B-Cell Outgrowth and Ligand-Specific Production of IL-10 Correlate with Th2 Dominance in Certain Parasitic Diseases

Palanivel, V.; Posey, C.; Hörauf, A.; Solbach, Werner; Piessens, Willy F.; Harn, Donald A.

doi:10.1006/expr.1996.0102

Cited by 90 publications

(69 citation statements)

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“…The hypothesis that these molecules are used by the pathogens to weaken the host immune response and that these are of central importance in the pathogenesis caused by the infection has been proposed (Reina-SanMartín et al 2000a). In this regard, it is worthy to note that infection with L major increases the splenic B220 ϩ B cell subset in BALB/c mice (Palanivel et al 1996). In line with this result, it can be speculated that Hsp70 and Hsp83 can serve Leishmania to deviate the immune response into a nonspecific activation of immune cells.…”

Section: Discussionsupporting

confidence: 58%

The heat shock proteins, Hsp70 and Hsp83, of Leishmania infantum are mitogens for mouse B cells

Rico¹,

Gironès²,

Fresno³

et al. 2002

Cell Stress Chaper

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Extending earlier studies, this report demonstrates that Leishmania infantum heat shock proteins (Hsps), Hsp70 and Hsp83, expressed as recombinant proteins fused to the Escherichia coli maltose-binding protein (MBP), are potent mitogens for murine splenocytes. The response was not due to lipopolysaccharide (LPS) because the stimulatory activity of Hsp preparations was sensitive to boiling and trypsin treatments, whereas the corresponding activity of LPS was resistant to both treatments. It was found that in vitro incubation of spleen cells with the Leishmania Hsps leads to the expansion of CD220-bearing populations, suggesting a direct effect of these proteins on B lymphocytes. In fact, splenocytes from B cell-deficient mice did not proliferate in response to the Leishmania Hsps. In contrast, spleen cells from athymic nude mice were significantly stimulated by these recombinant proteins as an indication that the MBP-Hsp70 and MBP-Hsp83 recombinant proteins behave as T cell-independent mitogens of B cells. Furthermore, both proteins were able to induce proliferation on B cell populations purified from BALB/c spleen.

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Section: Discussionsupporting

confidence: 58%

The heat shock proteins, Hsp70 and Hsp83, of Leishmania infantum are mitogens for mouse B cells

Rico¹,

Gironès²,

Fresno³

et al. 2002

Cell Stress Chaper

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“…The relationship between repeated exposure and development of fibrosis may result from the expansion egg-Ag specific lymphocytes because of shared Ags among developing larvae, adult worms, and ova (40). Some of these shared Ags have been identified as immunogenic carbohydrates that have been shown to preferentially promote T cell differentiation to a Th2-type phenotype (41,42) and may participate in TGF-␤ production. Therefore, repeated exposure to developing larvae and those released by adult worms (43) may preferentially expand this population of egg Agspecific lymphocytes compared with other immunogenic Ags unique to ova that stimulate a more Th1-type phenotype (44).…”

Section: Discussionmentioning

confidence: 99%

Repeated Exposure Induces Periportal Fibrosis inSchistosoma mansoni-Infected Baboons: Role of TGF-β and IL-4

Farah

Mola

Kariuki

et al. 2000

The Journal of Immunology

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Recently, we observed that repeated Schistosoma mansoni infection and treatment boost Th2-associated cytokines and TGF-β production in baboons. Other studies have shown that some chronically infected baboons develop hepatic fibrosis. Because TGF-β, IL-2, and IL-4 have been shown to participate in development of fibrosis in murine schistosomiasis, the present study examined whether repeated exposure stimulates hepatic fibrosis in olive baboons. To test this hypothesis, animals were exposed to similar numbers of S. mansoni cercariae given once or repeatedly. After 19 wk of infection, animals were cured with praziquantel and reinfected once or multiple times. Hepatic granulomatous inflammation and fibrosis were assessed from serial liver biopsies taken at weeks 6, 9, and 16 after reinfection and egg Ag (schistosome egg Ag)-specific cytokine production by PBMC were measured simultaneously. Periportal fibroblast infiltration and extracellular matrix deposition (fibrosis), angiogenesis, and biliary duct hyperplasia developed in some animals. The presence and amount of fibrosis directly correlated with the frequency of exposure. Fibrosis was not associated with adult worm or tissue egg burden. The amount of fibrosis correlated with increased schistosome egg Ag-driven TGF-β at 6, 9, and 16 wk postinfection (rs = 0.9, 0.8, and 0.54, respectively, all p < 0.01) and IL-4 production (p = 0.02) at 16 wk postinfection and not IFN-γ, IL-2, IL-5, or IL-10. These data suggest that repeated exposure is a risk factor for periportal fibrosis by a mechanism that primes lymphocytes to produce increased levels of profibrotic molecules that include TGF-β and IL-4.

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“…and Schistosoma spp.) there is also a nonspecific polyclonal B-cell proliferation event that contributes to the maintenance of the pathogen in vivo by down-regulating the humoral and cell-mediated immune response (Palanivel et al 1996). Observations reveal no apparent pathologic changes in elk due to T. cervi infection, suggesting more-subtle effects on the host by the parasite (Kingston et al 1981).…”

Section: Introductionmentioning

confidence: 86%

“…The identification of the B. abortus protein PrpA as a nonspecific B-cell mitogen and inducer of IL-10 has strengthened this hypothesis (Montes et al 2002;Spera et al 2006). Through this proliferation and IL-10 secretory events, it confers a specific advantage on the pathogen, allowing it to avoid specific and directed humoral and cell-mediated immune responses, leading to modulation of the host response (Palanivel et al 1996;Spera et al 2006). Some other endemic pathogens in elk are thought to utilize a similar mechanism.…”

Section: Introductionmentioning

confidence: 88%

“…Surveys in the 1970s showed that 71% of free-ranging elk in western Wyoming were infected with T. cervi (Kingston et al 1981). Trypanosoma cruzi and other blood parasites have been implicated in inducing chronic infections by modulating the host immune response via mechanisms such as those mediated by PrpA (Palanivel et al 1996;Montes et al 2002;Chamond et al 2005). We propose that T. cervi acts similar to other trypanosomes in suppressing immune activation.…”

Section: Introductionmentioning

confidence: 99%

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INFECTION OF C57BL/6 MICE BYTRYPANOSOMA MUSCULIMODULATES HOST IMMUNE RESPONSES DURINGBRUCELLA ABORTUSCOCOLONIZATION

Lowry

Leonhardt

Yao

et al. 2014

Journal of Wildlife Diseases

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ABSTRACT:Brucellosis, which results in fetal abortions in domestic and wildlife animal populations, is of major concern in the US and throughout much of the world. The disease, caused by Brucella abortus, poses an economic threat to agriculture-based communities. A moderately efficacious live attenuated vaccine (B. abortus strain RB51) exists. However, even with vaccine use, outbreaks occur. Evidence suggests that elk (Cervus canadensis), a wild host reservoir, are the source of recent outbreaks in domestic cattle herds in Wyoming, USA. Brucella abortus establishes a chronic, persistent infection in elk. The molecular mechanisms allowing the establishment of this persistent infective state are currently unknown. A potential mechanism could be that concurrent pathogen burdens contribute to persistence. In Wyoming, elk are chronically infected with Trypanosoma cervi, which may modulate host responses in a similar manner to that documented for other trypanosomes. To identify any synergistic relationship between the two pathogens, we simulated coinfection in the well-established murine brucellosis model using Trypanosoma musculi and B. abortus S19. Groups of C57BL/6 mice (Mus musculus) were infected with either B. abortus strain 19 (S19) or T. musculi or both. Sera were collected weekly; spleens from euthanized mice were tested to determine bacterial load near the end of normal brucellosis infection. Although changes in bacterial load were observed during the later stages of brucellosis in those mice coinfected with T. musculi, the most significant finding was the suppression of gamma interferon early during the infection along with an increase in interleukin-10 secretion compared with mice infected with either pathogen alone. These results suggest that immune modulatory events occur in the mouse during coinfection and that further experiments are warranted to determine if T. cervi impacts Brucella infection in elk.

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B-Cell Outgrowth and Ligand-Specific Production of IL-10 Correlate with Th2 Dominance in Certain Parasitic Diseases

Cited by 90 publications

References 0 publications

The heat shock proteins, Hsp70 and Hsp83, of Leishmania infantum are mitogens for mouse B cells

The heat shock proteins, Hsp70 and Hsp83, of Leishmania infantum are mitogens for mouse B cells

Repeated Exposure Induces Periportal Fibrosis inSchistosoma mansoni-Infected Baboons: Role of TGF-β and IL-4

INFECTION OF C57BL/6 MICE BYTRYPANOSOMA MUSCULIMODULATES HOST IMMUNE RESPONSES DURINGBRUCELLA ABORTUSCOCOLONIZATION

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