Skip to main page content
U.S. flag

An official website of the United States government

Dot gov

The .gov means it’s official.
Federal government websites often end in .gov or .mil. Before sharing sensitive information, make sure you’re on a federal government site.

Https

The site is secure.
The https:// ensures that you are connecting to the official website and that any information you provide is encrypted and transmitted securely.

Access keys NCBI Homepage MyNCBI Homepage Main Content Main Navigation
. 1974 Nov;27(5):815-24.

The nature of immunosuppression in Trypanosoma brucei infections in mice. I. The role of the macrophage

The nature of immunosuppression in Trypanosoma brucei infections in mice. I. The role of the macrophage

P K Murray et al. Immunology. 1974 Nov.

Abstract

The functional integrity of the mononuclear phagocytic system (MPS) in mice infected with Trypanosoma brucei was investigated with regard to its possible significance in the aetiology of the immunosuppression characteristic of this disease.

In infected mice the spleens and lymph nodes were grossly enlarged, and on histological examination it was shown that the MPS of the liver, lymph nodes, spleen and bone marrow was markedly expanded. Macrophages presented an active appearance and often contained cellular debris. Clearance of intravenously injected sheep red blood cells (SRBC) was increased, in that 1 hour after injection, 2–6 times more 51Cr-labelled SRBC had disappeared from the circulation of infected, compared to uninfected mice; this was due largely to an increased uptake by the expanded phagocytic system of the liver.

The intrinsic immunogenic potential of individual macrophages appeared to be unimpaired as judged by the ability of SRBC-containing macrophages from infected mice to elicit a response in syngeneic normal recipient mice.

It was concluded that the only evidence that immunosuppression might be associated with an altered activity of the MPS was an increased hepatic uptake of particulate antigen with a relative failure of splenic uptake. Together these might be responsible for a reduction in the concentration of antigen in the tissues of an enlarged spleen below the level necessary to initiate the formation of antibody.

PubMed Disclaimer

References

    1. J Reticuloendothel Soc. 1965 Dec;2(5):406-19 - PubMed
    1. J Immunol. 1967 Oct;99(4):744-50 - PubMed
    1. Trans R Soc Trop Med Hyg. 1970;64(6):797-817 - PubMed
    1. Clin Exp Immunol. 1971 Mar;8(3):467-78 - PubMed
    1. Br J Exp Pathol. 1972 Feb;53(1):40-3 - PubMed

MeSH terms

LinkOut - more resources