Cells and Signals of the Immune System/Major Histocompatibility Complex/Innate Immunity

The two types of immunity are innate and adaptive immunity. What cells mediate innate immunity?r

Adaptive immunity is composed of two responses. What cells mediate each response?

B and T cell proliferation in early lymphocyte maturation is stimulated by which cytokine?

What interacts with the T cell receptor (TCR) of an immature, double-positive T cell (CD4+/CD8+) to signal differentiation into a single-positive cell? In what organ does this occur?

What two processes eliminate immature T cells lacking proper antigen receptor specificities?

What mechanism drives cell elimination in positive selection?

Apoptosis of T-helper cells (CD4+, Th) or cytotoxic T cells (CD8+, Tc) bearing TCRs for self-proteins is the result of what process?

What cytokine released by activated Th further stimulates Th-cell survival/proliferation?

Name the two signals that are needed to activate T cells.

What is the result of an interaction between a T cell and an APC in the absence of costimulation?

What T cell protein displaces CD28 from B7, inhibiting T cell activation and ensuring T cell homeostasis?

What is a consequence to t cells that lack CTLA-4?

Which MHC class molecule presents processed antigens from organisms that have been phagocytosed? What cells possess this MHC class?

What cells function as professional APCs?

What is the source of antigen presented by MHC-1 molecules? What cells possess this class?

What is the cluster of polypeptides present in all T cells that is important in signal transduction by the TCR?

Induction of which of the T-cell helper lines (Th1 or Th2 elicits a more effective response against intracellular pathogens such as Mycobacterium tuberculosis?

Which cytokine released by Th1 cells is involved in macrophage activation?

What other signaling pathway results in macrophage activation?

What transcription factor is involved in both y-interferon and CD40/CD40L signaling?

How do macrophages respond to y-interferon and CD40/CD40L signaling?

Once activated, what are the major cytokines released by macrophages?

What are the microbidal substances produced by activated macrophages?

What are the main effector cells and cytokines of delayed hypersensitivity?

Against what pathogens is delayed hypersensitivity needed?

Patients with T cell deficiencies are most susceptible to what families of pathogens?

How is the of a T cell by a superantigen different from that by a typical antigen?

What is the result of superantigen activation of Th cells?

Which cytokine induces naive Th cells into mature Th2 cells?

What cytokines do Th2 cells produce? What properties do these cytokines share?

What cytokines aid B cells in antibody production?

What functions do IL-4 and IL-5 from Th2 cells serve in helminth immunity?

What cytokine is implicated as a mediator of asthma (airway hyperresponsiveness)?

By what two main methods do CD8+ cells kill virus-infected, graft and tumor cells?

MHC-1 molecules on allogenic donor cells have what role in graft rejections?

Which mature immune cell has receptors for whole, unprocessed antigens and does not require MHC presentation?

Which type of antigens can induce antibody production by B cells without the aid of helper T cells (ie T cell independent response)?

Where does B-cell differentiation occur?

What is the predominant antibody released in the initial stages of the primary humoral response?

What is class switching of antibodies?

What cells and signals are involved in class switching?

X-linked hyper IgM syndrome is an inherited disorder where the CD40 ligand on the T cells is defective. How would this affect B cells?

How would the same syndrome affect macrophages?

What are the main steps in B-cell presentation of antigens to helper T cells?

One of the causes of severe combined immunodeficiency (SCID) is a lack of functional IL-7 receptors. What cells are depleted? How is immunity affected?

What would be different about the T cells in a patient with DiGeorge syndrome compared to that of a person without it (DiGeorge syndrome results in thymic hypoplasia)?

What immune cell kills infected cells lacking MHC-1 proteins?

NK cells are activated by which cytokines?

Which cytokines are responsible for the increased production of C-reactive protein during an acute-phase response in innate immunity?

What cytokine is chemotactic for neutrophils?

Which cytokine has a similar function to granulocyte-macrophage colony-stimulating factor (GM-CSF)?

What is the major histocompability complex (MHC) also known as human leukocyte antigen (HLA) complex?

What chromosome contains the MHC in humans?

What are the two classes of MHC? What sets of HLA genes are associated with each class? what do these individual HLA genes actually encode for?

How are MHC inherited and expressed?

How many MHC molecules can an individual make?

Name the HLA haplotypes associated with each of the following diseases

What is the importance of MHC classes 1 and 2 proteins?

What is the structure of MHC class 1

Describe the a heavy chain's structure. Where is the peptide binding groove?

What are MHC class 1 proteins and where are they found?

What cells lack MHC class 1 proteins?

What is the function of MHC class 1 proteins?

MHC-TCR

How do proteins become associated with MHC class 1 molecules?

What are sources of foreign proteins associated with MHC class 1 molecules? What happens to cells presenting foreign antigens?

What is the structure of MHC class 2 molecules?

Describe the structure of the a and b chains. Where is the peptide binding groove located?

Where are MHC class 2 molecules expressed?

MHC class 2 molecules are cell surface proteins. What is their function?

How are MHC class 2 molecules loaded with peptide?

What prevents MHC class 2 molecules from binding peptides before fusion with vesicles containing endocytosed antigen?

What are the two main functions of innate immunity?

Which system is able to respond to a broader array of foreign motifs, innate or adaptive immunity? Why?

Which system is better at discriminating self from nonself, innate or adaptive immunity?

How does the innate immune system distinguish between foreign and self?

Why have microbes not adapted to avoid the motifs recognized by innate immunity?

Name the three different epithelial layers of the human body that are considered important aspects of innate immunity.

Name the principal effector cells of the innate immune system apart from epithelial cells:

What endothelial surface structure allows rolling of leukocytes along the endothelial wall adjacent to infection?

What endothelial surface structure allows for extravasation of leukocytes into the interstitial area of infection?

Mannose receptors and scavenger receptors are mechanisms to identify and ingest microbes utilized by what type of phagocyte?

How do NK cells identify selected cells?

How do NK cells kill infected cells?

Deficiencies of NK cells predispose to what types of infections?

Of the three effector cells of innate immunity (macrophages, neutrophils, NK cells), which is least likely to injure host tissue?

Which CD marker is useful for distinguishing NK cells from other immune cells? What is the function of this marker?

Which of the complement pathways is considered part of the adaptive immune system?

Antibodies/immunoglobulins (Igs) are synthesized by B cells and perform what general functions?

Define the following :

A simple Y shaped antibody is composed of two heavy chains and two light chains (named according to molecular weight) connected by disulfide bonds. Each chain is composed of variable and constant regions. What are the functions of these regions?

What are hypervariable regions?

How many heavy-chain constant domains (constituents of constant regions) are present on IgG, IgA, IgM and IgE?

What are the Fab and Fc fragments? Which one is at the amino terminus and which one is at the carboxyl terminus? What separates Fab and Fc fragments?

What is the function of the hinge region of the immunoglobulin?

What does the identification of the presence of both k and lambda light chains suggest about the sample of antibody?

What is the function of the J chain on IgA and IgM isotypes?

Define the following

What isotype has the highest avidity and why?

What isotypes of antibodies allow for B cells to achieve antigen presentation?

How does the structure of IgM in its secreted form differ from its membrane bound form? What is the function of secreted IgM?

IgG is the main antibody in the secondary response of humoral immunity, though both IgG and IgM can opsonize. How do they differ in this regard?

Microbial pathogens entering the nasopharynx will most likely encounter which immunoglobulin isotype?

What protects IgA from being digested by intestinal enzymes?

What two immune processes does IgE mediate?

Antibodies are found associated with the surfaces of which types of cells?

What isotype is most abundant in serum?

What isotype is produced in the largest amount?

Which immunoglobulin isotypes can initiate the classical complement cascade?

What is the most common immunoglobulin isotype found in fetal serum?

Why is IgG the only maternal isotype found in the fetus?

Why is IgA the predominant isotype found in milk?

What is the immunoglobulin isotype primarily produced by the fetus?

Define antibody-mediated cell cytotoxicity (ADCC). What two cells utilize ADCC? What two isotypes are involved in each case?

An overwhelming proportion of a single clone of IgM antibodies in serum is suggestive of what disease?

An overwhelming proportion of a single clone of IgG or IgA antibodies in serum is suggestive of what disease?

Name the three complement pathways and how they are activated.

Why do free IgM or IgG not activate the complement cascade?

How do IgM and IgG differ with respect to binding C1?

C3 convertase cleaves C3 to C3a (and C3b) in each complement pathway, but how does C3 convertase differ among pathways?

In the classical and lectin pathways what enzymes cleave C4 to C4b (and C4a) and C2 to C2a and (C2b)?

In the alternative pathway a small amount of C3b is generated. Once C3b binds B (forming C3bB) on a microbial surface, what enzyme cleaves B?