Blum JS, Wearsch PA, Cresswell P. 2013. Pathways of antigen processing. Annu Rev Immunol 31:443–473.[PubMed][CrossRef]
Campbell KS, Hasegawa J. 2013. Natural killer cell biology: an update and future directions. J Allergy Clin Immunol 132:536–544.[PubMed][CrossRef]
Clark MA, Hirst BH, Jepson MA. 1998. M-cell surface β1 integrin expression and invasin-mediated targeting of Yersinia pseudotuberculosis to mouse Peyer’s patch M cells. Infect Immun 66:1237–1243.[PubMed]
Cullen SP, Martin SJ. 2008. Mechanisms of granule-dependent killing. Cell Death Differ 15:251–262.[PubMed][CrossRef]
Dörner T, Jacobi AM, Lipsky PE. 2009. B cells in autoimmunity. Arthritis Res Ther 11:247.[PubMed][CrossRef]
Finlay CM, Walsh KP, Mills KH. 2014. Induction of regulatory cells by helminth parasites: exploitation for the treatment of inflammatory diseases. Immunol Rev 259:206–230.[PubMed][CrossRef]
Husband AJ, Gowans JL. 1978. The origin and antigen-dependent distribution of IgA-containing cells in the intestine. J Exp Med 148:1146–1160.[PubMed][CrossRef]
Kabelitz D, Peters C, Wesch D, Oberg HH. 2013. Regulatory functions of γδ T cells. Int Immunopharmacol 16:382–387.[PubMed][CrossRef]
Lochner M, Wang Z, Sparwasser T. 2015. The special relationship in the development and function of T helper 17 and regulatory T cells. Prog Mol Biol Transl Sci 136:99–129.[PubMed][CrossRef]
Mabbott NA, Donaldson DS, Ohno H, Williams IR, Mahajan A. 2013. Microfold (M) cells: important immunosurveillance posts in the intestinal epithelium. Mucosal Immunol 6:666–677.[PubMed][CrossRef]
Modlin RL. 1994. Th1-Th2 paradigm: insights from leprosy. J Invest Dermatol 102:828–832.[PubMed][CrossRef]
Oettgen HC, Burton OT. 2015. IgE and mast cells: the endogenous adjuvant. Adv Immunol 127:203–256.[PubMed][CrossRef]
Schroeder HW Jr, Cavacini L. 2010. Structure and function of immunoglobulins. J Allergy Clin Immunol 125(Suppl 2):S41–S52.[PubMed][CrossRef]
Slack E, Balmer ML, Macpherson AJ. 2014. B cells as a critical node in the microbiota-host immune system network. Immunol Rev 260:50–66.[PubMed][CrossRef]
Soypayrac L. 2016. How the Immune System Works, 5th ed. Wiley Blackwell, West Sussex, United Kingdom.
Questions
1. In the short statement that began the chapter, the innate immune system was likened to ordinary police and the adaptive immune system was likened to specialized backups such as snipers. For those of you who follow true crime or mystery stories, you might find it amusing—and helpful in your studies—to try to come up with other criminal justice analogies. For example, you might make an analogy between “antibody production by B cells” and “smart bombs, surveillance, and tracking devices.” See what you can do with T helper cells, cytokines, APCs, and NK cells.
2. Does the fact that sIgA does not activate complement make it less effective in preventing infection than IgG? Hint: Consider its location and function.
3. Explain how the structure of an antibody is designed to facilitate the function of the particular antibody (e.g., why an antibody has at least two active sites, why it has an Fc portion, and why it might be cross-linked as a multimer).
4. Why is a Th1 or Th2 cell needed to mediate APC-initiated antibody production? Why do the B cells not bind directly to the APCs?
5. Explain why direct antigen activation of cytotoxic T cells and B cells is more important than APC-initiated activation in subsequent encounters with a microbe. Why is the APC-initiated pathway needed at all?
6. There are many interactions between the innate and adaptive defense systems. List as many of them as you can and explain how they work. Why are these interactions important? Are all of them beneficial?
7. What are the two ways that polysaccharides, DNA, and lipid antigens can elicit an immune response? How are these responses different than that elicited by a peptide antigen?
8. Why is the level of specific IgM antibodies of diagnostic significance?
Solving Problems in Bacterial Pathogenesis
1. A group of researchers have isolated a new pathogenic bacterium Q from lungs and lymph nodes of cystic fibrosis patients that produces an unusual polysaccharide capsule, called QPS. They can see QPS on the surface of the bacteria in electron micrographs from fresh isolates (i.e., bacteria just obtained from patients). In addition to the capsule, bacterium Q produces a protease, called QP, which the researchers believe is responsible for degrading host sIgA.
a. The researchers propose that QPS and QP might make good targets for vaccine development against bacterium Q. What led the researchers
