title: Plasmodium chabaudi chabaudi infection in mice induces strong B cell responses and striking but temporary changes in splenic cell distribution.
abstract: B cells and Abs play a key role in controlling the erythrocytic stage of malaria. However, little is known about the way the humoral response develops during infection. We show that Plasmodium chabaudi chabaudi causes major, but temporary changes in the distribution of leukocytes in the spleen. Despite these changes, an ordered response to infection develops, which includes vigorous extrafollicular growth of plasmablasts and germinal center formation. Early in the response, the lymphocytes in the T zone and follicles become widely spaced, and the edges of these compartments blur. This effect is maximal around the peak of parasitemia. Germinal centers are apparent by day 8, peak at day 20, and persist through day 60. Extrafollicular foci of plasmablasts are visible from day 4 and initiate a very strong plasma cell response. Initially, the plasma cells have a conventional red pulp distribution, but by day 10 they are unconventionally sited in the periarteriolar region of the white pulp. In this region they form clusters occupying part of the area normally filled by T cells. B cells are absent from the marginal zone for at least 30 days after the peak of infection, although flow cytometry shows their continued presence in the spleen throughout infection. Relatively normal splenic architecture is regained by day 60 of infection. These results show that the changes in splenic cell distribution are linked to the presence of parasites and do not seem to interfere with the development of the humoral response.
authors.affiliation: Division of Parasitology, National Institute for Medical Research, London, United Kingdom.
authors.forename: Ariel H
authors.initials: AH
authors.lastname: Achtman
authors.forename: Mahmood
authors.initials: M
authors.lastname: Khan
authors.forename: Ian C M
authors.initials: IC
authors.lastname: MacLennan
authors.forename: Jean
authors.initials: J
authors.lastname: Langhorne
mesh_terms: D000818:Animals; D017209:Apoptosis / Q000276:immunology; D016175:B-Lymphocyte Subsets / Q000276:immunology* / Q000469:parasitology / Q000473:pathology*; D002454:Cell Differentiation / Q000276:immunology; D018450:Disease Progression; D005260:Female; D018858:Germinal Center / Q000276:immunology / Q000469:parasitology / Q000473:pathology; D018655:Lymphocyte Count; D008288:Malaria / Q000276:immunology* / Q000469:parasitology / Q000473:pathology*; D051379:Mice; D008810:Mice, Inbred C57BL; D016788:Plasmodium chabaudi / Q000276:immunology*; D013154:Spleen / Q000276:immunology* / Q000469:parasitology / Q000473:pathology*; D013158:Splenic Diseases / Q000276:immunology / Q000469:parasitology / Q000473:pathology; D013997:Time Factors