Transduce signals&#10;C) Anchor the TCR in the membrane&#10;D) Stabilize the interaction between the TCR and the APC

Accepted Answer

The CD3 complex is important for signal transduction because the TCR has only a short cytoplasmic tail that cannot carry the signal after binding of antigen. The CD3 complex does not interact with antigen during this process. The TCR has a hydrophobic transmembrane region that anchors the receptor in the membrane, and other markers, such as CD4 and CD8, serve to stabilize interactions between the TCR and APCs; the CD3 complex does not participate in these activities.

Question 10

The interaction between CTLA-4 and B7 leads to:&#10;A) Downregulation of T cell signaling&#10;B) Stabilization of the TCR/APC interaction&#10;C) B cell activation and generation of memory cells&#10;D) Production of proteins that regulate the cellular response to interleukin-2 (IL-2)

Accepted Answer

B7 molecules interact with either CD28, which leads to T cell activation, or CTLA-4, which prevents T cell activation and downregulates T cell signaling. The interaction of CD4 or CD8 molecules serves to stabilize the TCR/APC interaction. The CD40/CD40L interaction leads to B cell activation and generation of memory cells. The CD2/CD58 interaction leads to production of proteins that regulate the cellular response to IL-2.

Deck 6: Surface Interactions Between T Cells and Antigen-Presenting Cells