Immunoglobulin M production and immunosuppression in trypanosomiasis: a linking hypothesis

Terry, R. J.; Freeman, Joan; Hudson, K.M.; Longstaffe, J. A.

doi:10.1016/0035-9203(73)90167-3

Cited by 19 publications

(4 citation statements)

References 0 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…However, since these acids were first detected by a hemolytic assay and since anemia is so important in the pathogenesis of trypanosomiasis, it was necessary to determine whether these fatty acids contributed to hemolysis in vivo in a similar manner to that observed in blackwater fever (93). Further investigations showed that the hemolytic properties of these trypanosome-derived FFAs were probably not significant in vivo, at least not in cattle infected with T. congolense (172). The major reason for this is that FFAs are rapidly bound to serum albumin in vivo and cannot cause hemolysis when in the bound state (50,163,164).…”

Section: Factors Released By Living Trypanosomesmentioning

confidence: 99%

Biologically active products from African Trypanosomes.

Tizard¹,

Nielsen²,

Seed³

et al. 1978

Microbiological Reviews

View full text Add to dashboard Cite

Section: Factors Released By Living Trypanosomesmentioning

confidence: 99%

Biologically active products from African Trypanosomes.

Tizard¹,

Nielsen²,

Seed³

et al. 1978

Microbiological Reviews

View full text Add to dashboard Cite

“…Massive expansion of B-cells has often been used to explain the superabundance of IgM in trypanosome infections (Terry et al 1973;Urquhart et al 1973;Murray et al 1974), and one would therefore have expected much higher levels of IgM in group B. However, this lower level may have been attributable to the observation that the present study assayed IgM responses speci®c for the inducing trypanosome clone rather than just the measurement of hypergammaglobulinaemia, which indicates pathological changes in Ig levels during trypanosomosis without regard for parasite speci®city.…”

Section: Discussionmentioning

confidence: 82%

Changes in peripheral blood lymphocyte subpopulations and parasite-specific antibody responses in Trypanosoma evansi infection of sheep

Onah

Hopkins

Luckins

1999

Parasitology Research

View full text Add to dashboard Cite

This paper reports on changes in the lymphocyte composition of the peripheral blood in sheep infected with Trypanosoma evansi. In addition, parasite-specific IgG1 and IgM antibody responses were monitored using a double-sandwich enzyme-linked immunosorbent assay (ELISA) technique. Eight sheep were infected with 2 x 10(6) T. evansi TREU 2143. The infection was characterised by chronicity and ended in self-cure in two of the sheep. These two sheep were designated group A, whereas the other six sheep, which remained parasitaemic until treated, were designated group B. Analysis of the peripheral blood lymphocytes (PBLs) by indirect immunofluorescence staining and flow cytometry revealed significant alterations in the numbers of T- and B-cell subsets detected in all infected sheep. In group A, whereas the numbers of CD8+ cells decreased, CD4+ cells showed marginal decreases, remaining at or above pre-infection figures and resulting in increase in the CD4:CD8 ratio. In group B, CD8+ cells showed few marginal decreases, being at or above pre-infection figures most of the time, whereas CD4+ cells decreased significantly from day 26 post infection (p.i.) such that the CD4:CD8 ratio decreased. Infection also resulted in significant increases (P < 0.001) as of day 26 p.i. in circulating B-cells in group B as shown by the numbers of sIg+, CD45R+, CD1+ and major histocompatibility complex (MHC) II+ cells. The increases, however, were moderate and biphasic in group A. T. evansi-specific IgM and IgG1 antibody isotypes were detected in all infected sheep, but their levels were significantly higher in group A than in group B (IgM P < 0.05; IgGI P < 0.01). In addition, although an initially higher level of IgM response was subsequently replaced by a higher level of IgG1 response in group A, this was never the case in group B until after drug treatment.

show abstract

“…Consistent with previous data, a marked leucopenia could be observed in the animals around the same period when parasites could first be detected in peripheral blood. Strikingly, multiple peaks of white blood cell counts could be observed in subsequent days in all infected monkeys, suggesting that despite the immunosuppression described elsewhere for trypanosomiasis, 72 , 73 , 75 some myeloid precursor cells are still able to proliferate in response to the multiple waves of parasitemia. Combined, these observations suggest that non-murine models might be a better way forward in future vaccine research, as they would circumvent intrinsic artifacts that are related to experimental trypanosome infections in the mouse model.…”

Section: Murine Model For African Trypanosomiasis: Introducing Artifamentioning

confidence: 69%

“…A number of studies reported four decades ago, already described the following key facts of T. brucei infection: (1) The immune system is unable to react against unrelated new antigens upon infection 71 ; (2) there is a non-specific activation of immunoglobulin production 72 ; (3) the cellular components of the humoral response are no longer coordinated upon infection 73 ; (4) despite a sustained plasma cell hyperplasia, failure of antibody production (both IgM and IgG) at the cellular level occurs at 2–4 weeks post infection 74 . Those findings were directly associated to the presence of living trypanosomes, since the immune competence was restored after treatment, 75 and define the basis of immunosuppression, a hallmark of trypanosome infections.…”

Section: The Main Pitfalls Of Anti-trypanosome Vaccination: Antigenicmentioning

confidence: 99%

Vaccination against trypanosomiasis

Greca

Magez

2011

Human Vaccines

View full text Add to dashboard Cite

To date, human African trypanosomiasis (HAT) still threatens millions of people throughout sub-Sahara Africa, and new approaches to disease prevention and treatment remain a priority. It is commonly accepted that HAT is fatal unless treatment is provided. However, despite the well-described general symptoms of disease progression during distinct stages of the infection, leading to encephalitic complications, coma and death, a substantial body of evidence has been reported suggesting that natural acquired immunity could occur. Hence, if under favorable conditions natural infections can lead to correct immune activation and immune protection against HAT, the development of an effective anti-HAT vaccine should remain a central goal in the fight against this disease.
In this review, we will (1) discuss the vaccine candidates that have been proposed over the past years, (2) highlight the main obstacles that an efficient anti-trypanosomiasis vaccine needs to overcome and (3) critically reflect on the validity of the widely used murine model for HAT.

show abstract

Immunoglobulin M production and immunosuppression in trypanosomiasis: a linking hypothesis

Cited by 19 publications

References 0 publications

Biologically active products from African Trypanosomes.

Biologically active products from African Trypanosomes.

Changes in peripheral blood lymphocyte subpopulations and parasite-specific antibody responses in Trypanosoma evansi infection of sheep

Vaccination against trypanosomiasis

Contact Info

Product

Resources

About