1887

Chapter 20 : Immunity to Parasitic and Fungal Infections

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

Preview this chapter:
Zoom in
Zoomout

Immunity to Parasitic and Fungal Infections, Page 1 of 2

| /docserver/preview/fulltext/10.1128/9781555816148/9781555812461_Chap20-1.gif /docserver/preview/fulltext/10.1128/9781555816148/9781555812461_Chap20-2.gif

Abstract:

Infections with protozoa and helminths are typically chronic (often lasting for the remainder of the lifetime of the host), with the onset of disease symptoms in many instances developing years after the initial infection. Cutaneous leishmaniasis (also called Oriental sore) is probably the only major human parasitic infection for which there appears to be immunity to reinfection. As with many other intracellular infections, cell-mediated immunity seems to be the most important mechanism of resolving the infection, with little if any role for antibodies. T cells are critical in the control of all parasitic infections. Despite an apparent absence of protective immunity that protects against reinfection, the cell-mediated arm of the immune system is required to control parasitic infections. The most serious fungal infections are the systemic mycoses, including histoplasmosis, cryptococcosis, and coccidioidomycosis, which usually begin as lung infections and are acquired by inhaling the spores of free-living fungi. If macrophages are not activated, they are less potent at killing fungi than are neutrophils. Thus, the role of macrophages in resistance to fungal infection is more important in acquired immunity, where they become an effective tool of the specific immune response following activation by TH1-cell-derived cytokines.

Citation: Allen J, Liu L. 2004. Immunity to Parasitic and Fungal Infections, p 469-496. In Pier G, Lyczak J, Wetzler L (ed), Immunology, Infection, and Immunity. ASM Press, Washington, DC. doi: 10.1128/9781555816148.ch20

Key Concept Ranking

Tumor Necrosis Factor alpha
0.43029115
Transforming Growth Factor beta
0.40722525
0.43029115
Highlighted Text: Show | Hide
Loading full text...

Full text loading...

Figures

Image of Figure 20.1
Figure 20.1

Life cycle of malaria parasites. Malaria is transmitted by the bite of the female anopheline mosquito, which injects the sporozoite stage of species into the bloodstream. Sporozoites invade the liver, where they divide extensively without inducing a host inflammatory response. Eventually the infected liver cell ruptures, releasing merozoites into the bloodstream, where they invade erythrocytes and continue asexual division within the erythrocyte. Infected erythrocytes then lyse, releasing more merozoites to continue ongoing erythrocytic cycles of infection. Some of the merozoites develop into sexual stages (gametocytes) that are ingested by the mosquito, in which sexual development of the parasite proceeds, giving rise to infective sporozoites that are transmitted to the next host when the infected mosquito takes a second blood meal. Extensive hemolysis leads to severe anemia and splenomegaly. is particularly virulent because it can infect a high proportion of erythrocytes and cause cerebral disease due to microvascular occlusion. An antigenically variant family of proteins expressed on the erythrocyte cell surface mediate adherence of infected erythrocytes to postcapillary venule endothelium (see section on immune evasion by parasites, antigenic variation), which causes cerebral malaria. The circle containing a photo shows a photomicrograph of a trophozoite.

Citation: Allen J, Liu L. 2004. Immunity to Parasitic and Fungal Infections, p 469-496. In Pier G, Lyczak J, Wetzler L (ed), Immunology, Infection, and Immunity. ASM Press, Washington, DC. doi: 10.1128/9781555816148.ch20
Permissions and Reprints Request Permissions
Download as Powerpoint
Image of Figure 20.2
Figure 20.2

Leishmaniasis is an infection of rodents, canines, and other mammals, including humans. species are transmitted by the bite of an infected female sand fly. The infective-stage promastigotes enter the bite wound, activate complement, and are rapidly taken up by local macrophages. Within the phagolysosome of the macrophage, the promastigotes transform into amastigotes that replicate by binary fission within the cell, eventually filling the cytoplasm. Upon rupture of the infected macrophage, the released amastigotes are taken up by new macrophages. Amastigotes are engulfed from the infected mammal by the bite of another sand fly, develop into promastigotes within the insect's gut, migrate to the insect salivary glands, and are deposited on the skin of another host when the sand fly takes its next blood meal. The photograph shows a cutaneous ulcer due to .

Citation: Allen J, Liu L. 2004. Immunity to Parasitic and Fungal Infections, p 469-496. In Pier G, Lyczak J, Wetzler L (ed), Immunology, Infection, and Immunity. ASM Press, Washington, DC. doi: 10.1128/9781555816148.ch20
Permissions and Reprints Request Permissions
Download as Powerpoint
Image of Figure 20.3
Figure 20.3

Life cycle of . is transmitted among various mammalian hosts by hematophagous reduviid bugs native to parts of Central and South America. An infected bug defecates while feeding, discharging infective trypomastigotes in the feces. The trypomastigotes enter the bite wound, mucous membranes, or conjunctivae and infect a wide variety of cells. An indurated inflammatory lesion (chagoma) often appears at the site of the bite and parasite entry. Within host cells the trypomastigotes transform into amastigotes, replicating until the host cells rupture to release additional parasites. Trypomastigotes in the circulation can be ingested by reduviid bugs during a blood meal, thereby continuing the parasite life cycle. Chagas' disease can also be transmitted by blood transfusion because of the stages in the bloodstream. Early in the disease, heavy infection of the cardiac muscle occasionally causes acute heart failure and sudden cardiac death. The pathogenesis of chronic Chagas' disease is not well understood, but myocardial inflammation, fibrosis, and atrophy can develop with few or no detectable parasites. In some patients, focal inflammation and destruction of the myenteric nerve plexus of the gut result in loss of peristalsis and enormous dilatation of the esophagus or colon. The photomicrograph shows amastigotes.

Citation: Allen J, Liu L. 2004. Immunity to Parasitic and Fungal Infections, p 469-496. In Pier G, Lyczak J, Wetzler L (ed), Immunology, Infection, and Immunity. ASM Press, Washington, DC. doi: 10.1128/9781555816148.ch20
Permissions and Reprints Request Permissions
Download as Powerpoint
Image of Figure 20.4
Figure 20.4

Life cycle of . The family is the definitive host, and sexual stages of the parasite are found in the epithelial cells of the gut, and oocysts are shed in the feces. In the intermediate host (any mammal or bird), the parasite undergoes asexual division in one of two stages. The tachyzoite is rapidly dividing and can infect any nucleated cell. In the absence of a T-cell response, unrestricted growth of tachyzoites will kill the host. Normally, in the presence of a competent immune system, the tachyzoite stage is cleared from the tissues while the more slowly dividing form of the parasite, the bradyzoite, persists within pseudocysts. An active T-cell response to the parasite is required to prevent reemergence of the virulent tachyzoites from pseudocysts. There are three routes of transmission: (i) horizontal transmission via oocysts (i.e., cat to rodent), (ii) horizontal transmission via tissue cysts (i.e., rodent to cat or pig to human), and (iii) vertical transmission (congenital infection) via tachyzoites.

Citation: Allen J, Liu L. 2004. Immunity to Parasitic and Fungal Infections, p 469-496. In Pier G, Lyczak J, Wetzler L (ed), Immunology, Infection, and Immunity. ASM Press, Washington, DC. doi: 10.1128/9781555816148.ch20
Permissions and Reprints Request Permissions
Download as Powerpoint
Image of Figure 20.5
Figure 20.5

Life cycle of . Humans become infected with schistosome parasites by standing or swimming in fresh water infested with schistosome-infected snails. Infective schistosome larvae called cercariae emerge from infected snails and actively penetrate human skin. In the skin, the larvae of and transform into schistosomules, which migrate to the lungs and the portal vein, where the developing male and female schistosomes pair, settle in the mesenteric veins, and mature into adult worms. In these blood vessels, the female adult worm lives tightly ensconced within a longitudinal canal of the male worm and continuously produces eggs. Although most and eggs are passed out in the feces, others are carried retrograde by the portal venous system to the liver, where they become trapped in the portal triad. The life cycle of S. haematobium differs in that the adult worms of this species live in the bladder veins, and eggs of are expelled primarily in the urine, but some lodge in the bladder wall. Schistosome eggs passed in the feces or urine hatch in fresh water to release miracidia that infect snails and develop into infective larvae. The photo shows a patient with an enlarged spleen and liver due to infection.

Citation: Allen J, Liu L. 2004. Immunity to Parasitic and Fungal Infections, p 469-496. In Pier G, Lyczak J, Wetzler L (ed), Immunology, Infection, and Immunity. ASM Press, Washington, DC. doi: 10.1128/9781555816148.ch20
Permissions and Reprints Request Permissions
Download as Powerpoint
Image of Figure 20.6
Figure 20.6

Life cycle of . Lymphatic filariasis is caused primarily by and to a lesser extent by . The infection is transmitted by , , and species of mosquitos, which deposit infective larvae in the bite wound. The infective larvae migrate to the lymphatic vessels and lymph nodes, where they mature into adult worms. The offspring of adult worms are microfilariae, which enter the bloodstream. To complete the life cycle, microfilariae are ingested by another mosquito vector, in which they develop into new infective larvae. Chronic inflammation and lymphatic vessel damage can cause the gross lymphedema and skin changes of elephantiasis.

Citation: Allen J, Liu L. 2004. Immunity to Parasitic and Fungal Infections, p 469-496. In Pier G, Lyczak J, Wetzler L (ed), Immunology, Infection, and Immunity. ASM Press, Washington, DC. doi: 10.1128/9781555816148.ch20
Permissions and Reprints Request Permissions
Download as Powerpoint
Image of Figure 20.7
Figure 20.7

Life cycle of . Trichuriasis is transmitted directly by a human fecal-oral route with no intermediate vector. Adult whipworms (so called because of their broad posterior section and thin tapering anterior section) live in the colon and cecum. Adult female worms release thousands of unembryonated eggs daily, which pass via the feces and embryonate in the soil. Infection is acquired when infective eggs from the soil are accidentally transported to the mouth via unclean hands or contaminated food or water and are swallowed. After ingestion, the embryonated eggs hatch in the small bowel, releasing larvae that mature and then migrate to the large bowel.

Citation: Allen J, Liu L. 2004. Immunity to Parasitic and Fungal Infections, p 469-496. In Pier G, Lyczak J, Wetzler L (ed), Immunology, Infection, and Immunity. ASM Press, Washington, DC. doi: 10.1128/9781555816148.ch20
Permissions and Reprints Request Permissions
Download as Powerpoint
Image of Figure 20.8
Figure 20.8

IL-12 and parasite infection. (A) Early in infection with intracellular parasites, IL-12 is produced by phagocytic cells and induces the production of IFN-γ by NK cells and T cells. This early production of IFN-γ may help control infection by immediately activating macrophages. In addition, IL-12 and the IL-12- driven cytokine IFN-γ favor the development of parasite-specific TH1 cells, in addition to inducing the production of high levels of IFN-γ by already differentiated TH1 cells. (B) This early production of IL-12 is functionally analogous to the early induction of IL-4 synthesis by helminthic parasites, which drives TH2 development. That helminthic parasites do not induce production of IL-12 may contribute to the development of TH2 as a default pathway. (C) If IL-12 is added early during helminthic infection, the normal induction of TH2 cells is prevented, and responses such as IgE synthesis and eosinophil production are significantly reduced.

Citation: Allen J, Liu L. 2004. Immunity to Parasitic and Fungal Infections, p 469-496. In Pier G, Lyczak J, Wetzler L (ed), Immunology, Infection, and Immunity. ASM Press, Washington, DC. doi: 10.1128/9781555816148.ch20
Permissions and Reprints Request Permissions
Download as Powerpoint
Image of Figure 20.9
Figure 20.9

Murine leishmaniasis model. Experimental models of infection have provided the most dramatic illustrations of the impact of TH-cell subsets on disease outcome. Susceptible BALB/c or resistant C57BL/6 mice when inoculated in the footpad with L. major develop a local swelling at the site of infection. In BALB/c mice, the parasites disseminate throughout the body and the mice die by 8 weeks postinfection. However, in C57BL/6 mice, infection remains localized and the footpad swelling heals. These mice are resistant to reinfection. Susceptible BALB/c mice produce high levels of IL-4 and little IFN-γ in response to parasite antigen, while the reverse pattern is seen with the resistant C57BL/6 mice. Susceptible mice can be made resistant by the addition of antibody to IL-4 within the first few days of infection. In addition, normally resistant mice develop disseminated disease if given antibody to IFN-γ. Antibody to IL-4 blocks the induction of TH2 cells that downregulate protective TH1 responses, while antibody to IFN-γ blocks the ability of TH1 cells to activate macrophages.

Citation: Allen J, Liu L. 2004. Immunity to Parasitic and Fungal Infections, p 469-496. In Pier G, Lyczak J, Wetzler L (ed), Immunology, Infection, and Immunity. ASM Press, Washington, DC. doi: 10.1128/9781555816148.ch20
Permissions and Reprints Request Permissions
Download as Powerpoint
Image of Figure 20.10
Figure 20.10

Murine model. Experimental infection with the intestinal helminth provides a clear example of the ability of TH2 cells to mediate disease resolution. By 20 days postinfection, resistant BALB.K mice have expelled all the worms from the gut (top right). In contrast, the susceptible B10.BR mice establish a chronic infection and are incapable of expelling worms at any time point (top left). A strikingly different pattern of cytokine secretion is seen in these two strains. The resistant mice produce high levels of TH2 cytokines, which are detectable when parasites are cleared from the intestine. The susceptible mice produce low levels of TH2 cytokines but high levels of the TH1 cytokine IFN-γ soon after infection. Antibodies that block IL-4 cause BALB.K mice to establish chronic worm infection (bottom right), while antibodies that block IFN-γ help B10.BR mice to expel the worms (bottom left).

Citation: Allen J, Liu L. 2004. Immunity to Parasitic and Fungal Infections, p 469-496. In Pier G, Lyczak J, Wetzler L (ed), Immunology, Infection, and Immunity. ASM Press, Washington, DC. doi: 10.1128/9781555816148.ch20
Permissions and Reprints Request Permissions
Download as Powerpoint
Image of Figure 20.11
Figure 20.11

TNF and severe malaria. Large quantities of IL-1 and TNF believed to be important in pathogenesis are produced in people infected with . These cytokines, when administered exogenously, can reproduce the fever and nonspecific symptoms of malaria in humans. Overproduction of TNF is thought to be responsible for many of the life-threatening and severe pathologies associated with complicated malaria, including high fevers, hypoglycemia, and cerebral malaria. RBCs parasitized by adhere to small venule endothelial cells, causing microvascular occlusion. Parasites sequestered in brain vessels may stimulate local production of high levels of IL-1 and TNF. NO produced by cerebral endothelium in response to high levels of IL-1 and/or TNF may be directly responsible for neurologic symptoms of malaria by interfering with neurotransmission. Adapted from Fig. 14.3 (p. 317) of K. S. Warren (ed.), (Blackwell Science, Boston, Mass., 1993).

Citation: Allen J, Liu L. 2004. Immunity to Parasitic and Fungal Infections, p 469-496. In Pier G, Lyczak J, Wetzler L (ed), Immunology, Infection, and Immunity. ASM Press, Washington, DC. doi: 10.1128/9781555816148.ch20
Permissions and Reprints Request Permissions
Download as Powerpoint
Image of Figure 20.12
Figure 20.12

TH1/TH2-cell differentiation induced by eggs. The protective TH2 pattern of cytokine secretion in schistosomiasis begins only when the adult worms start to deposit eggs. However, the immune response that generates the egg granuloma is highly complex and involves a dynamic interplay between TH-cell subsets and a variety of inflammatory cells, including both activated macrophages and eosinophils. (A) The T-cell-dependent inflammatory response to the eggs is initially a mixed TH1 and TH2 response. TNF-α produced by both egg-specific T cells and macrophages recruited into the site is a key cytokine in the full development of the egg granuloma. (B) With time the overall inflammatory response subsides and the granuloma becomes fully TH2 mediated. Slow release of soluble egg antigens may be responsible for the shift to TH2 responses. Among these antigens are the Lewis trisaccharide, which stimulates (red arrow) a specific subset of B cells to proliferate and produce large quantities of IL-10. IL-10 can downregulate the expression of costimulatory molecules on antigen-presenting cells (APCs) and is the cytokine most responsible for the downmodulation of granuloma size that occurs over time.

Citation: Allen J, Liu L. 2004. Immunity to Parasitic and Fungal Infections, p 469-496. In Pier G, Lyczak J, Wetzler L (ed), Immunology, Infection, and Immunity. ASM Press, Washington, DC. doi: 10.1128/9781555816148.ch20
Permissions and Reprints Request Permissions
Download as Powerpoint
Image of Figure 20.13
Figure 20.13

Immune effector mechanisms involved in killing of schistosome larvae. (A) Direct killing by cytokine-activated macrophages. In the mouse model, infective schistosome larvae (schistosomulae) induce an initial TH1 response with secretion of IFN-γ, which activates macrophages to produce NO, which in turn kills the parasites. (B) In ADCC, a foreign organism is coated by specific antibody, which then binds effector cells that kill the pathogen. In vitro, schistosomulae of can be killed by a combination of eosinophils and antibodies from infected patients. IgE antibodies promote this reaction by binding to specific Fc receptors on the eosinophil surface. Eosinophils adhering to the antibody-coated schistosomulum degranulate and release reactive oxygen intermediates and other toxins that kill the organism over about 24 hours. Platelets and macrophages possess similar cytotoxic properties in vitro. Whether ADCC plays a major role in actual clinical immunity is unknown, however, and a protective role for eosinophils or IgE in human helminthic infections in vivo is supported only by circumstantial evidence and epidemiologic studies.

Citation: Allen J, Liu L. 2004. Immunity to Parasitic and Fungal Infections, p 469-496. In Pier G, Lyczak J, Wetzler L (ed), Immunology, Infection, and Immunity. ASM Press, Washington, DC. doi: 10.1128/9781555816148.ch20
Permissions and Reprints Request Permissions
Download as Powerpoint
Image of Figure 20.14
Figure 20.14

Immunity to the liver stages of malaria parasites. Vaccination of laboratory animals with irradiated sporozoites can provide protection against reinfection in experimental models. This immunity is T cell dependent and is due to the development of antibodies to the invading sporozoite and to cell-mediated immunity to the pre-erythrocytic liver stages (merozoites). The latter involves cytotoxic T cells that lyse the infected hepatocytes and the generation of cytokines that mediate resistance. In addition to killing directly, T cells produce IFN-γ, which inhibits growth of the parasite within the liver cells. Other lymphokines, such as IL-6, TNF, and IL-1, also inhibit intracellular development of the parasite. IL-6 can be produced directly by liver cells in response to IFN-γ, TNF, and IL-1. IL-6 and IFN-γ exert their effect on parasite development by inducing the production of NO by infected hepatocytes and by Kupffer cells (liver macrophages). These cytokines can also induce the expression of MHC class II molecules on hepatocytes, thereby allowing lysis by CD4 cells and by CD8 MHC class I-restricted cells. IL-6 along with IL-1 and TNF induces hepatocytes to release C-reactive protein (CRP), which can bind to the sporozoite and inhibit the early stages of development.

Citation: Allen J, Liu L. 2004. Immunity to Parasitic and Fungal Infections, p 469-496. In Pier G, Lyczak J, Wetzler L (ed), Immunology, Infection, and Immunity. ASM Press, Washington, DC. doi: 10.1128/9781555816148.ch20
Permissions and Reprints Request Permissions
Download as Powerpoint
Image of Figure 20.15
Figure 20.15

Cytokine and antibody profiles during lymphatic filariasis. Lymphatic filariasis presents as a wide spectrum of clinical situations in different patients, ranging from individuals with a high number of parasites but few clinical symptoms to those with chronic disease but few detectable parasites. The nature of the immune response in these individuals is equally diverse. Following infection with filarial nematodes, early immune responses are consistent with a TH1 profile. However, with the appearance of parasite microfilariae in the bloodstream, TH2 cytokines become dominant, with a rapid disappearance of T-cell proliferative responses and a striking increase in synthesis of parasite-specific IgG4. The induction of T-cell tolerance to the parasite is most apparent in the TH1 subset. In individuals with developed disease, this tolerance is broken, and responses of both the TH1 and TH2 types increase dramatically. Thus, both increased cell-mediated responses and extremely high levels of serum IgE have been implicated in pathogenesis. However, it should also be noted that both TH1 and TH2 responses to filarial antigens are present in individuals who are immune to reinfection; therefore, both types of TH response may be important in host protection as well as pathogenesis. Redrawn from Maizels and Lawrence, 7:271–275, 1992, with permission.

Citation: Allen J, Liu L. 2004. Immunity to Parasitic and Fungal Infections, p 469-496. In Pier G, Lyczak J, Wetzler L (ed), Immunology, Infection, and Immunity. ASM Press, Washington, DC. doi: 10.1128/9781555816148.ch20
Permissions and Reprints Request Permissions
Download as Powerpoint
Image of Figure 20.16
Figure 20.16

Antigenic variation in African trypanosomes. African trypanosomiasis (sleeping sickness) is characterized by successive waves of parasite proliferation in the bloodstream, the result of antigenic variation in the parasite population. The peaks of parasitemia are observed in mice infected experimentally with a single clone of as well as in natural infections in humans. Each wave is due to a new antigenic variant of the parasite (e.g., clone A, B, or C) that expresses a new VSG. Each decline is a result of a specific antibody response to that VSG. A few individual trypanosomes survive by expressing a different VSG, thus giving rise to a new wave of clonal parasites. The photo is of a blood smear showing a trypanosome.

Citation: Allen J, Liu L. 2004. Immunity to Parasitic and Fungal Infections, p 469-496. In Pier G, Lyczak J, Wetzler L (ed), Immunology, Infection, and Immunity. ASM Press, Washington, DC. doi: 10.1128/9781555816148.ch20
Permissions and Reprints Request Permissions
Download as Powerpoint
Image of Figure 20.17
Figure 20.17

erythrocyte membrane proteins (PfEMP1) mediate both antigenic variation and cytoadherence in malaria. Erythrocytes parasitized by express a variant antigen from the PfEMP1 family, which is concentrated on surface knobs and mediates attachment of the infected erythrocyte to the vascular endothelium. Different PfEMP1 proteins likely mediate binding to different endothelial cell surface receptors, including intercellular adhesion molecule 1 (ICAM-1), vascular cell adhesion molecule 1 (VCAM-1), E-selectin, CD36, and the matrix protein thrombospondin. The high frequency with which antigenic variants of PfEMP1 arise in the parasite population allow new antigenically variant malarial parasites to escape antibody-mediated immune destruction.

Citation: Allen J, Liu L. 2004. Immunity to Parasitic and Fungal Infections, p 469-496. In Pier G, Lyczak J, Wetzler L (ed), Immunology, Infection, and Immunity. ASM Press, Washington, DC. doi: 10.1128/9781555816148.ch20
Permissions and Reprints Request Permissions
Download as Powerpoint
Image of Figure 20.18
Figure 20.18

Systemic mycoses. Some fungal species grow only as molds; others grow only as yeast forms. Species that can grow in either form are known as dimorphic fungi and include many of the clinically important opportunistic fungal pathogens. Generally, these species grow in mycelial forms or as mold at room temperature but as yeast in the human body. (A) Invasive pulmonary aspergillosis in a patient with leukemia. (B) Growth of an sp. on an agar culture plate. (C) yeast cells in the spinal fluid of a patient with AIDS with cryptococcal meningitis. Slide is stained with India ink to highlight the yeast capsule. (D) Yeast cells of , stained with periodic acid-Schiff stain, in the liver of a patient with disseminated cryptococcosis. Some of the yeast cells have characteristic narrow-based buds.

Citation: Allen J, Liu L. 2004. Immunity to Parasitic and Fungal Infections, p 469-496. In Pier G, Lyczak J, Wetzler L (ed), Immunology, Infection, and Immunity. ASM Press, Washington, DC. doi: 10.1128/9781555816148.ch20
Permissions and Reprints Request Permissions
Download as Powerpoint

References

/content/book/10.1128/9781555816148.chap20
1. Beeson, J. G.,, and G. V. Brown. 2002. Pathogenesis of Plasmodium falciparum malaria: the roles of parasite adhesion and antigenic variation. Cell. Mol. Life Sci. 59:258271.
2. Behm, C. A.,, and K. S. Ovington. 2000. The role of eosinophils in parasitic helminth infections. Parasitol. Today 16:202209.
3. Carruthers, V. B. 2002. Host cell invasion by the opportunistic pathogen Toxoplasma gondii. Acta Trop. 81:111122.
4. Claudia, M.,, A. Bacci,, B. Silvia,, R. Gaziano,, A. Spreca,, and L. Romani. 2002. The interaction of fungi with dendritic cells: implications for TH immunity and vaccination. Curr. Mol. Med. 2:507524.
5. Crameri, R.,, and K. Blaser. 2002. Allergy and immunity to fungal infections and colonization. Eur. Respir. J. 19:151157.
6. Denkers, E.,, and R. T. Gazzinelli. 1998. Regulation and function of T-cell-mediated immunity during Toxoplasma gondii infection. Clin. Microbiol. Rev. 11:569588.
7. Engman, D. M.,, and J. S. Leon. 2002. Pathogenesis of Chagas heart disease: role of autoimmunity. Acta Trop. 81:123132.
8. Kennedy, M. W.,, and W. Harnett. (ed.). 2001. Parasitic Nematodes: Molecular Biology, Biochemistry and Immunology. CABI Publishing, Wallingford, Oxon, United Kingdom.
9. Lawrence, C. E. 2003. Is there a common mechanism of gastrointestinal nematode expulsion? Parasite Immunol. 25: 271281.
10. Lilic, D. 2002. New perspectives on the immunology of chronic mucocutaneous candidiasis. Curr. Opin. Infect. Dis. 15:143147.
11. Maizels, R. M.,, and M. Yazdanbakhsh. 2003. Immune regulation by helminth parasites: cellular and molecular mechanisms. Nat. Rev. Immunol. 3:733744.
12. Malaguarnera, L.,, and S. Musumeci. 2002. The immune response to Plasmodium falciparum malaria. Lancet Infect. Dis. 2:472478.
13. Markell, E.,, W. A. Krotoski,, and D. T. John. 1998. Markell and Voge’s Medical Parasitology, 8th ed. W. B. Saunders and Co., Philadelphia, Pa.
14. Pearce, E. J.,, and A. S. MacDonald. 2002. The immunobiology of schistosomiasis. Nat. Rev. Immunol. 2:499511.
15. Rogers, K. A.,, G. K. DeKrey,, M. L. Mbow,, R. D. Gillespie,, C. I. Brodskyn,, and R. G. Titus. 2002. Type 1 and type 2 responses to Leishmania major. FEMS Microbiol. Lett. 209:17.
16. Sacks, D.,, and A. Sher. 2002. Evasion of innate immunity by parasitic protozoa. Nat. Immunol. 3:10411047.
17. Zambrano-Villa, S.,, D. Rosales-Borjas,, J. C. Carrero,, and L. Ortiz-Ortiz. 2002. How protozoan parasites evade the immune response. Trends Parasitol. 18:272278.

Tables

Generic image for table
Table 20.1

Major parasitic infections of humans

Citation: Allen J, Liu L. 2004. Immunity to Parasitic and Fungal Infections, p 469-496. In Pier G, Lyczak J, Wetzler L (ed), Immunology, Infection, and Immunity. ASM Press, Washington, DC. doi: 10.1128/9781555816148.ch20
Generic image for table
Table 20.2

The potential role of T-cell subsets in parasitic diseases

Citation: Allen J, Liu L. 2004. Immunity to Parasitic and Fungal Infections, p 469-496. In Pier G, Lyczak J, Wetzler L (ed), Immunology, Infection, and Immunity. ASM Press, Washington, DC. doi: 10.1128/9781555816148.ch20
Generic image for table
Table 20.3

Some mechanisms of parasite immune evasion

Citation: Allen J, Liu L. 2004. Immunity to Parasitic and Fungal Infections, p 469-496. In Pier G, Lyczak J, Wetzler L (ed), Immunology, Infection, and Immunity. ASM Press, Washington, DC. doi: 10.1128/9781555816148.ch20

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