Antibodies And B Lymphocyte Development Assignment

Assignment Task

Module 1: Antibodies and B Lymphocyte Development

1. Make a model of an IgG antibody using pipe cleaners or some other material, or make a drawing using different colours or symbols. Make a short video or take a series of pictures, pointing out the various important regions of the antibody (H- and L-chains, constant and variable regions, antigen binding sites, Fc effector region, hinge) and explaining the functions of each. Be sure to include a key for any different colours and/or symbols you use. Include these pictures (with written commentary) or video (with spoken commentary) in your assignment. 

2. Antibodies help to protect unborn children and young babies from the same infectious organisms that their mothers are exposed to. Explain how antibodies are passed from mother to fetus (before birth) and mother to infant (after birth) to provide them with passive immunity. During what period of time would infants be most susceptible to infection and why? What does this suggest about the period of time most beneficial for breastfeeding?

3. ADCC is an important mechanism for eliminating parasites and pathogen-infected cells. Go back and review the toxic materials present in eosinophils and NK cells. List 5 of these toxins and state their effects on the target cells that have been tagged with antibodies. What kinds of antibodies are involved in triggering ADCC in each case (by eosinophils and by NK cells)? 

4. See the instructions below:

1. Create a video or a series of photos/drawings or a comic strip to illustrate the steps involved in recombination of the V, D and J segments of an antibody H chain gene to produce a unique combination of segments, with additional nucleotides in the coding joints. Be sure to show what happens to the chromosomal DNA that lies between the chosen V, D and J segments and where the recombination signal sequences are located before and after rearrangement of the gene.
   (For example, for this project you could use a paper streamer or ribbon to represent your germline chromosome. You don't need to include all of the possible V, D and J segments, but include 3 or 4 of each to be representative. You could use a stapler or tape as the recombinase).
2. Next, show what would happen to the heavy chain gene in an activated B cell in the presence of interleukin 4, which causes class switching to IgE. 

5. In Chapters 6 and 13 of the textbook, several immunodeficiency diseases and tumors are mentioned that are associated with defects in B cell development See Chapter 6, sections 6-4 (p. 167-169), 6-7 and 6-8 (p. 171-174); also see Chapter 4, section 4-14 (p. 116-118) and Chapter 13, sections 13-12 and 13-13 (p. 388- 390). Explain the processes that are defective in the following situations and list the major symptoms shown by patients affected by these mutations. Give a common name for each condition.

1. Both copies of the gene for l5 (part of the surrogate L chain) are defective. 
2. A mutation in the Btk gene (Bruton's tyrosine kinase, coding for a protein involved in signal transduction from Iga and Igb). Why is this disease more common in boys than girls? 
3. Both copies of the gene for AID (activation-induced deaminase) are defective. 
4. Defects in the CD40 gene or the CD40 ligand gene. Which one occurs more frequently in boys and why? Why are low numbers of neutrophils observed during an infection in patients with defects in either of these genes? 
5. Translocation and fusion of one of the immunoglobulin genes to the BCL2 gene. What is the normal role of the Bcl-2 protein in cells? Why are B cells primarily affected, even if the translocation appears in other cell types? 

6. In Chapter 10, section 10-15 (p. 300-301) of the textbook a condition known as "selective IgA deficiency" is discussed, in which individuals do not switch from making IgM to IgA. Explain why people, especially children, with this condition often appear perfectly healthy and why the lungs rather than the gut are more often affected by infections, especially in populations of developed/industrialized countries. List 3 possible genetic defects that might lead to selective IgA deficiency. 

7. What would be the consequences of allowing the expression of more than one H and/or L chain gene (having no allelic exclusion) during B cell development? (See section 6-4 (p. 168) in the textbook). How many types of BCRs could be made if the cell expressed 2 kinds of H chains but only one kind of L chain? How many types of BCRs could be made if there were 2 H chains and 2 L chains expressed? Why would this be a bad thing for B cells?

8. Case Study:

A boy of 8 months of age who has stopped breast-feeding presents with ongoing repeated infections with encapsulated bacteria (Streptococcus and Haemophilus). The child has virtually no antibodies and you suspect a B cell deficiency.

1. Outline how you could use flow cytometry to confirm your diagnosis. What B cell-specific monoclonal antibodies could you use for this test? How do you make sure that it is only B cells that are missing in this patient and not both B cells and T cells? 
2. If your diagnosis was correct, what treatments would you advise?
3. What are 3 genetic defects that could lead to B cell deficiency? 
4. Why doesn’t B cell deficiency generally show up until a child is a few months old and being weaned? 

9. Outline the principles of a simple “dipstick test” (similar to a pregnancy test) you could develop using monoclonal antibodies to see if your drinking water contained measurable amounts of a contaminant such as bisphenol A. How many kinds of monoclonal antibodies, specific for the contaminant, would you need for the test?

What kind of immunoassay would be more quantitative?

Module 2: T Cell Receptors, MHCs, and Antigen Presentation 

1. Complete the following: 

Summarize the similarities and differences between BCRs/antibodies and TCRs including structure, generation of diversity in antigen binding sites, generation of isotypes, mechanism of antigen recognition, subunits responsible for signal transduction, and function of co-receptors. 

Include drawings of the TCR and BCR complexes, showing how the receptors and the accessory proteins are arranged in the lymphocyte membrane, indicating the variable and constant regions and the antigen binding sites, and showing how the receptor subunits and signalling components are linked to each other. Include the B cell and T cell co-receptors in your drawings. 

2. Case Study:

Two children in a family present with repeated viral infections that are difficult to resolve but so far have not been fatal. Flow cytometry shows very low levels of HLA class I proteins on leukocytes and reduced numbers of CD8⁺ lymphocytes, but normal levels of CD4⁺ lymphocytes and B cells, and increased numbers of activated NK cells.

What genetic defect might explain these results? Give your reasoning. Be sure to account for all of the observations. 

3. Listeria monocytogenes is a bacterium that evades digestion by macrophages. How does it do this and how would a healthy person usually terminate the infection?

4. Where are g:d T cells generally found in the body and what kinds of antigens do they recognize? What do they do when they become activated? 

5. Why are pigs considered to be good candidates as a source of organs for xenotransplantation? What are three barriers to xenotransplantation of pig organs?

6. What is the primary cause of chronic rejection of an organ transplant? How would Rituximab work to prevent chronic rejection?

7. What is an "MHC haplotype" and how many of these would be carried by an individual? Given that most MHC haplotypes are inherited intact from parents to offspring, what would be the expected frequency of haplo-identical siblings (i.e., siblings with identical MHCs) in a family, given that both parents are heterozygous for different MHC haplotypes?

8. Explain the advantage for an individual of being heterozygous for as many MHC alleles as possible and indicate what natural forces might favour the frequency of heterozygotes in a population. 

9. What are CD1 proteins? In what ways do they resemble, and in what ways do they differ from, Class I MHCs? What antigens can be presented by CD1 and what cell types carry TCRs that recognize these antigens?  

10. Fill in the table below.

Module 6: Development and Activation of T Cells

1. Compare and contrast the steps in development of B cells and a:b T cells, including the following: 

• Where does the majority of B and T cell development occur? 
• What signals and cellular interactions are needed to promote commitment of lymphocyte progenitor cells to the B or T cell lineage? 
• What are the first steps in gene rearrangement that take place in pro-B and pro-T cells? (i.e., which genes are rearranged first in progenitor cells; you don’t need to discuss all the details of gene rearrangement). What percentage of pro-B and pro-T lymphocytes are successful at rearranging their first receptor genes and thus become pre-B or pre-T cells? 
• Describe the structure of the pre-B and pre-T cell receptors and what happens to a lymphocyte that is successful at making one of these pre-receptors.
• What accessory molecules, associated with the pre-BCR and pre-TCR, are expressed on the cell surface at the pre-B and DP (double positive) pre-T cell stage? 
• Which receptor genes are rearranged next (at the pre-B/pre-T cell stage)? How many genes can be rearranged at this stage of B cell development and what proportion of each kind are expressed in the mature B cell receptor repertoire? 
• When (at what stage of development) and where does positive and negative selection of immature B and T cells take place? What is the purpose of each kind of selection and what percentage of each type of lymphocyte survives both processes?
• What is "receptor editing" and what is its purpose? When in B and T cell development does it takes place?

2. Autoimmune diseases develop when tolerance to self-antigens is lost. Two such diseases are due to defects in the gene for AIRE or the gene for FOXP3. What is the normal role of the proteins encoded by these genes? List the symptoms associated with these diseases and explain what has gone wrong with the systems that are normally responsible for tolerance to self-antigens when these genes are defective. 

3. Both B cells and T cells can become “anergic.” What is “anergy” and what conditions promote anergy in B cells and T cells? What is the purpose of making some lymphocytes anergic? 

4. Leprosy is a disease caused by persistent infection of macrophages by Mycobacterium leprae. The disease can present in two forms, tuberculoid and lepromatous, depending on the type of TH response that is mounted. Discuss the symptoms associated with each form of the disease and how the progression of the disease relates to the immune response that is mounted in each case.

5. Answer ONE of the following questions

1. In Chapter 12, sections 12-9 (p. 352-355) and 3-21 (p. 86-87) of the textbook, the topic of uterine NK (uNK) cell involvement in formation of the placenta is discussed. Summarize how uNK cells interact with fetal trophoblast cells to control the remodeling of maternal blood vessels in the placenta. Include a discussion of the kinds of HLA molecules that the uNK cells interact with and how uNKs promote blood vessel formation and remodeling in the placenta. What may happen to the placenta if there are reduced numbers of inhibitory interactions between the uNK cells and the trophoblast cells or too many inhibitory interactions due to the paternal HLA-C haplotype?

Why doesn’t the immune system reject the fetal trophoblast cells?

OR

1. In Chapter 12, section 12-18 (p. 368-369) of the textbook the topic of mucosal-associated invariant T cells (MAIT cells) is discussed. Summarize characteristics of MAIT cells and how they act to help control infections by certain bacteria and fungi.

What antigens do MAIT cells recognize and how are they presented to the MAIT cell TCRs? What is special about the MAIT cell TCRs? Where do MAIT cells develop and where are mature MAIT cells found in the body? In what proportions are MAIT cells present compared to other lymphocytes? What is the phenotype of most MAIT cells in the adult? How do they act to control infection?

6. Make a video or a comic strip or produce some other way of presenting the activation of clones of CD4⁺ TH1 and T_FH1 helper T cells, and CD8⁺ cytotoxic T cells in a lymph node in response to a viral infection. You will have to illustrate/show the activating interactions between naïve T cells and the APCs, as well as the cytokines responsible for clonal expansion and differentiation of the activated TH1 and T_FH1 Show where the T_FH1 cells will go to accomplish their tasks of supporting B cell development (what kind of antibodies will be made?), and how the TH1 and CTLs cells will assist the innate immune system in eliminating the viral infection. Be sure to include and label the cells and antibodies involved. 

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