1887

Chapter 17 : Mucosal Immunity

MyBook is a cheap paperback edition of the original book and will be sold at uniform, low price.

Preview this chapter:
Zoom in
Zoomout

Mucosal Immunity, Page 1 of 2

| /docserver/preview/fulltext/10.1128/9781555816148/9781555812461_Chap17-1.gif /docserver/preview/fulltext/10.1128/9781555816148/9781555812461_Chap17-2.gif

Abstract:

The mucosal immune system consists of an integrated network of anatomic sites, immune effector cells, and tissues, commonly called (MALT). The functions of MALT can be subdivided into three main categories: (i) primary lymphoid development, (ii) induction and amplification of local mucosal immune responses, and (iii) production of the effector mechanisms of local mucosal immunity. (GALT), the best characterized component of MALT, consists of both highly organized local sites, where lymphocytes collect and are responsible for the inductive phase of the mucosal immune response, and vast diffuse effector sites, where activated cells reside. MALTs have evolved an elaborate set of protective mechanisms to prevent infection or colonization. These defenses can be categorized as specific and innate. Specific mucosal defense mechanisms consist of both the humoral and cellular immune systems. Pathogens, particulate antigens, or macromolecules are taken up only via a type of highly restricted active vesicular transport across epithelial cells at a site termed the follicle-associated epithelium (FAE). Oral tolerance is not mediated by a single immunologic mechanism; the primary mechanisms are active suppression, clonal anergy, and clonal deletion. The protective mechanisms that defend mucosal sites from colonization or invasion by microorganisms are essential for health and survival since this is the route of entry of inhaled, ingested, or sexually encountered pathogens.

Citation: Simpson S, Wetzler L. 2004. Mucosal Immunity, p 399-423. In Pier G, Lyczak J, Wetzler L (ed), Immunology, Infection, and Immunity. ASM Press, Washington, DC. doi: 10.1128/9781555816148.ch17

Key Concept Ranking

Major Histocompatibility Complex
0.71645826
Immune Systems
0.70165944
Infection and Immunity
0.67446834
Immune Response
0.5074442
0.71645826
Highlighted Text: Show | Hide
Loading full text...

Full text loading...

Figures

Image of Figure 17.1
Figure 17.1

Schematic diagram of various MALTs showing the route of entry of ingested antigens and the recirculatory patterns used by some gut leukocytes to populate other MALTs after encounter with antigen.

Citation: Simpson S, Wetzler L. 2004. Mucosal Immunity, p 399-423. In Pier G, Lyczak J, Wetzler L (ed), Immunology, Infection, and Immunity. ASM Press, Washington, DC. doi: 10.1128/9781555816148.ch17
Permissions and Reprints Request Permissions
Download as Powerpoint
Image of Figure 17.2
Figure 17.2

Antigens can be sampled at mucosal surfaces and transported to lymphoid tissue by several means. At stratified epithelium, DCs that capture antigen at the mucosal surface can migrate to organized MALT or to peripheral lymph nodes. Such migratory DCs can also sample antigens in the airway epithelia, after which they can migrate to organized MALT or to peripheral lymph nodes. Last, intestine and airways have specialized antigen-sampling cells known as M cells that transport intact antigens across the epithelial layer where the antigens can then encounter the underlying organized MALT. Redrawn from M. R. Neutra et al., 275–300, 1996, with permission.

Citation: Simpson S, Wetzler L. 2004. Mucosal Immunity, p 399-423. In Pier G, Lyczak J, Wetzler L (ed), Immunology, Infection, and Immunity. ASM Press, Washington, DC. doi: 10.1128/9781555816148.ch17
Permissions and Reprints Request Permissions
Download as Powerpoint
Image of Figure 17.3
Figure 17.3

M cells are found within the intestinal and airway epithelia and serve the function of transporting antigens (Ag) across the epithelial layer so they can encounter the immune cells of the host. The schematic diagram of an M cell shows the large pocket in its basolateral membrane in which macrophages (Mϕ) and lymphocytes (L) reside. DCs are also closely associated with M cells. Antigens in the intestinal lumen contact the apical membrane of the M cell and are transcytosed to its basolateral pocket. Redrawn from M. R. Neutra et al., 275–300, 1996, with permission.

Citation: Simpson S, Wetzler L. 2004. Mucosal Immunity, p 399-423. In Pier G, Lyczak J, Wetzler L (ed), Immunology, Infection, and Immunity. ASM Press, Washington, DC. doi: 10.1128/9781555816148.ch17
Permissions and Reprints Request Permissions
Download as Powerpoint
Image of Figure 17.3-1
Figure 17.3-1

Organization of the BALT showing the pathways of lymphocyte recirculation and points of exchange between the mucosal and systemic immune systems.

Citation: Simpson S, Wetzler L. 2004. Mucosal Immunity, p 399-423. In Pier G, Lyczak J, Wetzler L (ed), Immunology, Infection, and Immunity. ASM Press, Washington, DC. doi: 10.1128/9781555816148.ch17
Permissions and Reprints Request Permissions
Download as Powerpoint
Image of Figure 17.4
Figure 17.4

Antibacterial peptides are proteins of 30 to 40 amino acids that have cytotoxic activity due to their ability to permeabilize membranes. Amino acid sequences of antibacterial peptides of several species. See the inside front cover for the amino acid code. Reprinted from A. L. Hughes, 94–103, 1999, with permission. Model for permeabilization of a phospholipid bilayer by antibacterial peptides.

Citation: Simpson S, Wetzler L. 2004. Mucosal Immunity, p 399-423. In Pier G, Lyczak J, Wetzler L (ed), Immunology, Infection, and Immunity. ASM Press, Washington, DC. doi: 10.1128/9781555816148.ch17
Permissions and Reprints Request Permissions
Download as Powerpoint
Image of Figure 17.5
Figure 17.5

Diagram showing the several locations of MALT immune activation (inductive sites) and the spectra of effector sites usually populated by immune cells originally activated at each inductive site.

Citation: Simpson S, Wetzler L. 2004. Mucosal Immunity, p 399-423. In Pier G, Lyczak J, Wetzler L (ed), Immunology, Infection, and Immunity. ASM Press, Washington, DC. doi: 10.1128/9781555816148.ch17
Permissions and Reprints Request Permissions
Download as Powerpoint
Image of Figure 17.6
Figure 17.6

Schematic diagram of a Peyer's patch. Each nodule is composed of a follicle (comprising a germinal center, B-cell-rich corona, and T-cell-rich dome), T-cell-rich interfollicular area, and M-cell-containing dome epithelium. The germinal center contains actively dividing lymphocytes and tingible body macrophages (TBM). At the left is a postcapillary venule containing HEV, a site of leukocyte influx. At the right is a lymphatic, a site of leukocyte efflux.

Citation: Simpson S, Wetzler L. 2004. Mucosal Immunity, p 399-423. In Pier G, Lyczak J, Wetzler L (ed), Immunology, Infection, and Immunity. ASM Press, Washington, DC. doi: 10.1128/9781555816148.ch17
Permissions and Reprints Request Permissions
Download as Powerpoint
Image of Figure 17.7
Figure 17.7

Trafficking of B cells and T cells following activation at the Peyer's patch. () Lymphocytes residing at or near an M cell will encounter M-cell-transported antigens and will migrate to a local lymphoid follicle, where activation is facilitated by FDCs. Some lymphocytes activated in this local follicle will enter the lymphatic circulation and are carried via an afferent lymphatic (AL) to a mesenteric lymph node, where further immune activation may occur due to APCs and T cells residing in the lymph node. Activated lymphocytes can then leave the mesenteric node via an efferent lymphatic (EL) and merge with the peripheral blood at the thoracic duct. These peripheral blood lymphocytes can then home to any of a number of mucosal and nonmucosal sites at postcapillary venules. () Lymphocytes activated in the GALT preferentially home back to the intestine, where they reside below the intestinal epithelium and secrete sIgA, which is transcytosed into the intestinal lumen.

Citation: Simpson S, Wetzler L. 2004. Mucosal Immunity, p 399-423. In Pier G, Lyczak J, Wetzler L (ed), Immunology, Infection, and Immunity. ASM Press, Washington, DC. doi: 10.1128/9781555816148.ch17
Permissions and Reprints Request Permissions
Download as Powerpoint
Image of Figure 17.8
Figure 17.8

Diagram of an IgA1 monomer () and two different models of the IgA2 dimer (). The locations of intermonomer disulfide binds (S-S) and J chain (J) differ between these two models.

Citation: Simpson S, Wetzler L. 2004. Mucosal Immunity, p 399-423. In Pier G, Lyczak J, Wetzler L (ed), Immunology, Infection, and Immunity. ASM Press, Washington, DC. doi: 10.1128/9781555816148.ch17
Permissions and Reprints Request Permissions
Download as Powerpoint
Image of Figure 17.9
Figure 17.9

Diagram of the pIgR. The extracellular region consists of five immunoglobulin-like domains D1 to D5 and contains the binding site for polymeric immunoglobulin. The intracellular region contains signal sequences for membrane targeting, endocytosis, and transcytosis. The two arrows indicate the binding site for IgA. Ser, serine; Tyr, tyrosine.

Citation: Simpson S, Wetzler L. 2004. Mucosal Immunity, p 399-423. In Pier G, Lyczak J, Wetzler L (ed), Immunology, Infection, and Immunity. ASM Press, Washington, DC. doi: 10.1128/9781555816148.ch17
Permissions and Reprints Request Permissions
Download as Powerpoint
Image of Figure 17.10
Figure 17.10

Transcytosis of secretory, polymeric immunoglobulin. The pIgR is synthesized in the rough endoplasmic reticulum (RER) glycosylated in the Golgi apparatus and then transported to the basolateral membrane Dimeric IgA or polymeric IgM then binds to the pIgR and is transcytosed from the basolateral membrane of the epithelial cell to the apical membrane and released at the apical membrane . During step 6 or 7, the pIgR is cleaved so that the extracellular region of the pIgR (now called SC) remains associated with the immunoglobulin, while the transmembrane and intracellular regions of the pIgR remain on the apical membrane of the epithelial cell.

Citation: Simpson S, Wetzler L. 2004. Mucosal Immunity, p 399-423. In Pier G, Lyczak J, Wetzler L (ed), Immunology, Infection, and Immunity. ASM Press, Washington, DC. doi: 10.1128/9781555816148.ch17
Permissions and Reprints Request Permissions
Download as Powerpoint
Image of Figure 17.11
Figure 17.11

IgA can protect mucosal surfaces by three mechanisms. Polymeric immunoglobulin can be secreted into a gland lumen to bind luminal antigens. During transcytosis, polymeric immunoglobulin can bind and inactivate intracellular viruses. Polymeric immunoglobulin that binds to antigen in the submucosal space (to form IgA or IgM ICs) can be transcytosed to the lumen, thus removing the antigen complexed to the immunoglobulin.

Citation: Simpson S, Wetzler L. 2004. Mucosal Immunity, p 399-423. In Pier G, Lyczak J, Wetzler L (ed), Immunology, Infection, and Immunity. ASM Press, Washington, DC. doi: 10.1128/9781555816148.ch17
Permissions and Reprints Request Permissions
Download as Powerpoint
Image of Figure 17.12
Figure 17.12

Mechanisms of oral tolerance induction.

Citation: Simpson S, Wetzler L. 2004. Mucosal Immunity, p 399-423. In Pier G, Lyczak J, Wetzler L (ed), Immunology, Infection, and Immunity. ASM Press, Washington, DC. doi: 10.1128/9781555816148.ch17
Permissions and Reprints Request Permissions
Download as Powerpoint

References

/content/book/10.1128/9781555816148.chap17
1. Bassler, B. L. 2002. Small talk. Cell-to-cell communication in bacteria. Cell 109:421424.
2. Beeching N. J.,, D. A. Dance,, A. R. Miller,, and R. C. Spencer. 2002. Biological warfare and bioterrorism. Br. Med. J. 324: 336339.
3. Beutler, B. 2002. Toll-like receptors: how they work and what they do. Curr. Opin. Hematol. 9:210.
4. Bhatnagar, R.,, and S. Batra. 2001. Anthrax toxin. Crit. Rev. Microbiol. 27:167200.
5. Casadevall, A. 2002. Passive antibody administration (immediate immunity) as a specific defense against biological weapons. Emerg. Infect. Dis. 8:833841.
6. Cornelis, G. R. 2000. Molecular and cell biology aspects of plague. Proc. Natl. Acad. Sci. USA 97:87788783.
7. Dehio, C.,, S. D. Gray-Owen,, and T. F. Meyer. 2000. Host cell invasion by pathogenic Neisseriae. Subcell. Biochem. 33:6196.
8. Galan, J. E. 2001. Salmonella interactions with host cells: type III secretion at work. Annu. Rev. Cell Dev. Biol. 17:5386.
9. Green, D. W. 2002. The bacterial cell wall as a source of antibacterial targets. Expert Opin. Ther. Targets 6:119.
10. Hunter, C. A.,, and S. L. Reiner. 2000. Cytokines and T cells in host defense. Curr. Opin. Immunol. 12:413418.
11. Lyczak, J. B.,, C. L. Cannon,, and G. B. Pier. 2002. Lung infections associated with cystic fibrosis. Clin. Microbiol. Rev. 15:194222.
12. Wilson J. W.,, M. J. Schurr,, C. L. LeBlanc,, R. Ramamurthy,, K. L. Buchanan,, and C. A. Nickerson. 2002. Mechanisms of bacterial pathogenicity. Postgrad. Med. J. 78:216224.

Tables

Generic image for table
Table 17.1

Isotypes and functions of mucosal immunoglobulins

Citation: Simpson S, Wetzler L. 2004. Mucosal Immunity, p 399-423. In Pier G, Lyczak J, Wetzler L (ed), Immunology, Infection, and Immunity. ASM Press, Washington, DC. doi: 10.1128/9781555816148.ch17

This is a required field
Please enter a valid email address
Please check the format of the address you have entered.
Approval was a Success
Invalid data
An Error Occurred
Approval was partially successful, following selected items could not be processed due to error